高频振荡通气联合部分液体通气治疗吸入性损伤的实验研究
|
摘要
吸入性损伤的发病率及死亡率一直很高,重度烧伤合并吸入性损伤病人是烧伤临床治疗上的重点和难点,病死率仍然高达50-60%。机械通气是治疗重度烧伤合并吸入性损伤不可缺少的手段之一,但常规机械通气可能产生和加重肺损伤。作为一种“保护性肺通气策略,高频振荡通气和部分液体通气日益受到重视。
本研究将新西兰大白兔制成蒸气吸入性损伤并急性呼吸衰竭模型,随机分组后采用四种机械通气模式进行治疗(CMV,CMV+PLV,HFOV及HFOV+PLV),分别在治疗后0.5,1.5,2.5及3.5h取动脉血行血气分析、血流动力学监测。通气治疗3.5h后,为评估四种机械通气模式对通气肺组织的炎症反应及肺损伤程度的影响,作了大体标本、组织病理学观察及肺组织损伤评分;使用酶联免疫吸附法(ELISA)检测肺组织匀浆中和血清中可溶性E-选择素、P-选择素、ICAM-1和ET-1的含量,用RT- PCR法测肺组织中E-选择素、P-选择素、ICAM-1和ET-1 mRNA表达。为评价四种机械通气模式对通气肺组织细胞凋亡的影响,应用TUNEL DNA片段末端标记方式(FragELTM)法检测肺组织细胞凋亡,采用RT- PCR法测肺组织匀浆中caspsase-3含量,应用逆转录聚合酶链反应(RT-PCR)技术检测肺组织caspsase-3 mRNA表达水平,用凝胶电泳条带成像系统照相分析结果。收集肺泡灌洗液细胞后分离出中性粒细胞,使用流式细胞仪Annexin V-FITC法检测中性粒细胞凋亡及坏死;肺泡灌洗上清液则进行各种炎性因子(E-选择素、P-选择素、ICAM-1和ET-1)总蛋白、丙二醛检测。结果:1.血气分析: 1)伤后各组动物PaO2均降至60mm Hg以下,各组致伤前与致伤后比较均有显著性差异(P<0.01),各组致伤前、致伤后(治疗前)血气组间比较均无显著性差异(P >0.05)。2).四个治疗组的PaO2在通气治疗0.5h后均明显上升,通气治疗3.5h内一直有良好的PaO2。3).HFOV组和HFOV+PLV组的PaO2、PaO2/FiO2在治疗治疗各时间点均分别高于相应时间点的CMV组和CMV+PLV组(P<0.05和P<0.01);CMV+PLV组在治疗1.5h、2.5h PaO2优于CMV组(P<0.05);HFOV+PLV组在治疗3.5h PaO2优于HFOV组(P<0.01)。4)肺泡气-动脉血氧分压差[P(A-a)O2]在各治疗组无统计学差异(P >0.05)。5)四个治疗组伤后各时相点的PaCO2均无明显变化(P >0.05)。2.肺组织病理学检查:HFOV组的损伤程度较CMV组明显减轻,HFOV+PLV组损伤最轻,CMV+PLV组次之,CMV组损伤最重。3.炎症反应:E-选择素、P-选择素和ICAM-1在肺组织和血清中的含量及其在肺组织中mRNA表达,在HFOV组及HFOV+PLV组分别低于CMV组及CMV+PLV组,组间比较统计学上有显著差异(p<0.01)。E-选择素、P-选择素和ICAM-1在肺组织和血清中的含量及其在肺组织中mRNA表达在CMV组和HFOV组分别高于CMV+PLV组及HFOV+PLV组.ET-1在肺组织和血清中的含量及其在肺组织中mRNA表达在CMV、HFOV、HFOV+PLV,及CMV+PLV四组间比较统计学上无显著性差异(P>0.05)。4.细胞凋亡:肺组织细胞凋亡及评分指数,HFOV组及HFOV+PLV组分别较CMV、CMV+PLV明显减少,两组比较有显著差异(p<0.01)。而CMV+PLV组和HFOV+PLV组又较CMV组和HFOV组减少,两组比较也有显著性差异(p<0.05)。caspsase-3活性及caspsase-3 mRNA表达,在HFOV及HFOV+PLV组,分别较CMV,CMV+PLV组明显减少,组间比较有显著差异(p<0.01)。而HFOV+PLV及CMV+PLV组又分别较HFOV和CMV组减少,两组比较也有显著性差异(p<0.05)。5.肺泡灌洗液: HFOV+PLV组中性粒细胞凋亡率和早期凋亡率较其它三组高,同时坏死细胞数量也最少。HFOV组及HFOV+PLV组中中性粒细胞早期凋亡率较CMV组和CMV+PLV组明显升高,差别有显著性(P<0.01);CMV组和CMV+PLV组中性粒细胞晚期凋亡率较HFOV组及HFOV+PLV组高,差异明显(P<0.01)。四个治疗组中CMV组中性粒细胞凋亡率最低,但与CMV+PLV组比较无明显差异(P>0.05)。总蛋白、丙二醛浓度各治疗组间的差异无统计学意义(P>0.05)。肺泡灌洗液E-选择素、P-选择素、ICAM-1和ET-1浓度各治疗组间的差异无统计学意义(P>0.05)。结论:与其它三种通气模式相比,HFOV联合PLV能提高蒸汽吸入性损伤兔的氧合水平,降低肺组织内粘附分子浓度及mRNA表达,减少肺组织调亡,减少肺组织内caspsase-3活性及caspsase-3 mRNA表达,提高肺泡中性粒细胞凋亡,减少肺组织内炎性细胞浸润,减轻肺损伤。是治疗吸入性损伤并呼吸衰竭较好的方法。
Inhalation injury with respiratory failure or acute lung injury has high morality, need to be supported with ventilator .Conventional mandatory ventilation could cause ventilator-induced lung injury and could deteriorate pulmonary injury. As the protective lung ventilation strategy, high frequency oscillatory ventilation (HFOV) and partial liquid ventilation have important significance. Methods Thirty-two New Zealand rabbits were randomly divided into four groups after acute respiratory failure models caused by severe steam inhalation injury were established. Then they were ventilated by CMV,HFOV,CMV+PLV or HFOV+PLV,respectively. Femoral arterial blood samples were obtained respectively at 0.5,1.5,2.5,3.5h treatment timepoints for blood gas examination. respiratory mechanics and hemodynamic parameters were recorded. After the experimental period,the lowest lobe of the right lung was weighed for calculating weight ratio of lung water and lung tissue [(W-D)/W] , the middle lobe in the right lung were excised for histological sections. The right middle lobe of rabbit was excised for the examination of mRNA expression of E-selectin, P-selectin,ICAM-1 and ET-1 and their contents by the method of RT-PCR ( reverse transcription polymerase chain reaction ) and enzyme linked immunosorbent assay (ELISA) respectively. Partial excised lung tissue was used for pathological assessment and histological sections. The middle lobe in the right lung were excised for examination of mRNA expression of caspase-3 by the method of Real Time PCR (real time polymerase chain reaction ). Caspase-3 contents in lung tissue homogenates was examined by the method of colorimetric assay. Apoptosis indexes in the lung tissue were assessed with TUNEL FragELTM(Fragment End Labeling). Each one underwent whole-lung lavage. Cells were removed from bronchoalveolar lavage fluid (BALF) by low-speed centrifugation, and the resulting pellets were analyzed for total cell﹑differential counts and apoptosis analysis . Total white-cell numbers were determined by manual counting. Cell-free lavage fluid was processed for total protein (TP) and malondialdehyde (MDA) determinations.
Results 1.(A) PaO2 in the four groups all decreased below 60mmHg and PaO2 of postinjury had statistical significance compared with pre-injury at the same group(P<0.01). PaO2 of postinjury and pre-injury between-group comparison showed no significance(P>0.05). (B) PaO2 in the four groups had increased since 0.5h treatment timepont,and values of PaO2 sustained continuously within 3.5 h treatment time. PaO2、PaO2/FiO2 in the HFOV and HFOV+PLV groups were higher than the corresponding data in CMV and CMV+PLV groups respectively (P<0.05, P<0.01). PaO2 in the CMV+PLV group at 1.5h and 2.5h treatment timepoint and PaO2 in HFOV+PLV group at 3.5h treatment timepoints showed significant advantages over the data in the corresponding non-PLV groups at the same timepoints (P<0.05, P<0.01). (C) Histological injury score found the HFOV groups were more alleviated than the CMV group,the lowest in the HFOV+PLV group and the highest in the CMV group. 2. (A) The contents of E-selectin,P-selectin, ICAM-1 and their mRNA expression in lung tissue homogenates in HFOV group, HFOV+PLV group were lower than them in CMV group ,CMV+PLV group respectively, and their comparison showed statistical significance(p<0.01). The contents of E-selectin, P-selectin, ICAM-1 and their mRNA expression in lung tissue homogenates in HFOV group, CMV group were higher than them in HFOV+PLV group , CMV+PLV group respectively , and their comparison showed statistical significance (p<0.01). The contents of ET-1 and mRNA expression in lung tissue homogenates in HFOV, HFOV+PLV, CMV, CMV+PLV showed no statistical significance (P>0.05). (B) Histological injury found the HFOV groups were more alleviated than the CMV group,the lowest in the HFOV+PLV group and the highest in the CMV group. 3. (A) Lung tissue apoptosis indexes in HFOV group and HFOV+PLV group were lower than them in CMV group and CMV+PLV group , between-group comparison had significant difference(P<0.01). HFOV+PLV group showed lowest apoptosis indexes.(B) caspase-3 and caspase-3 mRNA expression in the lung tissue in HFOV group and HFOV+PLV group were lower than them in CMV group and CMV+PLV group (P<0.01). caspase-3 and caspase-3 mRNA expression in the lung tissue in CMV+PLV group and HFOV+PLV group were lower than them in CMV group and HFOV group (P<0.05). 4. (A)in the CMV group ,the number of total and polymorphonuclear cell was obviously increased compared with other group( P<0.01) , HFOV+PLV have the lowest total and polymorphonuclear cell number .polymorphonuclear cell number in the CMV+PLV and HFOV+PLV groups comparison showed significance( P>0.05). (B) polymorphonuclear cell apoptosis in HFOV+PLV group were higher than other group, There was significant difference when compared with CMV,HFOV or CMV+PLV group. CMV group have the lowest polymorphonuclear cell apoptosis, There was no significant difference between CMV and CMV+PLV group. Conclusion high frequency oscillatory ventilation ; combined with partial liquid ventilation can improve arterial oxygenation; decreased the concentration and mRNA expression of E-selectin, P-selectin, ICAM-1 ;suppress lung tissue apoptosis induced by inhalation injury ,reduced the caspase-3 concentration and mRNA expression ;HFOV combined with PLV can increase polymorphonuclear cell apoptosis,alleviate polymorphonuclear cell infiltration in inhalation lung injury , reduce lung injury.high frequency oscillatory ventilation combined with partial liquid ventilation may be a optimal method for the treatment of acute respiratory failure caused by inhalation injury .
本研究将新西兰大白兔制成蒸气吸入性损伤并急性呼吸衰竭模型,随机分组后采用四种机械通气模式进行治疗(CMV,CMV+PLV,HFOV及HFOV+PLV),分别在治疗后0.5,1.5,2.5及3.5h取动脉血行血气分析、血流动力学监测。通气治疗3.5h后,为评估四种机械通气模式对通气肺组织的炎症反应及肺损伤程度的影响,作了大体标本、组织病理学观察及肺组织损伤评分;使用酶联免疫吸附法(ELISA)检测肺组织匀浆中和血清中可溶性E-选择素、P-选择素、ICAM-1和ET-1的含量,用RT- PCR法测肺组织中E-选择素、P-选择素、ICAM-1和ET-1 mRNA表达。为评价四种机械通气模式对通气肺组织细胞凋亡的影响,应用TUNEL DNA片段末端标记方式(FragELTM)法检测肺组织细胞凋亡,采用RT- PCR法测肺组织匀浆中caspsase-3含量,应用逆转录聚合酶链反应(RT-PCR)技术检测肺组织caspsase-3 mRNA表达水平,用凝胶电泳条带成像系统照相分析结果。收集肺泡灌洗液细胞后分离出中性粒细胞,使用流式细胞仪Annexin V-FITC法检测中性粒细胞凋亡及坏死;肺泡灌洗上清液则进行各种炎性因子(E-选择素、P-选择素、ICAM-1和ET-1)总蛋白、丙二醛检测。结果:1.血气分析: 1)伤后各组动物PaO2均降至60mm Hg以下,各组致伤前与致伤后比较均有显著性差异(P<0.01),各组致伤前、致伤后(治疗前)血气组间比较均无显著性差异(P >0.05)。2).四个治疗组的PaO2在通气治疗0.5h后均明显上升,通气治疗3.5h内一直有良好的PaO2。3).HFOV组和HFOV+PLV组的PaO2、PaO2/FiO2在治疗治疗各时间点均分别高于相应时间点的CMV组和CMV+PLV组(P<0.05和P<0.01);CMV+PLV组在治疗1.5h、2.5h PaO2优于CMV组(P<0.05);HFOV+PLV组在治疗3.5h PaO2优于HFOV组(P<0.01)。4)肺泡气-动脉血氧分压差[P(A-a)O2]在各治疗组无统计学差异(P >0.05)。5)四个治疗组伤后各时相点的PaCO2均无明显变化(P >0.05)。2.肺组织病理学检查:HFOV组的损伤程度较CMV组明显减轻,HFOV+PLV组损伤最轻,CMV+PLV组次之,CMV组损伤最重。3.炎症反应:E-选择素、P-选择素和ICAM-1在肺组织和血清中的含量及其在肺组织中mRNA表达,在HFOV组及HFOV+PLV组分别低于CMV组及CMV+PLV组,组间比较统计学上有显著差异(p<0.01)。E-选择素、P-选择素和ICAM-1在肺组织和血清中的含量及其在肺组织中mRNA表达在CMV组和HFOV组分别高于CMV+PLV组及HFOV+PLV组.ET-1在肺组织和血清中的含量及其在肺组织中mRNA表达在CMV、HFOV、HFOV+PLV,及CMV+PLV四组间比较统计学上无显著性差异(P>0.05)。4.细胞凋亡:肺组织细胞凋亡及评分指数,HFOV组及HFOV+PLV组分别较CMV、CMV+PLV明显减少,两组比较有显著差异(p<0.01)。而CMV+PLV组和HFOV+PLV组又较CMV组和HFOV组减少,两组比较也有显著性差异(p<0.05)。caspsase-3活性及caspsase-3 mRNA表达,在HFOV及HFOV+PLV组,分别较CMV,CMV+PLV组明显减少,组间比较有显著差异(p<0.01)。而HFOV+PLV及CMV+PLV组又分别较HFOV和CMV组减少,两组比较也有显著性差异(p<0.05)。5.肺泡灌洗液: HFOV+PLV组中性粒细胞凋亡率和早期凋亡率较其它三组高,同时坏死细胞数量也最少。HFOV组及HFOV+PLV组中中性粒细胞早期凋亡率较CMV组和CMV+PLV组明显升高,差别有显著性(P<0.01);CMV组和CMV+PLV组中性粒细胞晚期凋亡率较HFOV组及HFOV+PLV组高,差异明显(P<0.01)。四个治疗组中CMV组中性粒细胞凋亡率最低,但与CMV+PLV组比较无明显差异(P>0.05)。总蛋白、丙二醛浓度各治疗组间的差异无统计学意义(P>0.05)。肺泡灌洗液E-选择素、P-选择素、ICAM-1和ET-1浓度各治疗组间的差异无统计学意义(P>0.05)。结论:与其它三种通气模式相比,HFOV联合PLV能提高蒸汽吸入性损伤兔的氧合水平,降低肺组织内粘附分子浓度及mRNA表达,减少肺组织调亡,减少肺组织内caspsase-3活性及caspsase-3 mRNA表达,提高肺泡中性粒细胞凋亡,减少肺组织内炎性细胞浸润,减轻肺损伤。是治疗吸入性损伤并呼吸衰竭较好的方法。
Inhalation injury with respiratory failure or acute lung injury has high morality, need to be supported with ventilator .Conventional mandatory ventilation could cause ventilator-induced lung injury and could deteriorate pulmonary injury. As the protective lung ventilation strategy, high frequency oscillatory ventilation (HFOV) and partial liquid ventilation have important significance. Methods Thirty-two New Zealand rabbits were randomly divided into four groups after acute respiratory failure models caused by severe steam inhalation injury were established. Then they were ventilated by CMV,HFOV,CMV+PLV or HFOV+PLV,respectively. Femoral arterial blood samples were obtained respectively at 0.5,1.5,2.5,3.5h treatment timepoints for blood gas examination. respiratory mechanics and hemodynamic parameters were recorded. After the experimental period,the lowest lobe of the right lung was weighed for calculating weight ratio of lung water and lung tissue [(W-D)/W] , the middle lobe in the right lung were excised for histological sections. The right middle lobe of rabbit was excised for the examination of mRNA expression of E-selectin, P-selectin,ICAM-1 and ET-1 and their contents by the method of RT-PCR ( reverse transcription polymerase chain reaction ) and enzyme linked immunosorbent assay (ELISA) respectively. Partial excised lung tissue was used for pathological assessment and histological sections. The middle lobe in the right lung were excised for examination of mRNA expression of caspase-3 by the method of Real Time PCR (real time polymerase chain reaction ). Caspase-3 contents in lung tissue homogenates was examined by the method of colorimetric assay. Apoptosis indexes in the lung tissue were assessed with TUNEL FragELTM(Fragment End Labeling). Each one underwent whole-lung lavage. Cells were removed from bronchoalveolar lavage fluid (BALF) by low-speed centrifugation, and the resulting pellets were analyzed for total cell﹑differential counts and apoptosis analysis . Total white-cell numbers were determined by manual counting. Cell-free lavage fluid was processed for total protein (TP) and malondialdehyde (MDA) determinations.
Results 1.(A) PaO2 in the four groups all decreased below 60mmHg and PaO2 of postinjury had statistical significance compared with pre-injury at the same group(P<0.01). PaO2 of postinjury and pre-injury between-group comparison showed no significance(P>0.05). (B) PaO2 in the four groups had increased since 0.5h treatment timepont,and values of PaO2 sustained continuously within 3.5 h treatment time. PaO2、PaO2/FiO2 in the HFOV and HFOV+PLV groups were higher than the corresponding data in CMV and CMV+PLV groups respectively (P<0.05, P<0.01). PaO2 in the CMV+PLV group at 1.5h and 2.5h treatment timepoint and PaO2 in HFOV+PLV group at 3.5h treatment timepoints showed significant advantages over the data in the corresponding non-PLV groups at the same timepoints (P<0.05, P<0.01). (C) Histological injury score found the HFOV groups were more alleviated than the CMV group,the lowest in the HFOV+PLV group and the highest in the CMV group. 2. (A) The contents of E-selectin,P-selectin, ICAM-1 and their mRNA expression in lung tissue homogenates in HFOV group, HFOV+PLV group were lower than them in CMV group ,CMV+PLV group respectively, and their comparison showed statistical significance(p<0.01). The contents of E-selectin, P-selectin, ICAM-1 and their mRNA expression in lung tissue homogenates in HFOV group, CMV group were higher than them in HFOV+PLV group , CMV+PLV group respectively , and their comparison showed statistical significance (p<0.01). The contents of ET-1 and mRNA expression in lung tissue homogenates in HFOV, HFOV+PLV, CMV, CMV+PLV showed no statistical significance (P>0.05). (B) Histological injury found the HFOV groups were more alleviated than the CMV group,the lowest in the HFOV+PLV group and the highest in the CMV group. 3. (A) Lung tissue apoptosis indexes in HFOV group and HFOV+PLV group were lower than them in CMV group and CMV+PLV group , between-group comparison had significant difference(P<0.01). HFOV+PLV group showed lowest apoptosis indexes.(B) caspase-3 and caspase-3 mRNA expression in the lung tissue in HFOV group and HFOV+PLV group were lower than them in CMV group and CMV+PLV group (P<0.01). caspase-3 and caspase-3 mRNA expression in the lung tissue in CMV+PLV group and HFOV+PLV group were lower than them in CMV group and HFOV group (P<0.05). 4. (A)in the CMV group ,the number of total and polymorphonuclear cell was obviously increased compared with other group( P<0.01) , HFOV+PLV have the lowest total and polymorphonuclear cell number .polymorphonuclear cell number in the CMV+PLV and HFOV+PLV groups comparison showed significance( P>0.05). (B) polymorphonuclear cell apoptosis in HFOV+PLV group were higher than other group, There was significant difference when compared with CMV,HFOV or CMV+PLV group. CMV group have the lowest polymorphonuclear cell apoptosis, There was no significant difference between CMV and CMV+PLV group. Conclusion high frequency oscillatory ventilation ; combined with partial liquid ventilation can improve arterial oxygenation; decreased the concentration and mRNA expression of E-selectin, P-selectin, ICAM-1 ;suppress lung tissue apoptosis induced by inhalation injury ,reduced the caspase-3 concentration and mRNA expression ;HFOV combined with PLV can increase polymorphonuclear cell apoptosis,alleviate polymorphonuclear cell infiltration in inhalation lung injury , reduce lung injury.high frequency oscillatory ventilation combined with partial liquid ventilation may be a optimal method for the treatment of acute respiratory failure caused by inhalation injury .
引文
[1]杨宗城,吸入性损伤研究进展。中华烧伤杂志,2000,16:(3):137-140
[2]郭光华,姚学俊,姚世红,等.吸入性损伤与机械通气.江西高校出版社. 1995,10.
[3] Ingrid Steinvall , Zoltan Bak , Folke Sjoberg et al. Acute respiratory distress syndrome is as important as inhalation injury for the development of respiratory dysfunction in major burns. Burns . 2007,10(7):1-11
[4] Susan Jain, Geoff Bellingan. Basic science of acute lung injury. Surgery (Oxford). 2007, 25(3):112-116
[5] Schmidt R, Luboeinski T, Markart P, et al. Alveolar antioxidant status in patients with acute respiratory distress syndrome. Eur Respir J 2004,(24): 994–999
[6] New insights into the pathology of acute respiratory failure. Jose L. Mendez and Rolf D. Hubmayr. Curr Opin Crit Care 2005, ( 11):29–36.
[7] Rabinder Randhawa, Geoff Bellingan. Acute lung injury. Anaesthesia And Intensive Care Medicine 2007,8(11) 477-480
[8] Arthur P Wheeler, Gordon R Bernard. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet 2007,(369): 1553–1565
[9] You-Lan Yang, Gau-Jun Tang, Yuh-Lin Wu, et al. Exacerbation of wood smoke-induced acute lung injury by mechanical ventilation using moderately high tidal volume in mice. Respiratory Physiology Neurobiology, 2008, 60(1): 99-108
[10] Matthay MA, Bhattacharya S, Gaver D, et al. Ventilation induced lung injury : in vivo and in vitro mechanism. Am J Physiol lung Cell Mol Physiol, 2002, Vol. 283(4):678-682
[11] Dhanireddy S, Altemeier WA, Matute-Bello G, et al. Mechanical ventilation induces inflammation, lung injury, and extra-pulmonary organ dysfunction in experimental pneumonia. Lab Invest. 2006, 86(8):790-799.
[12] Eumorfia Kondili, Nectaria Xirouchaki, Katerina Vaporidi, Short-term Cardio respiratory Effects of Proportional Assist and Pressure-support Ventilation in Patients with Acute Lung Injury/Acute Respiratory Distress Syndrome Anesthesiology 2006, 105:703–8
[13] Tsangaris I, Lekka M.E, Kitsiouli E, et al. Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury. Eur Respir J 2003, 21: 495–501
[14] P. Dahlem , A.P. Bos, J.J. Haitsma, et al. Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury Eur Respir J 2006, 28: 992–998
[15] H.A. Vreugdenhil, C.J. Heijnen, F.B. Plotz, et al. Mechanical ventilation of healthy rats suppresses peripheral immune function. Eur Respir J 2004, 23: 122–128
[16] S.-C. KO, H. ZHANG, J. J. HAITSMA et al. Effects of PEEP levels following repeated recruitment maneuvers on ventilator-induced lung injury. Acta Anaesthesiol Scand 2008: 1–8
[17] Emilie Lam and Claudia C. dos Santos .et al. Advances in molecular acute lung injury/acuterespiratory distress syndrome and ventilator-induced lung injury: the role of genomics, proteomics, bioinformatics and translational biology. Curr Opin Crit Care 2008, 14:3–10
[18] Imai Y,Parodo J,Kajikawa O, et al. Injurious mechanical ventilation and end organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome.JAMA,2003,289(16):2104-2112.
[19] James A. Frank, Charlie M. Wray, Danny F. Mcauley, et al. Alveolar macrophages contribute to alveolar barrier dysfunction in ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol 2006, 291: 1191–1198
[20] Belperio JA, Keane MP, Lynch JP 3rd,etal. The role of cytokines during the pathogenesis of ventilator assosiated and ventilator-induced lung Injury. Semin Respir Crit Care Med, 2006, 27(4):350-364.
[21] Okutani D, Han B, Mura M, et al. High-volume ventilation induces pentraxin 3 expression in multiple acute lung injury models in rats. Am J Physiol Lung Cell Mol. Physiol, 2007, 292(1): 144-153
[22] Hammerschmidt S, Kuhn H, Grasenack T, et al. Apoptosis and necrosis induced by cyclic mechanical stretching in alveolar typeⅡcells influence of captopril and L-Arginine. Pneumologie, 2004, 58(4):222-229
[23] Saito S,Ogawa J, Minamiya Y. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. AM J Physiol Lung Cell Mol Physiol, 2005, 289(3): 400-406
[24]胡国栋,蔡绍曦,陈英华,等.不同潮气量机械通气对大鼠支气管和肺组织细胞凋亡的影响.第一军医大学学报,2005,25(5):508-512
[25] May M,Strobel P, Preisshofen T, et al. Apoptosis and proliferation in lungs of ventilated and oxygen-treated preterm infants. Eur Respir J, 2004, 23(1):113-121
[26] Jerng JS, Hsu YC, Wu HD, et al. Role of the rennin-angitensin system in Ventilator-induced ung injury: An in vivo study in a rat model. Thorax. 2007, 18: 758-762
[27] Takenaka K, Nishimura Y, Nishiuma T, et al. Ventilator-induced lung injury is reduced in transgenic mice that overexpress endothelial nitric oxide synthase. Am J Physiol Lung Cell Mol Physiol, 2006, 290(6):1078-1086
[28] Li M, Qin YZ, MA LJ. Study of the effects on the heart function when different positive end expiratory pressure levels were used on patients treated with mechanical ventilation. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 2007, 19(2):86-89
[29] Rotta AT, Gunnarsson B, Fuhrman BP,et al. Comparison of lung protective ventilation strategies in a rabbit model of acute lung injury. Crit Care Med. 2001, 29(11):2176-2184.
[30] Van kaam AH, Haotsma JJ, De Jaegere A, et al. Open lung ventilation improves gas exchange and attenuates secondary lung injury in a piglet model of meconium aspiration. Crit Care Med.2004, 32(2):443-449
[31] Serge J.C.Verbrugge, Burkhard Lachmann and Jozef Kesecioglu. Lung protective ventilatory strategies in acute lung injury and acute respiratory distress syndrome: from experimental findings to clinical application Clin Physiol Funct Imaging .2007, 27:67–90.
[32] Peter Delong, James A. Murray, and Christopher K. Cook. Mechanical Ventilation in the Management of Acute Respiratory Distress Syndrome. Seminars in Dialysis. 2006, 19(6):517–524
[33] James E. Lynch, BS, RRT, J. Mark Cheek, BS, et al. Adjuncts to Mechanical Ventilation in ARDS. Semin Thorac Cardiovasc Surg 2006, 18:20-27
[34] Esther K. Wolthuis, Goda Choi, Mark C. Dessing, Mechanical Ventilation with Lower Tidal Volumes and Positive End-expiratory Pressure Prevents Pulmonary Inflammation in Patients without Preexisting Lung Injury. Anesthesiology 2008,108:46–54
[35] Nakazawa K, Yokoyama K, Yamakawa K, et al. Effect of positive end-expiratory pressure on inflammatory response in oleic acid-induced lung injury and whole lung lavage induced lung injury. J Anesth, 2007, 21(1):47-54
[36] Imai Y, Nakagawa S, Ito Y,et al. Comparison of lung protection strategies using conventional and high-frequency oscillatory ventilation. J Appl Physiol, 2001, 91(4): 1836-1844.
[37] Anton H. van Kaam, Jack J. Haitsma, Anne De Jaegere, et al. Open lung ventilation improves gas exchange and attenuates secondary lung injury in a piglet model of meconium aspiration。Crit Care Med 2004 ,32(2): 443-449
[38] Meyer J, Cox PN, Mckerlie C, et al. Protective strategies of high frequency oscillatory ventilation in a rabbit model. Pediatr Res, 2006, 60(4):401-406
[39] M. David and W. Heinrichs .High frequency oscillatory ventilation and an interventional lung assist device to treat hypoxaemia and hypercapnia. British Journal of Anaesthesia 2004,93 (4): 582–586
[40]Cacciari A, Ruggeri G, Mordenti M,et al. High-frequency oscillatory ventilation versus conventional mechanical ventilation in congenital diaphragmatic hernia. Eur J Pediatr Surg, 2001, 11(1):3-7.
[41] Dembinski R, Max M,Bensberg R, et al. High frequency oscillatory ventilation in experimental lung injury: effects on gas exchange. Intensive Care Med, 2002, 28(6):768-774
[42] Katharina Von Der Hardt, Michael Andreas Kandler, Ludger Fink, et al. High Frequency Oscillatory Ventilation Suppresses Inflammatory response in Lung Tissue and Microdissected Alveolar Macrophages in Surfactant Depleted Piglets Pediatric Research Vol. 55, No. 2, 2004
[43] Yoder BA, Siler-Khodr T, Winter VT, et al. High-frequency oscillatory ventilation: effects on lung function, mechanics, and airway cytokines in the immature baboon model for neonatal chronic lung disease. Am J Respir Crit Care Med, 2000, 162(5):1867-1876.
[44] John H. Arnold, ; Nick G. Anas, Peter Luckett, High-frequency oscillatory ventilation in pediatric respiratory failure: A multicenter experience; Crit Care Med 2000, 28(12): 3913- 3919
[45] Ben Jaballah N, Khaldi A, Mnif K,et al. High-frequency oscillatory ventilation in pediatric patients with acute respiratory failure. P ediatr Crit Care Med,2006, 7(4):362-367.
[46] Angela T Wratney , Michael A Gentile , Donna S Hamel , et al. Successful Treatment ofAcute Chest Syndrome With High-Frequency Oscillatory Ventilation in Pediatric Patients. Respir Care 2004, 49(3):263–269.
[47] Gerstmann DR, Wood K, Miller A, et al . Childhood outcome after early high frequency oscillation ventilation for neonatal respiratory distress syndrome. Pediatrics,2001, 108(3): 617-662.
[48] N. Gullberg, P. Winberg and H. Sellde N,et al. Changes in mean airway pressure during HFOV influences cardiac output in neonates and infants. Acta Anaesthesiol Scand. 2004, 48: 218—223
[49] Sangeeta Mehta, John Granton, Rod J. MacDonald, et al. High Frequency Oscillatory Ventilation in Adults .CHEST 2004, 126:519-527
[50] Bollen CW, Van Well GT, Sherry T, et al. High frequeney oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a ramdomized controlled trial. Crit Care, 2005, 9 (4):430-439.
[51] Sangeeta Mehta, MD, FRCPC; Stephen E. Lapinsky, et al. Prospective trial of high- frequency oscillation in adults with acute respiratory distress syndrome. Crit Care Med 2001 29(7): 1360-1369
[52] Fort P, Farmer C, Westerman J, et al. High frequency oscillatory ventilation for adult respiratory distress syndrome, a pilot study. Crit Care Med,1997 ,25:937-947
[53] F. A. Andersen, A. B. Guttormsen and H. K. Flaatten. High frequency oscillatory ventilation in adult patients with acute respiratory distress syndrome a retrospective study. Acta Anaesthesiol Scand 2002, 46: 1082–1088
[54] Stephen Derdak, DO。High-frequency oscillatory ventilation for acute respiratory distress syndrome in adult patients。Crit Care Med 2003,31(4): (Suppl.) 317-323
[55] Rob Cartotto, Andrew B. Cooper, John R. Esmond, et al. Early Clinical Experience with High-Frequency Oscillatory Ventilation for ARDS in Adult Burn Patients. Journal of Burn Care & Rehabilitation. 2003,22(5): 325-333
[56] Cartotto R, Ellis S, Gomez M, et al.Use of high frequency oscillatory ventilation in burn patients. Crit Care Med, 2005, 33( suppl):175-181.
[57] Cartotto R, Ellis S, Gomez M, et al. High frequency oscillatory ventilation in burn patients with the acute respiratory distress. Burns, 2004, 30 (5):453-463.
[58] Kao KC,Tsai YH, WU YK, et al. High frequency oscillatory ventilation for surgical patients with acute respiratory distress syndrome. J Trauma, 2006, 61(4):837-843.
[59] Andrew B. Cooper, Avinash Islur Bsc, et al. Hypercapnic respiratory failure and partial upper airway obstruction during high frequency oscillatory ventilation in an adult burn patient. Can J Anesth 2002, 49(7): 724–728.
[60] Jaarsma AS, Braaksma MA, Geven WB, et al. Early activation of inflammation and clotting in the preterm lamb with neonatal RDS: comparison of conventional ventilation and high frequency oscillatory ventilation. Pediatr Res. 2001 ,50(5):650-657
[61] Demory D, Michelet P, Arnal JM, et al. High-frequency oscillatory ventilation following prone positioning prevents a further impairment in oxygenation. Crit Care Med, 2007, 35(1):564-568
[62] Alexandre T. Rotta, MD; Mário Eduardo G. Viana, MD; Budi Wiryawan, Combining lung-protective strategies in experimental acute lung injury: The impact of high frequency partial liquid ventilation. Pediatr Crit Care Med 2006,7(6): 562-570
[63] Chang Won Choi, Sun Young Koh Yun Sil Chang, Effects of perfluorocarbon Associated High Frequency Oscillatory Ventilation on Hemodynamics and Gas Exchange in the Newborn Piglets with Respiratory Distress. J Korean Med Sci 2003, 18: 663-8
[64] Kohelet D. Nitric oxide inhalation and high frequency oscillatory ventilation for hypoxemic respiratory failure in infants.Isr Med Assoc J, 2003, 5(1):19-23.
[65] Dobyns EL, Anas NG, Fortenberry JD, et al. Interactive effects of high-frequency oscillatory ventilation and inhaled nitric oxide in acute hypoxemic respiratory failure in pediatrics. Crit Care Med, 2002, 30(11):2425-2429.
[66]胡庆宏郭光华,等.吸入伤犬部分液体通气后血生化指标变化与动脉血氧分压分压的关系。中华烧伤杂志,2002,18:142-144
[67] Jurgen P. Meinhardta, Ulrike Friessa, Hans Joachim Bendera, Relationship among cardiac index, inspiration/expiration ratio, and perfluorocarbon dose during partial liquid ventilation in an oleic acid model of acute lung injury in sheep. Journal of Pediatric Surgery. 2005. 40, 1395–1403
[68] K. W. Southern, W. K. Funkhouser, I. Kazachkova. Airway surface liquid recovered by lavage with perfluorocarbon liquid in cats. European Journal of Clinical Investigation. 2002,32; 956–961
[69] G.F. Vazquez de Anda, R.A. Lachmann, S.J.C. Verbrugge, Partial liquid ventilation improves lung function in ventilation induced lung injury .Eur Respir J 2001, 18: 93–99
[70] Jean-Damien Ricard, Franck Iserin, Didier Dreyfuss, et al. Perflubron dosing affects ventilator-induced lung injury in rats with previous lung injury Crit Care Med 2007, 35(2): 561-567
[71] Juergen P. Meinhardt, Marc Schmittner, Peter Herrmann. Comparison of Different Inhalational Perfluorocarbons in a Rabbit Model of Acute Lung Injury. Asaio Journal 2005, 51:85–91.
[72] Scot T. Bateman, MD; Allan Doctor, MD; Barry Price, et al. Optimizing intrapulmonary perfluorocarbon distribution: Fluoroscopic comparison of mode of ventilation and body position.Crit Care Med. 2001, 29(3): 601-608
[73] Wolf S, Lohbrunner H, Busch T, et al. Small dose of exogenous surfactant combined with partial liquid ventilation in experimental acute lung injury: effects on gas exchange, haemodynamics, lung mechanics, and lung pathology.Br J Anaesth, 2001, 87(4):593-601.
[74] Fellery de Lange, Kenji Yoshitani, Alan D. Proia, MD, et al. Perfluorocarbon Administration During Cardiopulmonary Bypass in Rats: An Inflammatory Link to Adverse Outcome?Anesth Analg 2008, 106:24–31)
[75] Ellen Schoof, Katharina von der Hardt, Michael A. Kandler, et al. Aerosolized perfluorocarbon reduces adhesion molecule gene expression and neutrophil sequestration in acute respiratory distress.European Journal of Pharmacology,. 2002, 457(2):Pages 195-200.
[76] Allan Doctor, MD; Barry Price, RRT; Neeraj Bhargava, BA, et al. High frequency oscillatory ventilation of the perfluorocarbon-filled lung: Dose-response relationships in an animal model of acute lung injury Crit Care Med. 2001, 29(4): 847-854
[77] Anne Greenough . High frequency oscillation and liquid ventilation. Paediatric respiratory reviews. 2006, 7:186–188
[78]郭光华,钱克俭,朱峰,等.高频部分液体通气对吸入犬呼吸循环功能的影响。中华烧伤杂志,2002,18(6):346-349
[79]Wang SG, Guo GH, FU ZH,et al. Effects of high-frequency oscillatory ventilation and partial liquid ventilation on acute lung injury induced by steam inhalation in new Zealand rabbits. Annals of Burns and Fire Disasters, 2006,ⅪⅩ(2):88-94.
[80]朱佩芳,黎鳌,姜坤元,等.重度呼吸道蒸汽烧伤动物(狗)模型的制作.解放军医学杂志.1983,8(1):7-10.
[81] Ren-Feng Guo, Peter A. Ward. Mediators and regulation of neutrophil accumulation in inflammatory responses in lung: insights from the IgG immune complex model.Free Radical Biology and Medicine, 2002, 33(3):303-310
[82] Mayumi Hirose, Toshiyuki Murai, Hiroto Kawashima. Elevation of rat plasma P-selectin in acute lung injury. Biochimica Biophysica Acta (BBA) - Molecular Basis of Disease, 2007, 1772(3):382-389
[83] Frank Hildebrand, Hans-Christoph Pape, Paul Harwood, et al. Role of adhesion molecule ICAM in the pathogenesis of polymicrobial sepsis.Experimental and Toxicologic Pathology, 2005,56(21):281-290
[84]孙萌,井丽娟, E选择素与急性肺损伤国际儿科学杂志2007,34(2):93-95
[85] Hidemi Ishii, Kimihiko Takada. Bleomycin Induces E-selectin Expression in Cultured Umbilical Vein Endothelial Cells by Increasing Its mRNA Levels through Activation of NF-κB/Rel.Toxicology and Applied Pharmacology, 2002, 184(2):88-97
[86]马希刚,曹相原,张珍祥,等.火把花根片抑制大鼠急性肺损伤黏附分子表达中国病理生理杂志.2007, 23 (12):2394-2397
[87] Hirotsugu Hayashi, Haruhiko Koike, Yukiko Kurata, et al. Protective effects of sialyl Lewis X and anti-P-selectin antibody against lipopolysaccharide induced acute lung injury in rabbits. European Journal of Pharmacology, 1999, 370 (1):47-56
[88] Allen E. Haddrell, Stephen F. van Eeden, George R. Agnes.Dose response studies involving controlled deposition of less than 100 particles generated and levitated in an ac trap onto lung cells, in vitro, and quantitation of ICAM-1 differential expression.Toxicology in Vitro, 2006, 20(6): 1030-1039
[89] Ndukauba M. Eleghasim, Allen E. Haddrell, Stephen van Eeden,et al. The preparation of 100particles per trial having the same mole fraction of 12 inorganic compounds at diameters of 6.8, 3.8, or 2.6μm followed by their deposition onto human lung cells (A549) with measurement of the relative downstream differential expression of ICAM-1.International Journal of Mass Spectrometry, 2006, 258(3):Pages 134-141.
[90] M. Tufano, I. Paoletti, B. Perfetto,P1762 Effect of moxifioxacin and human beta-defensin 2 on ICAM-1 and cytokines expression in human lung epithelial cell line.International Journal of Antimicrobial Agents, Volume 29, 2007, 29(Suppl): 501.
[91] Ruijin Li, Ziqiang Meng, Jingfang Xie.Effects of sulfur dioxide on the expressions of MUC5AC and ICAM-1 in airway of asthmatic rats.Regulatory Toxicology and Pharmacology, 2007, ,48(3): 284-291
[92] Kymberly Gowdy, Quentin T. Krantz, Mary Daniels,et al. Modulation of pulmonary inflammatory responses and antimicrobial defenses in mice exposed to diesel exhaust.Toxicology and Applied Pharmacology, In Press, Corrected Proof, Available online 15 February 2008
[93] K. Maeda, K. Kai, T. Hayashi, K. Hasegawa, T. Matsumura. et al.Intercellular Adhesion Molecule-1 (ICAM-1) and Lymphocyte Function associated Antigen-1 (LFA-1) Contribute to the Elimination of Equine Herpesvirus Type 1 (EHV-1) from the Lungs of Intranasally Infected BALB/c Mice. Journal of Comparative Pathology, 2004, 130(3): Pages 162-170
[94]陈雯,许国根,陈颖,等.急性肺损伤患者血管内皮生长因子改变的意义内科急危重症杂志2007,13(2):74-75
[95] Janet D. Pierce, Dsn, Arnp, Ccrn Jana Pierce, et al. The role of apoptosis in respiratory diseases. Clinical nursespecialist.2007; 21: 22-28J, 2004, 23(1):113-121.
[96]李文军,杨宗城,杨晓东,等.烟雾吸入伤大鼠肺组织细胞凋亡及凋亡调控基因表达的变化.解放军医学杂志,2002,27(2):142-144
[97]农凌波,急性肺损伤中细胞的凋亡及凋亡的调控。国外医学呼吸系统分册,2002,22(3):149-151
[98] Reinout A. Bem, Albert P. Bos, Gustavo Matute Bello, et al. Lung epithelial cell apoptosis during acute lung injury in infancy. Pediatr Crit Care Med 2007 Vol. 8, No. 2 132-137
[99]张国友,邓小川.细胞凋亡与急性呼吸窘迫综合征。国际麻醉学与复苏杂志,2005,26(6):375-377
[100] Saito S,Ogama J,Minamiya Y. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol.,2005, 289(3):400-406
[101] Tadaaki Yamada, Yoshinobu Iwasaki, Kazuhiro Nagata,et al.Thioredoxin-1 protects against hyperoxia-induced apoptosis in cells of the alveolar walls. Pulmonary Pharmacology & Therapeutics, 2007, , 20(6):650-659
[102]黄英,刘国祥.肺泡Ⅱ型上皮细胞凋亡在急性肺损伤中的作用.中国现代医学杂志, 2002,12(3):35-37.
[103] Leanne M. Sutherland, Yasmin S. Edwards, Andrew W. Murray. Alveolar type II cell apoptosis. Comparative Biochemistry and Physiology - Part A: Molecular & IntegrativePhysiology, 2001, , 129(1): 267-285
[104]宋勇,毛宝龄,钱桂生,等.急性肺损伤大鼠肺组织细胞凋亡和FasPFasL表达的改变及其意义.中华医学杂志,1999,79(3):230-232.
[105] Stefan Hammerschmidt, Hartmut Kuhn, Christian Gessner,et al. Stretch-Induced Alveolar Type II Cell Apoptosisl. Role of Endogenous Bradykinin and PI3K-Akt Signaling American Journal of Respiratory Cell and Molecular Biology. 2007,( 37): 699-705
[106] Stefan Hammerschmidt, Hartmut Kuhn, Thomas Grasenack et al. Apoptosis and Necrosis Induced by Cyclic Mechanical Stretching in Alveolar Type II Cells .American Journal of Respiratory Cell and Molecular Biology. 2004, 30:396-402
[107] Yumiko Imai, Jean Parodo, Osamu Kajikawa,et al. Injurious Mechanical Ventilation and End-Organ Epithelial Cell Apoptosis and Organ Dysfunction in an Experimental Model of Acute Respiratory Distress Syndrome JAMA.2003, 289:2104-2112
[108] Mantell LL, Shaffer TH, Horowitz S, et al. Distinct patterns of apoptosis in the lung during liquid ventilation compared with gas ventilation. Am J Physiol Lung Cell Mol Physiol, 2002, 283(1):31-41.
[109] Vertrees RA, Nason R,Hold . Smoke/burn injury-induced respiratory failure elicits apoptosis in ovine lungs and cultured lung cells, ameliorated with Arteriovenous CO2 removal.Chest, 2004, 125(4):1472-1482.
[110]刘忠令,李强.呼吸疾病介入诊疗学。(M)北京:人民军医出版社。2003:81-86。
[111]中华医学会呼吸病学分会支气管肺泡灌洗液细胞学检测技术规范(草案)中华结核和呼吸杂志2002 ,25(7):390-391
[112] Merdad V. Parsey, Debra Kaneko, Robert Shenkar, et al. Neutrophil Apoptosis in the Lung after Hemorrhage or Endotoxemia: Apoptosis and Migration Are Independent of IL-1β. Clinical Immunology, 1999, , 91(2): Pages 219-225
[113] Keu Sung Lee, Young Hwa Choi, Young Sun Kim, et al. Evaluation of bronchoalveolar lavage fluid from ARDS patients with regard to apoptosis. Respiratory Medicine, 2008, 102(3): 464-469
[114] M.W.R. Pletz, M. Ioanas, A. de Roux .et al. Reduced spontaneous apoptosis in peripheral blood neutrophils during exacerbation of COPD. Eur Respir J, 2004, 23: 532–537
[115] M. Muller, J. Grunewald, C. Olgart Hoglund. et al. Altered apoptosis in bronchoalveolar lavage lymphocytes after allergen exposure of atopic asthmatic subjects. Eur Respir J 2006, 28: 513–522
[116]许国根,陈雯,陈颖,等.急性肺损伤病人中性粒细胞凋亡变化的研究.中国急救医学,2004,24(4):242-244
[117] Naveed Hussain, Fengying Wu, Li Zhu,et al. Neutrophil Apoptosis during the Development and Resolution of Oleic Acid-Induced Acute Lung Injury in the Rat. Am. J. Respir. Cell Mol. Biol.1998, 19(6):867-874
[118] Patricia M de Souza, Mark A Lindsay. Apoptosis as a therapeutic target for the treatment of lung disease.Current Opinion in Pharmacology, 2005, 5(3): 232-237
[1]刘忠令、李强主编呼吸疾病介入诊疗学。人民军医出版社。2003:81-86。
[2]李强,呼吸内镜学.上海:上海科技出版社, 2003: 315-318
[3]俞森祥,张进川1当代呼吸疗法[M]1第1版1北京:北京医科大学.中国协和医科大学联合出版社,1994 ,202～2201 [4 ] Noel2Georis I ,Bernard A , Falmagne P , et al . Database of bronchoalveolar lavage fluid proteins[J ] . J Chromatogr B Analyt Technol Biomed Life Sci , 2002 , 771 (122) :221-236.
[5]中华医学会呼吸病学分会支气管肺泡灌洗液细胞学检测技术规范(草案)中华结核和呼吸杂志2002 ,25(7):390-391
[6]代华平王辰Ulrich Costabel特发性间质性肺炎的分类中华医学杂志2002 , 82(12) 861-862。
[7] Blondeau K,Dupont L,Mertens V. Gastroesophageal reflux and aspiration of gastric contents in adult patients with cystic fibrosis. Gut. 2008 Mar 27.
[8] Steinberg KP , Mitchell DR , Maunder RJ , et al. Safety of bronchoalveolar lavage in patients with adult respiratory distress syndrome [ J ] 1 Am Rev Respir Dis ,1993 ,148 :556～5691
[9] Hamacher J ,Lucas R ,Lijnen HR , et al . Tumor necrosis factor-alpha and angiostatin are mediators of endothelial cytotoxicity in bronchoalveolar lavages of patients with acute respiratory distress syndrome [ J ] . Am J Respir Crit Care Med ,2002 ,166 (5) :651-656.
[10] Drent M, Wagenaar SS , Mulder PH , et al。Chest ,1994 ,105(2) :514-519。
[11] Mills NE , Fishman CL , Scholes J , et al. J Natl Cancer inst1995, 87(14):1056-1060.
[12] Gustavo Matute-Bello .Mark M. Wurfel .Janet S. Lee. et al .Essential role of MMP-12 in FAS-induced lung fibrosis. Am J Respir Cell Mol Biol. 2007;4:19-25。
[13] P.R.M. Rocco, D.P. Momesso, R.C. Figueira, et al .Therapeutic potential of a new phosphodiesterase inhibitor in acute lung injury. Eur Respir J 2003; 22: 20–27。
[14] I. Tsangaris, .M.E. Lekka, E. Kitsiouli, et al . Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury. Eur Respir J 2003; 21: 495–501
[15] R. Schmidt, T. Luboeinski, P. Markart, et al. Alveolar antioxidant status in patients with acute respiratory. distress syndrome Eur Respir J 2004; 24: 994–999
[16] Nussbaum E. Pediatric fiberoptic bronchoscopy :Clinical experience with 2 ,836 bronchoscopies[J ] . Pediatr Crit Care Med ,2002 ,3 (2) :171-176.
[17] Marguet C ,Dean T ,Warner JO. Soluble intercellular adhesion molecule-1( sICAM-1 ) and interferon-gamma in bronchoalveolar lavage fluid from children with airway diseases [J ] . Am J Respir Crit Care Med , 2000 , 162(3):1016-1022.
[18]吕培中,周苏明,邹春英,等.机械通气下支气管肺泡灌洗治疗老年重症肺部感染.实用老年医学, 2002, 16(5) : 264-265
[19]周凤丽,唐英春.支气管肺泡灌洗在呼吸道感染诊治中的应用[M]医学综述, 2000 , 7(6) :306～3071
[20] Koh YY, Park Y,Lee HJ ,et al . Levels of I nterleukin-2 , interferon-gamma ,and interleukin-4 in bronchoalveolar lavage fluid from patients with Mycoplasma pneumonia : implication of tendency toward increasedimmunoglobulin E production [J ] . Pediatrics ,2001 ,107 (3) :E39.
[21] Sekizawa K,Ujud Y, Itabashi S, et al. Lack of Cough in aspiration pneumonia. Lancet, 1999, 355 (6) : 1228-1229
[1] Janet D. Pierce, Dsn, Arnp, Ccrn Jana Pierce, et al. The role of apoptosis in respiratory diseases. Clinical nursespecialist. 2004, 23(1):113-121.
[2] Susan Jain, Geoff Bellingan. Basic science of acute lung injury. Surgery (Oxford), 2007, 25(3): 112-116
[3] Schmidt R, Luboeinski T, Markart P, et al. Alveolar antioxidant status in patients with acute respiratory distress syndrome. Eur Respir J. 2004, 24: 994–999
[4] New insights into the pathology of acute respiratory failure. Jose L. Mendez and Rolf D. Hubmayr. Curr Opin Crit Care . 2005 11:29–36.
[5] Rabinder Randhawa, Geoff Bellingan. Acute lung injury. Anaesthesia And Intensive Care Medicine .2007; 8(11): 477-480
[6] Arthur P Wheeler, Gordon R Bernard. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007; 369: 1553–1565
[7] Reinout A. Bem, Albert P. Bos, Gustavo Matute Bello, et al. Lung epithelial cell apoptosis during acute lung injury in infancy. Pediatr Crit Care Med 2007 , 8(2): 132-137
[8]张国友,邓小川。细胞凋亡与急性呼吸窘迫综合征。国际麻醉学与复苏杂志,2005,26(6):375-377
[9] Saito S,Ogama J, Minamiya Y. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol.,2005, 289(3): L400-406
[10]陈娟,许峰,蒋静等。氧化应激状态下肺泡Ⅱ型上皮细胞凋亡及细胞外信号调节激酶信号转导机制的研究。中国危重病急救医学。2007,4(19):193-196
[11]何琳,李涛平。肺泡Ⅱ型上皮细胞钠通道在肺水清除中信号转导的研究进展。国际呼吸杂志。2007,27(12):919-921
[12]陈力黎檀实。肺泡上皮细胞在ALI、ARDS中的研究进展。世界危重病医学杂志。2006,3(4):1409-1412。
[13]潘芳,李文志.肺泡Ⅱ型上皮细胞的体外培养及其在麻醉学研究领域的应用.国外医学麻醉学与复苏分册。2000,21(6):368—371.
[14] Crandall ED,Matthay MA.Alveolar epithelial transport.Am J Respir Crit Care Med. 2001,163:1021.
[15] Sartori C,Matthay MA.Alveolar epithelial fluid transport in acute lung injury :new insights.Eur Respir J. 2002,20:1299—1313.
[16] Matthay MA Clerici C ,Saumon G.Active fluid clearance from the distal air spaces of the lung.J Appl Physiol. 2002,93:1533.
[17]张秋金,李银平。肺泡上皮细胞功能特性与内毒素性急性肺损伤。中国危重病急救医学2005,17(6):382-384。
[18]农凌波,急性肺损伤中细胞的凋亡及凋亡的调控。国外医学呼吸系统分册。2002,22(3):149-151
[19] Tadaaki Yamada, Yoshinobu Iwasaki, Kazuhiro Nagata,et al.Thioredoxin-1 protects againsthyperoxia-induced apoptosis in cells of the alveolar walls. Pulmonary Pharmacology & Therapeutics, 2007, 20(6): 650-659
[20]黄英,刘国祥.肺泡Ⅱ型上皮细胞凋亡在急性肺损伤中的作用.中国现代医学杂志, 2002, 12(3):35-37.
[21] Ashkenszi A,Dixil VM,Death receptors signaling and modulation.Science.1998,281:1305-1308
[22]官健,金大地,金丽娟.多发伤合并休克大鼠肺脏中细胞凋亡的实验研究.中国危重病急救医学.1998.10:479-483
[23]王疑,张淑文等,细胞凋亡在大鼠急性肺损伤发生机制中的意义。中国危重急救医学.2002,13(2):90-94
[24] Hengarther M0.The biochemistry of apoptosis.Nature。2000.407 (68O5): 770-776
[25] Tesfaigzi J.Wild MB.Johnson NF,et al。Apoptosis is a pathway responsible for the resolution of endotoxin—induced alveolar type II cell hyperplasia in the rat.Love Respir Res Ins.1998;79(5):303-3ll
[26] Gruener,Dieter C,Walter E,et al.Culture and transformation of human airway epithelia cells.Am J Physiol,1995;268:347-360
[27]张玉芹,欧阳静萍,李瑞祥.硫氮唑酮在失血性休克犬肺泡Ⅱ型细胞的影响.中国现代医学杂志,2000, 10(6):9-11
[28] Dawicki DD,Chatterjee D,Wyche J,et al.Extracelluar ATP and adenosine cause apoptosis of pulmonary artery endothelial cells.Am J Physiol Lung Cell Mol Physiol,1997,273(2):L485-L494
[29] Merdad V. Parsey, Debra Kaneko, Robert Shenkar, et al. Neutrophil Apoptosis in the Lung after Hemorrhage or Endotoxemia: Apoptosis and Migration Are Independent of IL-1β. Clinical Immunology, Volume 91, Issue 2, May 1999, Pages 219-225
[30] Keu Sung Lee, Young Hwa Choi, Young Sun Kim, et al. Evaluation of bronchoalveolar lavage fluid from ARDS patients with regard to apoptosis.Respiratory Medicine, 2008, 102(4):464-469
[31] M.W.R. Pletz, M. Ioanas, A. de Roux .et al. Reduced spontaneous apoptosis in peripheral blood neutrophils during exacerbation of COPD. Eur Respir J 2004; 23: 532–537
[32] M. Muller, J. Grunewald, C. Olgart Hoglund. et al. Altered apoptosis in bronchoalveolar lavage lymphocytes after allergen exposure of atopic asthmatic subjects. Eur Respir J. 2006; 28: 513–522
[33]许国根,陈雯,陈颖,等.急性肺损伤病人中性粒细胞凋亡变化的研究.中国急救医学,2004,24(4):242-244
[34] Naveed Hussain, Fengying Wu, Li Zhu,et al. Neutrophil Apoptosis during the Development and Resolution of Oleic Acid-Induced Acute Lung Injury in the Rat. Am. J. Respir. Cell Mol. Biol.1998, 19(6):867-874
[35] Patricia M de Souza, Mark A Lindsay. Apoptosis as a therapeutic target for the treatment of lung disease.Current Opinion in Pharmacology, 2005, 283(4): 232-237
[36] You-Lan Yang, Gau-Jun Tang, Yuh-Lin Wu, et al. Exacerbation of wood smoke-induced acute lung injury by mechanical ventilation using moderately high tidal volume in mice. Respiratory Physiology Neurobiology, 2008, 160(1): 99-108
[37] Matthay MA, Bhattacharya S, Gaver D, et al. Ventilation induced lung injury : in vivo and in vitro mechanism. Am J Physiol lung Cell Mol Physiol, 2002, 283(4):678-682
[38] Dhanireddy S, Altemeier WA, Matute-Bello G, et al. Mechanical ventilation induces inflammation, lung injury, and extra-pulmonary organ dysfunction in experimental pneumonia. Lab Invest. 2006, 86(8):790-799.
[39] Eumorfia Kondili, Nectaria Xirouchaki, Katerina Vaporidi, Short-term Cardio respiratory Effects of Proportional Assist and Pressure-support Ventilation in Patients with Acute Lung Injury/Acute Respiratory Distress Syndrome Anesthesiology, 2006, 105:703–8
[40] Tsangaris I, Lekka M.E, Kitsiouli E, et al. Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury. Eur Respir J. 2003, 21: 495–501
[41] P. Dahlem , A.P. Bos, J.J. Haitsma, et al. Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury Eur Respir J , 2006, 28: 992–998
[42] H.A. Vreugdenhil, C.J. Heijnen, F.B. Plotz, et al. Mechanical ventilation of healthy rats suppresses peripheral immune function. Eur Respir J, 2004, 23: 122–128
[43] S.-C. KO, H. ZHANG, J. J. HAITSMA et al. Effects of PEEP levels following repeated recruitment maneuvers on ventilator-induced lung injury. Acta Anaesthesiol Scand 2008: 1–8
[44] Emilie Lam and Claudia C. dos Santos .et al. Advances in molecular acute lung injury/acute respiratory distress syndrome and ventilator-induced lung injury: the role of genomics, proteomics, bioinformatics and translational biology. Curr Opin Crit Care, 2008 ,14:3–10
[45] Imai Y,Parodo J,Kajikawa O, et al. Injurious mechanical ventilation and end organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome.JAMA, 2003,289(16):2104-2112.
[46] James A. Frank, Charlie M. Wray, Danny F. Mcauley, et al. Alveolar macrophages contribute to alveolar barrier dysfunction in ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol . 2006,291: 1191–1198
[47] Mantell LL,Shaffer TH,Horowitz S,et al.Distinct patterns of apoptosis in the lung during liquid ventilation compared with gas ventilation.Am J Physiol Lung Cell Mol Physiol,2002,283(1):31-41.
[48] May M,Strobel P,Preisshofen T,et al.Apoptosis and proliferation in lungs of ventilated and oxygen-treated preterm infants.Eur Respir J,2004,23(1): 113- 121.
[49]不同潮气量机械通气对大鼠支气管和肺组织细胞凋亡的影响。第一军医大学学报。2005,(4):536-542.
[2]郭光华,姚学俊,姚世红,等.吸入性损伤与机械通气.江西高校出版社. 1995,10.
[3] Ingrid Steinvall , Zoltan Bak , Folke Sjoberg et al. Acute respiratory distress syndrome is as important as inhalation injury for the development of respiratory dysfunction in major burns. Burns . 2007,10(7):1-11
[4] Susan Jain, Geoff Bellingan. Basic science of acute lung injury. Surgery (Oxford). 2007, 25(3):112-116
[5] Schmidt R, Luboeinski T, Markart P, et al. Alveolar antioxidant status in patients with acute respiratory distress syndrome. Eur Respir J 2004,(24): 994–999
[6] New insights into the pathology of acute respiratory failure. Jose L. Mendez and Rolf D. Hubmayr. Curr Opin Crit Care 2005, ( 11):29–36.
[7] Rabinder Randhawa, Geoff Bellingan. Acute lung injury. Anaesthesia And Intensive Care Medicine 2007,8(11) 477-480
[8] Arthur P Wheeler, Gordon R Bernard. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet 2007,(369): 1553–1565
[9] You-Lan Yang, Gau-Jun Tang, Yuh-Lin Wu, et al. Exacerbation of wood smoke-induced acute lung injury by mechanical ventilation using moderately high tidal volume in mice. Respiratory Physiology Neurobiology, 2008, 60(1): 99-108
[10] Matthay MA, Bhattacharya S, Gaver D, et al. Ventilation induced lung injury : in vivo and in vitro mechanism. Am J Physiol lung Cell Mol Physiol, 2002, Vol. 283(4):678-682
[11] Dhanireddy S, Altemeier WA, Matute-Bello G, et al. Mechanical ventilation induces inflammation, lung injury, and extra-pulmonary organ dysfunction in experimental pneumonia. Lab Invest. 2006, 86(8):790-799.
[12] Eumorfia Kondili, Nectaria Xirouchaki, Katerina Vaporidi, Short-term Cardio respiratory Effects of Proportional Assist and Pressure-support Ventilation in Patients with Acute Lung Injury/Acute Respiratory Distress Syndrome Anesthesiology 2006, 105:703–8
[13] Tsangaris I, Lekka M.E, Kitsiouli E, et al. Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury. Eur Respir J 2003, 21: 495–501
[14] P. Dahlem , A.P. Bos, J.J. Haitsma, et al. Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury Eur Respir J 2006, 28: 992–998
[15] H.A. Vreugdenhil, C.J. Heijnen, F.B. Plotz, et al. Mechanical ventilation of healthy rats suppresses peripheral immune function. Eur Respir J 2004, 23: 122–128
[16] S.-C. KO, H. ZHANG, J. J. HAITSMA et al. Effects of PEEP levels following repeated recruitment maneuvers on ventilator-induced lung injury. Acta Anaesthesiol Scand 2008: 1–8
[17] Emilie Lam and Claudia C. dos Santos .et al. Advances in molecular acute lung injury/acuterespiratory distress syndrome and ventilator-induced lung injury: the role of genomics, proteomics, bioinformatics and translational biology. Curr Opin Crit Care 2008, 14:3–10
[18] Imai Y,Parodo J,Kajikawa O, et al. Injurious mechanical ventilation and end organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome.JAMA,2003,289(16):2104-2112.
[19] James A. Frank, Charlie M. Wray, Danny F. Mcauley, et al. Alveolar macrophages contribute to alveolar barrier dysfunction in ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol 2006, 291: 1191–1198
[20] Belperio JA, Keane MP, Lynch JP 3rd,etal. The role of cytokines during the pathogenesis of ventilator assosiated and ventilator-induced lung Injury. Semin Respir Crit Care Med, 2006, 27(4):350-364.
[21] Okutani D, Han B, Mura M, et al. High-volume ventilation induces pentraxin 3 expression in multiple acute lung injury models in rats. Am J Physiol Lung Cell Mol. Physiol, 2007, 292(1): 144-153
[22] Hammerschmidt S, Kuhn H, Grasenack T, et al. Apoptosis and necrosis induced by cyclic mechanical stretching in alveolar typeⅡcells influence of captopril and L-Arginine. Pneumologie, 2004, 58(4):222-229
[23] Saito S,Ogawa J, Minamiya Y. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. AM J Physiol Lung Cell Mol Physiol, 2005, 289(3): 400-406
[24]胡国栋,蔡绍曦,陈英华,等.不同潮气量机械通气对大鼠支气管和肺组织细胞凋亡的影响.第一军医大学学报,2005,25(5):508-512
[25] May M,Strobel P, Preisshofen T, et al. Apoptosis and proliferation in lungs of ventilated and oxygen-treated preterm infants. Eur Respir J, 2004, 23(1):113-121
[26] Jerng JS, Hsu YC, Wu HD, et al. Role of the rennin-angitensin system in Ventilator-induced ung injury: An in vivo study in a rat model. Thorax. 2007, 18: 758-762
[27] Takenaka K, Nishimura Y, Nishiuma T, et al. Ventilator-induced lung injury is reduced in transgenic mice that overexpress endothelial nitric oxide synthase. Am J Physiol Lung Cell Mol Physiol, 2006, 290(6):1078-1086
[28] Li M, Qin YZ, MA LJ. Study of the effects on the heart function when different positive end expiratory pressure levels were used on patients treated with mechanical ventilation. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 2007, 19(2):86-89
[29] Rotta AT, Gunnarsson B, Fuhrman BP,et al. Comparison of lung protective ventilation strategies in a rabbit model of acute lung injury. Crit Care Med. 2001, 29(11):2176-2184.
[30] Van kaam AH, Haotsma JJ, De Jaegere A, et al. Open lung ventilation improves gas exchange and attenuates secondary lung injury in a piglet model of meconium aspiration. Crit Care Med.2004, 32(2):443-449
[31] Serge J.C.Verbrugge, Burkhard Lachmann and Jozef Kesecioglu. Lung protective ventilatory strategies in acute lung injury and acute respiratory distress syndrome: from experimental findings to clinical application Clin Physiol Funct Imaging .2007, 27:67–90.
[32] Peter Delong, James A. Murray, and Christopher K. Cook. Mechanical Ventilation in the Management of Acute Respiratory Distress Syndrome. Seminars in Dialysis. 2006, 19(6):517–524
[33] James E. Lynch, BS, RRT, J. Mark Cheek, BS, et al. Adjuncts to Mechanical Ventilation in ARDS. Semin Thorac Cardiovasc Surg 2006, 18:20-27
[34] Esther K. Wolthuis, Goda Choi, Mark C. Dessing, Mechanical Ventilation with Lower Tidal Volumes and Positive End-expiratory Pressure Prevents Pulmonary Inflammation in Patients without Preexisting Lung Injury. Anesthesiology 2008,108:46–54
[35] Nakazawa K, Yokoyama K, Yamakawa K, et al. Effect of positive end-expiratory pressure on inflammatory response in oleic acid-induced lung injury and whole lung lavage induced lung injury. J Anesth, 2007, 21(1):47-54
[36] Imai Y, Nakagawa S, Ito Y,et al. Comparison of lung protection strategies using conventional and high-frequency oscillatory ventilation. J Appl Physiol, 2001, 91(4): 1836-1844.
[37] Anton H. van Kaam, Jack J. Haitsma, Anne De Jaegere, et al. Open lung ventilation improves gas exchange and attenuates secondary lung injury in a piglet model of meconium aspiration。Crit Care Med 2004 ,32(2): 443-449
[38] Meyer J, Cox PN, Mckerlie C, et al. Protective strategies of high frequency oscillatory ventilation in a rabbit model. Pediatr Res, 2006, 60(4):401-406
[39] M. David and W. Heinrichs .High frequency oscillatory ventilation and an interventional lung assist device to treat hypoxaemia and hypercapnia. British Journal of Anaesthesia 2004,93 (4): 582–586
[40]Cacciari A, Ruggeri G, Mordenti M,et al. High-frequency oscillatory ventilation versus conventional mechanical ventilation in congenital diaphragmatic hernia. Eur J Pediatr Surg, 2001, 11(1):3-7.
[41] Dembinski R, Max M,Bensberg R, et al. High frequency oscillatory ventilation in experimental lung injury: effects on gas exchange. Intensive Care Med, 2002, 28(6):768-774
[42] Katharina Von Der Hardt, Michael Andreas Kandler, Ludger Fink, et al. High Frequency Oscillatory Ventilation Suppresses Inflammatory response in Lung Tissue and Microdissected Alveolar Macrophages in Surfactant Depleted Piglets Pediatric Research Vol. 55, No. 2, 2004
[43] Yoder BA, Siler-Khodr T, Winter VT, et al. High-frequency oscillatory ventilation: effects on lung function, mechanics, and airway cytokines in the immature baboon model for neonatal chronic lung disease. Am J Respir Crit Care Med, 2000, 162(5):1867-1876.
[44] John H. Arnold, ; Nick G. Anas, Peter Luckett, High-frequency oscillatory ventilation in pediatric respiratory failure: A multicenter experience; Crit Care Med 2000, 28(12): 3913- 3919
[45] Ben Jaballah N, Khaldi A, Mnif K,et al. High-frequency oscillatory ventilation in pediatric patients with acute respiratory failure. P ediatr Crit Care Med,2006, 7(4):362-367.
[46] Angela T Wratney , Michael A Gentile , Donna S Hamel , et al. Successful Treatment ofAcute Chest Syndrome With High-Frequency Oscillatory Ventilation in Pediatric Patients. Respir Care 2004, 49(3):263–269.
[47] Gerstmann DR, Wood K, Miller A, et al . Childhood outcome after early high frequency oscillation ventilation for neonatal respiratory distress syndrome. Pediatrics,2001, 108(3): 617-662.
[48] N. Gullberg, P. Winberg and H. Sellde N,et al. Changes in mean airway pressure during HFOV influences cardiac output in neonates and infants. Acta Anaesthesiol Scand. 2004, 48: 218—223
[49] Sangeeta Mehta, John Granton, Rod J. MacDonald, et al. High Frequency Oscillatory Ventilation in Adults .CHEST 2004, 126:519-527
[50] Bollen CW, Van Well GT, Sherry T, et al. High frequeney oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a ramdomized controlled trial. Crit Care, 2005, 9 (4):430-439.
[51] Sangeeta Mehta, MD, FRCPC; Stephen E. Lapinsky, et al. Prospective trial of high- frequency oscillation in adults with acute respiratory distress syndrome. Crit Care Med 2001 29(7): 1360-1369
[52] Fort P, Farmer C, Westerman J, et al. High frequency oscillatory ventilation for adult respiratory distress syndrome, a pilot study. Crit Care Med,1997 ,25:937-947
[53] F. A. Andersen, A. B. Guttormsen and H. K. Flaatten. High frequency oscillatory ventilation in adult patients with acute respiratory distress syndrome a retrospective study. Acta Anaesthesiol Scand 2002, 46: 1082–1088
[54] Stephen Derdak, DO。High-frequency oscillatory ventilation for acute respiratory distress syndrome in adult patients。Crit Care Med 2003,31(4): (Suppl.) 317-323
[55] Rob Cartotto, Andrew B. Cooper, John R. Esmond, et al. Early Clinical Experience with High-Frequency Oscillatory Ventilation for ARDS in Adult Burn Patients. Journal of Burn Care & Rehabilitation. 2003,22(5): 325-333
[56] Cartotto R, Ellis S, Gomez M, et al.Use of high frequency oscillatory ventilation in burn patients. Crit Care Med, 2005, 33( suppl):175-181.
[57] Cartotto R, Ellis S, Gomez M, et al. High frequency oscillatory ventilation in burn patients with the acute respiratory distress. Burns, 2004, 30 (5):453-463.
[58] Kao KC,Tsai YH, WU YK, et al. High frequency oscillatory ventilation for surgical patients with acute respiratory distress syndrome. J Trauma, 2006, 61(4):837-843.
[59] Andrew B. Cooper, Avinash Islur Bsc, et al. Hypercapnic respiratory failure and partial upper airway obstruction during high frequency oscillatory ventilation in an adult burn patient. Can J Anesth 2002, 49(7): 724–728.
[60] Jaarsma AS, Braaksma MA, Geven WB, et al. Early activation of inflammation and clotting in the preterm lamb with neonatal RDS: comparison of conventional ventilation and high frequency oscillatory ventilation. Pediatr Res. 2001 ,50(5):650-657
[61] Demory D, Michelet P, Arnal JM, et al. High-frequency oscillatory ventilation following prone positioning prevents a further impairment in oxygenation. Crit Care Med, 2007, 35(1):564-568
[62] Alexandre T. Rotta, MD; Mário Eduardo G. Viana, MD; Budi Wiryawan, Combining lung-protective strategies in experimental acute lung injury: The impact of high frequency partial liquid ventilation. Pediatr Crit Care Med 2006,7(6): 562-570
[63] Chang Won Choi, Sun Young Koh Yun Sil Chang, Effects of perfluorocarbon Associated High Frequency Oscillatory Ventilation on Hemodynamics and Gas Exchange in the Newborn Piglets with Respiratory Distress. J Korean Med Sci 2003, 18: 663-8
[64] Kohelet D. Nitric oxide inhalation and high frequency oscillatory ventilation for hypoxemic respiratory failure in infants.Isr Med Assoc J, 2003, 5(1):19-23.
[65] Dobyns EL, Anas NG, Fortenberry JD, et al. Interactive effects of high-frequency oscillatory ventilation and inhaled nitric oxide in acute hypoxemic respiratory failure in pediatrics. Crit Care Med, 2002, 30(11):2425-2429.
[66]胡庆宏郭光华,等.吸入伤犬部分液体通气后血生化指标变化与动脉血氧分压分压的关系。中华烧伤杂志,2002,18:142-144
[67] Jurgen P. Meinhardta, Ulrike Friessa, Hans Joachim Bendera, Relationship among cardiac index, inspiration/expiration ratio, and perfluorocarbon dose during partial liquid ventilation in an oleic acid model of acute lung injury in sheep. Journal of Pediatric Surgery. 2005. 40, 1395–1403
[68] K. W. Southern, W. K. Funkhouser, I. Kazachkova. Airway surface liquid recovered by lavage with perfluorocarbon liquid in cats. European Journal of Clinical Investigation. 2002,32; 956–961
[69] G.F. Vazquez de Anda, R.A. Lachmann, S.J.C. Verbrugge, Partial liquid ventilation improves lung function in ventilation induced lung injury .Eur Respir J 2001, 18: 93–99
[70] Jean-Damien Ricard, Franck Iserin, Didier Dreyfuss, et al. Perflubron dosing affects ventilator-induced lung injury in rats with previous lung injury Crit Care Med 2007, 35(2): 561-567
[71] Juergen P. Meinhardt, Marc Schmittner, Peter Herrmann. Comparison of Different Inhalational Perfluorocarbons in a Rabbit Model of Acute Lung Injury. Asaio Journal 2005, 51:85–91.
[72] Scot T. Bateman, MD; Allan Doctor, MD; Barry Price, et al. Optimizing intrapulmonary perfluorocarbon distribution: Fluoroscopic comparison of mode of ventilation and body position.Crit Care Med. 2001, 29(3): 601-608
[73] Wolf S, Lohbrunner H, Busch T, et al. Small dose of exogenous surfactant combined with partial liquid ventilation in experimental acute lung injury: effects on gas exchange, haemodynamics, lung mechanics, and lung pathology.Br J Anaesth, 2001, 87(4):593-601.
[74] Fellery de Lange, Kenji Yoshitani, Alan D. Proia, MD, et al. Perfluorocarbon Administration During Cardiopulmonary Bypass in Rats: An Inflammatory Link to Adverse Outcome?Anesth Analg 2008, 106:24–31)
[75] Ellen Schoof, Katharina von der Hardt, Michael A. Kandler, et al. Aerosolized perfluorocarbon reduces adhesion molecule gene expression and neutrophil sequestration in acute respiratory distress.European Journal of Pharmacology,. 2002, 457(2):Pages 195-200.
[76] Allan Doctor, MD; Barry Price, RRT; Neeraj Bhargava, BA, et al. High frequency oscillatory ventilation of the perfluorocarbon-filled lung: Dose-response relationships in an animal model of acute lung injury Crit Care Med. 2001, 29(4): 847-854
[77] Anne Greenough . High frequency oscillation and liquid ventilation. Paediatric respiratory reviews. 2006, 7:186–188
[78]郭光华,钱克俭,朱峰,等.高频部分液体通气对吸入犬呼吸循环功能的影响。中华烧伤杂志,2002,18(6):346-349
[79]Wang SG, Guo GH, FU ZH,et al. Effects of high-frequency oscillatory ventilation and partial liquid ventilation on acute lung injury induced by steam inhalation in new Zealand rabbits. Annals of Burns and Fire Disasters, 2006,ⅪⅩ(2):88-94.
[80]朱佩芳,黎鳌,姜坤元,等.重度呼吸道蒸汽烧伤动物(狗)模型的制作.解放军医学杂志.1983,8(1):7-10.
[81] Ren-Feng Guo, Peter A. Ward. Mediators and regulation of neutrophil accumulation in inflammatory responses in lung: insights from the IgG immune complex model.Free Radical Biology and Medicine, 2002, 33(3):303-310
[82] Mayumi Hirose, Toshiyuki Murai, Hiroto Kawashima. Elevation of rat plasma P-selectin in acute lung injury. Biochimica Biophysica Acta (BBA) - Molecular Basis of Disease, 2007, 1772(3):382-389
[83] Frank Hildebrand, Hans-Christoph Pape, Paul Harwood, et al. Role of adhesion molecule ICAM in the pathogenesis of polymicrobial sepsis.Experimental and Toxicologic Pathology, 2005,56(21):281-290
[84]孙萌,井丽娟, E选择素与急性肺损伤国际儿科学杂志2007,34(2):93-95
[85] Hidemi Ishii, Kimihiko Takada. Bleomycin Induces E-selectin Expression in Cultured Umbilical Vein Endothelial Cells by Increasing Its mRNA Levels through Activation of NF-κB/Rel.Toxicology and Applied Pharmacology, 2002, 184(2):88-97
[86]马希刚,曹相原,张珍祥,等.火把花根片抑制大鼠急性肺损伤黏附分子表达中国病理生理杂志.2007, 23 (12):2394-2397
[87] Hirotsugu Hayashi, Haruhiko Koike, Yukiko Kurata, et al. Protective effects of sialyl Lewis X and anti-P-selectin antibody against lipopolysaccharide induced acute lung injury in rabbits. European Journal of Pharmacology, 1999, 370 (1):47-56
[88] Allen E. Haddrell, Stephen F. van Eeden, George R. Agnes.Dose response studies involving controlled deposition of less than 100 particles generated and levitated in an ac trap onto lung cells, in vitro, and quantitation of ICAM-1 differential expression.Toxicology in Vitro, 2006, 20(6): 1030-1039
[89] Ndukauba M. Eleghasim, Allen E. Haddrell, Stephen van Eeden,et al. The preparation of 100particles per trial having the same mole fraction of 12 inorganic compounds at diameters of 6.8, 3.8, or 2.6μm followed by their deposition onto human lung cells (A549) with measurement of the relative downstream differential expression of ICAM-1.International Journal of Mass Spectrometry, 2006, 258(3):Pages 134-141.
[90] M. Tufano, I. Paoletti, B. Perfetto,P1762 Effect of moxifioxacin and human beta-defensin 2 on ICAM-1 and cytokines expression in human lung epithelial cell line.International Journal of Antimicrobial Agents, Volume 29, 2007, 29(Suppl): 501.
[91] Ruijin Li, Ziqiang Meng, Jingfang Xie.Effects of sulfur dioxide on the expressions of MUC5AC and ICAM-1 in airway of asthmatic rats.Regulatory Toxicology and Pharmacology, 2007, ,48(3): 284-291
[92] Kymberly Gowdy, Quentin T. Krantz, Mary Daniels,et al. Modulation of pulmonary inflammatory responses and antimicrobial defenses in mice exposed to diesel exhaust.Toxicology and Applied Pharmacology, In Press, Corrected Proof, Available online 15 February 2008
[93] K. Maeda, K. Kai, T. Hayashi, K. Hasegawa, T. Matsumura. et al.Intercellular Adhesion Molecule-1 (ICAM-1) and Lymphocyte Function associated Antigen-1 (LFA-1) Contribute to the Elimination of Equine Herpesvirus Type 1 (EHV-1) from the Lungs of Intranasally Infected BALB/c Mice. Journal of Comparative Pathology, 2004, 130(3): Pages 162-170
[94]陈雯,许国根,陈颖,等.急性肺损伤患者血管内皮生长因子改变的意义内科急危重症杂志2007,13(2):74-75
[95] Janet D. Pierce, Dsn, Arnp, Ccrn Jana Pierce, et al. The role of apoptosis in respiratory diseases. Clinical nursespecialist.2007; 21: 22-28J, 2004, 23(1):113-121.
[96]李文军,杨宗城,杨晓东,等.烟雾吸入伤大鼠肺组织细胞凋亡及凋亡调控基因表达的变化.解放军医学杂志,2002,27(2):142-144
[97]农凌波,急性肺损伤中细胞的凋亡及凋亡的调控。国外医学呼吸系统分册,2002,22(3):149-151
[98] Reinout A. Bem, Albert P. Bos, Gustavo Matute Bello, et al. Lung epithelial cell apoptosis during acute lung injury in infancy. Pediatr Crit Care Med 2007 Vol. 8, No. 2 132-137
[99]张国友,邓小川.细胞凋亡与急性呼吸窘迫综合征。国际麻醉学与复苏杂志,2005,26(6):375-377
[100] Saito S,Ogama J,Minamiya Y. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol.,2005, 289(3):400-406
[101] Tadaaki Yamada, Yoshinobu Iwasaki, Kazuhiro Nagata,et al.Thioredoxin-1 protects against hyperoxia-induced apoptosis in cells of the alveolar walls. Pulmonary Pharmacology & Therapeutics, 2007, , 20(6):650-659
[102]黄英,刘国祥.肺泡Ⅱ型上皮细胞凋亡在急性肺损伤中的作用.中国现代医学杂志, 2002,12(3):35-37.
[103] Leanne M. Sutherland, Yasmin S. Edwards, Andrew W. Murray. Alveolar type II cell apoptosis. Comparative Biochemistry and Physiology - Part A: Molecular & IntegrativePhysiology, 2001, , 129(1): 267-285
[104]宋勇,毛宝龄,钱桂生,等.急性肺损伤大鼠肺组织细胞凋亡和FasPFasL表达的改变及其意义.中华医学杂志,1999,79(3):230-232.
[105] Stefan Hammerschmidt, Hartmut Kuhn, Christian Gessner,et al. Stretch-Induced Alveolar Type II Cell Apoptosisl. Role of Endogenous Bradykinin and PI3K-Akt Signaling American Journal of Respiratory Cell and Molecular Biology. 2007,( 37): 699-705
[106] Stefan Hammerschmidt, Hartmut Kuhn, Thomas Grasenack et al. Apoptosis and Necrosis Induced by Cyclic Mechanical Stretching in Alveolar Type II Cells .American Journal of Respiratory Cell and Molecular Biology. 2004, 30:396-402
[107] Yumiko Imai, Jean Parodo, Osamu Kajikawa,et al. Injurious Mechanical Ventilation and End-Organ Epithelial Cell Apoptosis and Organ Dysfunction in an Experimental Model of Acute Respiratory Distress Syndrome JAMA.2003, 289:2104-2112
[108] Mantell LL, Shaffer TH, Horowitz S, et al. Distinct patterns of apoptosis in the lung during liquid ventilation compared with gas ventilation. Am J Physiol Lung Cell Mol Physiol, 2002, 283(1):31-41.
[109] Vertrees RA, Nason R,Hold . Smoke/burn injury-induced respiratory failure elicits apoptosis in ovine lungs and cultured lung cells, ameliorated with Arteriovenous CO2 removal.Chest, 2004, 125(4):1472-1482.
[110]刘忠令,李强.呼吸疾病介入诊疗学。(M)北京:人民军医出版社。2003:81-86。
[111]中华医学会呼吸病学分会支气管肺泡灌洗液细胞学检测技术规范(草案)中华结核和呼吸杂志2002 ,25(7):390-391
[112] Merdad V. Parsey, Debra Kaneko, Robert Shenkar, et al. Neutrophil Apoptosis in the Lung after Hemorrhage or Endotoxemia: Apoptosis and Migration Are Independent of IL-1β. Clinical Immunology, 1999, , 91(2): Pages 219-225
[113] Keu Sung Lee, Young Hwa Choi, Young Sun Kim, et al. Evaluation of bronchoalveolar lavage fluid from ARDS patients with regard to apoptosis. Respiratory Medicine, 2008, 102(3): 464-469
[114] M.W.R. Pletz, M. Ioanas, A. de Roux .et al. Reduced spontaneous apoptosis in peripheral blood neutrophils during exacerbation of COPD. Eur Respir J, 2004, 23: 532–537
[115] M. Muller, J. Grunewald, C. Olgart Hoglund. et al. Altered apoptosis in bronchoalveolar lavage lymphocytes after allergen exposure of atopic asthmatic subjects. Eur Respir J 2006, 28: 513–522
[116]许国根,陈雯,陈颖,等.急性肺损伤病人中性粒细胞凋亡变化的研究.中国急救医学,2004,24(4):242-244
[117] Naveed Hussain, Fengying Wu, Li Zhu,et al. Neutrophil Apoptosis during the Development and Resolution of Oleic Acid-Induced Acute Lung Injury in the Rat. Am. J. Respir. Cell Mol. Biol.1998, 19(6):867-874
[118] Patricia M de Souza, Mark A Lindsay. Apoptosis as a therapeutic target for the treatment of lung disease.Current Opinion in Pharmacology, 2005, 5(3): 232-237
[1]刘忠令、李强主编呼吸疾病介入诊疗学。人民军医出版社。2003:81-86。
[2]李强,呼吸内镜学.上海:上海科技出版社, 2003: 315-318
[3]俞森祥,张进川1当代呼吸疗法[M]1第1版1北京:北京医科大学.中国协和医科大学联合出版社,1994 ,202～2201 [4 ] Noel2Georis I ,Bernard A , Falmagne P , et al . Database of bronchoalveolar lavage fluid proteins[J ] . J Chromatogr B Analyt Technol Biomed Life Sci , 2002 , 771 (122) :221-236.
[5]中华医学会呼吸病学分会支气管肺泡灌洗液细胞学检测技术规范(草案)中华结核和呼吸杂志2002 ,25(7):390-391
[6]代华平王辰Ulrich Costabel特发性间质性肺炎的分类中华医学杂志2002 , 82(12) 861-862。
[7] Blondeau K,Dupont L,Mertens V. Gastroesophageal reflux and aspiration of gastric contents in adult patients with cystic fibrosis. Gut. 2008 Mar 27.
[8] Steinberg KP , Mitchell DR , Maunder RJ , et al. Safety of bronchoalveolar lavage in patients with adult respiratory distress syndrome [ J ] 1 Am Rev Respir Dis ,1993 ,148 :556～5691
[9] Hamacher J ,Lucas R ,Lijnen HR , et al . Tumor necrosis factor-alpha and angiostatin are mediators of endothelial cytotoxicity in bronchoalveolar lavages of patients with acute respiratory distress syndrome [ J ] . Am J Respir Crit Care Med ,2002 ,166 (5) :651-656.
[10] Drent M, Wagenaar SS , Mulder PH , et al。Chest ,1994 ,105(2) :514-519。
[11] Mills NE , Fishman CL , Scholes J , et al. J Natl Cancer inst1995, 87(14):1056-1060.
[12] Gustavo Matute-Bello .Mark M. Wurfel .Janet S. Lee. et al .Essential role of MMP-12 in FAS-induced lung fibrosis. Am J Respir Cell Mol Biol. 2007;4:19-25。
[13] P.R.M. Rocco, D.P. Momesso, R.C. Figueira, et al .Therapeutic potential of a new phosphodiesterase inhibitor in acute lung injury. Eur Respir J 2003; 22: 20–27。
[14] I. Tsangaris, .M.E. Lekka, E. Kitsiouli, et al . Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury. Eur Respir J 2003; 21: 495–501
[15] R. Schmidt, T. Luboeinski, P. Markart, et al. Alveolar antioxidant status in patients with acute respiratory. distress syndrome Eur Respir J 2004; 24: 994–999
[16] Nussbaum E. Pediatric fiberoptic bronchoscopy :Clinical experience with 2 ,836 bronchoscopies[J ] . Pediatr Crit Care Med ,2002 ,3 (2) :171-176.
[17] Marguet C ,Dean T ,Warner JO. Soluble intercellular adhesion molecule-1( sICAM-1 ) and interferon-gamma in bronchoalveolar lavage fluid from children with airway diseases [J ] . Am J Respir Crit Care Med , 2000 , 162(3):1016-1022.
[18]吕培中,周苏明,邹春英,等.机械通气下支气管肺泡灌洗治疗老年重症肺部感染.实用老年医学, 2002, 16(5) : 264-265
[19]周凤丽,唐英春.支气管肺泡灌洗在呼吸道感染诊治中的应用[M]医学综述, 2000 , 7(6) :306～3071
[20] Koh YY, Park Y,Lee HJ ,et al . Levels of I nterleukin-2 , interferon-gamma ,and interleukin-4 in bronchoalveolar lavage fluid from patients with Mycoplasma pneumonia : implication of tendency toward increasedimmunoglobulin E production [J ] . Pediatrics ,2001 ,107 (3) :E39.
[21] Sekizawa K,Ujud Y, Itabashi S, et al. Lack of Cough in aspiration pneumonia. Lancet, 1999, 355 (6) : 1228-1229
[1] Janet D. Pierce, Dsn, Arnp, Ccrn Jana Pierce, et al. The role of apoptosis in respiratory diseases. Clinical nursespecialist. 2004, 23(1):113-121.
[2] Susan Jain, Geoff Bellingan. Basic science of acute lung injury. Surgery (Oxford), 2007, 25(3): 112-116
[3] Schmidt R, Luboeinski T, Markart P, et al. Alveolar antioxidant status in patients with acute respiratory distress syndrome. Eur Respir J. 2004, 24: 994–999
[4] New insights into the pathology of acute respiratory failure. Jose L. Mendez and Rolf D. Hubmayr. Curr Opin Crit Care . 2005 11:29–36.
[5] Rabinder Randhawa, Geoff Bellingan. Acute lung injury. Anaesthesia And Intensive Care Medicine .2007; 8(11): 477-480
[6] Arthur P Wheeler, Gordon R Bernard. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007; 369: 1553–1565
[7] Reinout A. Bem, Albert P. Bos, Gustavo Matute Bello, et al. Lung epithelial cell apoptosis during acute lung injury in infancy. Pediatr Crit Care Med 2007 , 8(2): 132-137
[8]张国友,邓小川。细胞凋亡与急性呼吸窘迫综合征。国际麻醉学与复苏杂志,2005,26(6):375-377
[9] Saito S,Ogama J, Minamiya Y. Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol.,2005, 289(3): L400-406
[10]陈娟,许峰,蒋静等。氧化应激状态下肺泡Ⅱ型上皮细胞凋亡及细胞外信号调节激酶信号转导机制的研究。中国危重病急救医学。2007,4(19):193-196
[11]何琳,李涛平。肺泡Ⅱ型上皮细胞钠通道在肺水清除中信号转导的研究进展。国际呼吸杂志。2007,27(12):919-921
[12]陈力黎檀实。肺泡上皮细胞在ALI、ARDS中的研究进展。世界危重病医学杂志。2006,3(4):1409-1412。
[13]潘芳,李文志.肺泡Ⅱ型上皮细胞的体外培养及其在麻醉学研究领域的应用.国外医学麻醉学与复苏分册。2000,21(6):368—371.
[14] Crandall ED,Matthay MA.Alveolar epithelial transport.Am J Respir Crit Care Med. 2001,163:1021.
[15] Sartori C,Matthay MA.Alveolar epithelial fluid transport in acute lung injury :new insights.Eur Respir J. 2002,20:1299—1313.
[16] Matthay MA Clerici C ,Saumon G.Active fluid clearance from the distal air spaces of the lung.J Appl Physiol. 2002,93:1533.
[17]张秋金,李银平。肺泡上皮细胞功能特性与内毒素性急性肺损伤。中国危重病急救医学2005,17(6):382-384。
[18]农凌波,急性肺损伤中细胞的凋亡及凋亡的调控。国外医学呼吸系统分册。2002,22(3):149-151
[19] Tadaaki Yamada, Yoshinobu Iwasaki, Kazuhiro Nagata,et al.Thioredoxin-1 protects againsthyperoxia-induced apoptosis in cells of the alveolar walls. Pulmonary Pharmacology & Therapeutics, 2007, 20(6): 650-659
[20]黄英,刘国祥.肺泡Ⅱ型上皮细胞凋亡在急性肺损伤中的作用.中国现代医学杂志, 2002, 12(3):35-37.
[21] Ashkenszi A,Dixil VM,Death receptors signaling and modulation.Science.1998,281:1305-1308
[22]官健,金大地,金丽娟.多发伤合并休克大鼠肺脏中细胞凋亡的实验研究.中国危重病急救医学.1998.10:479-483
[23]王疑,张淑文等,细胞凋亡在大鼠急性肺损伤发生机制中的意义。中国危重急救医学.2002,13(2):90-94
[24] Hengarther M0.The biochemistry of apoptosis.Nature。2000.407 (68O5): 770-776
[25] Tesfaigzi J.Wild MB.Johnson NF,et al。Apoptosis is a pathway responsible for the resolution of endotoxin—induced alveolar type II cell hyperplasia in the rat.Love Respir Res Ins.1998;79(5):303-3ll
[26] Gruener,Dieter C,Walter E,et al.Culture and transformation of human airway epithelia cells.Am J Physiol,1995;268:347-360
[27]张玉芹,欧阳静萍,李瑞祥.硫氮唑酮在失血性休克犬肺泡Ⅱ型细胞的影响.中国现代医学杂志,2000, 10(6):9-11
[28] Dawicki DD,Chatterjee D,Wyche J,et al.Extracelluar ATP and adenosine cause apoptosis of pulmonary artery endothelial cells.Am J Physiol Lung Cell Mol Physiol,1997,273(2):L485-L494
[29] Merdad V. Parsey, Debra Kaneko, Robert Shenkar, et al. Neutrophil Apoptosis in the Lung after Hemorrhage or Endotoxemia: Apoptosis and Migration Are Independent of IL-1β. Clinical Immunology, Volume 91, Issue 2, May 1999, Pages 219-225
[30] Keu Sung Lee, Young Hwa Choi, Young Sun Kim, et al. Evaluation of bronchoalveolar lavage fluid from ARDS patients with regard to apoptosis.Respiratory Medicine, 2008, 102(4):464-469
[31] M.W.R. Pletz, M. Ioanas, A. de Roux .et al. Reduced spontaneous apoptosis in peripheral blood neutrophils during exacerbation of COPD. Eur Respir J 2004; 23: 532–537
[32] M. Muller, J. Grunewald, C. Olgart Hoglund. et al. Altered apoptosis in bronchoalveolar lavage lymphocytes after allergen exposure of atopic asthmatic subjects. Eur Respir J. 2006; 28: 513–522
[33]许国根,陈雯,陈颖,等.急性肺损伤病人中性粒细胞凋亡变化的研究.中国急救医学,2004,24(4):242-244
[34] Naveed Hussain, Fengying Wu, Li Zhu,et al. Neutrophil Apoptosis during the Development and Resolution of Oleic Acid-Induced Acute Lung Injury in the Rat. Am. J. Respir. Cell Mol. Biol.1998, 19(6):867-874
[35] Patricia M de Souza, Mark A Lindsay. Apoptosis as a therapeutic target for the treatment of lung disease.Current Opinion in Pharmacology, 2005, 283(4): 232-237
[36] You-Lan Yang, Gau-Jun Tang, Yuh-Lin Wu, et al. Exacerbation of wood smoke-induced acute lung injury by mechanical ventilation using moderately high tidal volume in mice. Respiratory Physiology Neurobiology, 2008, 160(1): 99-108
[37] Matthay MA, Bhattacharya S, Gaver D, et al. Ventilation induced lung injury : in vivo and in vitro mechanism. Am J Physiol lung Cell Mol Physiol, 2002, 283(4):678-682
[38] Dhanireddy S, Altemeier WA, Matute-Bello G, et al. Mechanical ventilation induces inflammation, lung injury, and extra-pulmonary organ dysfunction in experimental pneumonia. Lab Invest. 2006, 86(8):790-799.
[39] Eumorfia Kondili, Nectaria Xirouchaki, Katerina Vaporidi, Short-term Cardio respiratory Effects of Proportional Assist and Pressure-support Ventilation in Patients with Acute Lung Injury/Acute Respiratory Distress Syndrome Anesthesiology, 2006, 105:703–8
[40] Tsangaris I, Lekka M.E, Kitsiouli E, et al. Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury. Eur Respir J. 2003, 21: 495–501
[41] P. Dahlem , A.P. Bos, J.J. Haitsma, et al. Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury Eur Respir J , 2006, 28: 992–998
[42] H.A. Vreugdenhil, C.J. Heijnen, F.B. Plotz, et al. Mechanical ventilation of healthy rats suppresses peripheral immune function. Eur Respir J, 2004, 23: 122–128
[43] S.-C. KO, H. ZHANG, J. J. HAITSMA et al. Effects of PEEP levels following repeated recruitment maneuvers on ventilator-induced lung injury. Acta Anaesthesiol Scand 2008: 1–8
[44] Emilie Lam and Claudia C. dos Santos .et al. Advances in molecular acute lung injury/acute respiratory distress syndrome and ventilator-induced lung injury: the role of genomics, proteomics, bioinformatics and translational biology. Curr Opin Crit Care, 2008 ,14:3–10
[45] Imai Y,Parodo J,Kajikawa O, et al. Injurious mechanical ventilation and end organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome.JAMA, 2003,289(16):2104-2112.
[46] James A. Frank, Charlie M. Wray, Danny F. Mcauley, et al. Alveolar macrophages contribute to alveolar barrier dysfunction in ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol . 2006,291: 1191–1198
[47] Mantell LL,Shaffer TH,Horowitz S,et al.Distinct patterns of apoptosis in the lung during liquid ventilation compared with gas ventilation.Am J Physiol Lung Cell Mol Physiol,2002,283(1):31-41.
[48] May M,Strobel P,Preisshofen T,et al.Apoptosis and proliferation in lungs of ventilated and oxygen-treated preterm infants.Eur Respir J,2004,23(1): 113- 121.
[49]不同潮气量机械通气对大鼠支气管和肺组织细胞凋亡的影响。第一军医大学学报。2005,(4):536-542.
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |