HVHF对ALI/ARDS患者肺血管通透性及血浆中性粒细胞弹性蛋白酶和血管内皮生长因子的影响
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摘要
目的:ALI/ARDS(Acute Lung Injury/Acute Respiratory Distress Syndrome)是ICU(Intensive Care Unit)危重病患者的常见病,病死率高。渗透性肺水肿是ALI/ARDS的重要特征,应用脉波指示剂连续心排血量(Pulse Indicator Contious Cadiac Output, PICCO)技术测得的肺血管通透性(Pulmonary Vascular Permeability Index, PVPI)、血管外肺水指数(Extra Vascular Lung Water Index, EVLWI)是判断肺水肿类型和评价肺水肿程度的指标,动态监测EVLW可了解肺水肿的病情变化,为临床防止和治疗肺水肿提供直观依据。ALI/ARDS患者肺毛细血管内皮细胞与肺泡上皮细胞屏障的通透性增高,肺泡与肺间质内积聚大量的水肿液,其中富含蛋白如中性粒细胞弹性蛋白酶(Neutrophil Elastase,NE)及以中性粒细胞为主的多种炎症细胞。此外,肺泡上皮细胞以及成纤维细胞也能产生多种细胞因子如血管内皮生长因子(Vascular Endothel- ial Growth Factor,VEGF),进而加剧炎症反应过程。NE和VEGF具有强效的促炎作用,被认为是全身炎症反应的关键介质,可导致肺上皮和肺毛细血管内皮通透性增高从而引起不同程度的肺水肿。随着对ARDS的发病机制和连续性血液净化(Continuous Bood Purification, CBP)的作用机制的研究,20世纪80年代开始人们把血液净化引入ARDS的治疗,特别是持续高容量血液滤过(High volume Hemofiltration, HVHF)通过增加置换液输入量进一步提高对大中分子溶质的对流清除。本实验15例ALI/ARDS患者通过HVHF治疗前后应用PICCO技术观察EVLWI变化及氧合状态改善情况,同时检测HVHF治疗前后患者血浆NE和VEGF的变化,探讨血浆NE和VEGF在ALI/ARDS患者的作用机制及HVHF的清除作用对血管外肺水的影响。
方法:按1994年欧美联合会议(American-European Consensus Coference, AECC)定义的诊断标准选择ALI/ARDS患者15例,且这些患者具有应用HVHF治疗指征,给予HVHF治疗,并应用PiCCO监测仪(单指示剂经肺热稀释技术)记录患者入选时(T0)和HVHF治疗后24h(T1)、48h(T2)、72h(T3)的血管外肺水指数(EVLWI)、肺血管通透性指数(Pulmonary Vascular Permeability Index, PVPI)、胸腔内血容积指数(Intrathoracic Blood Volume Index,ITBVI)及氧合指数(Oxygenation ratio, PaO2/FiO2 ratio),中心静脉压(Central Venous Pressure, CVP),急性肺损伤评分(Lung Injury Score, LIS)和急性生理和慢性健康( Acute Physiology and Chronic Health Evaluation ,APACHEⅡ)评分,同时抽静脉血用酶联免疫吸附法(Enzyme Linked Immunosorbent Assay, ELISA)的方法测定患者血浆中性粒细胞弹性蛋白酶(NE)和血管内皮生长因子(VEGF)。根据患者预后分为存活组及死亡组,以及20名健康体检的志愿者作为血浆NE和VEGF水平的健康对照。
结果:
1 HVHF治疗后ALI/ARDS患者PICCO监测指标及PaO2/FiO2的变化:所有患者HVHF治疗过程后CVP,T3与T0时间点相比有统计学意义(P<0.05)。ITBVI各时间点没有统计学差异。EVLWI呈下降趋势,T2和T3与T0时间点相比均有统计学意义(P<0.05),比较PVPI发现T2与T0时间点差异有统计学意义(P<0.05),T3与T0时间点比较有显著统计学意义(P<0.01)。PaO2/FiO2升高,T1、T2与T0时间点比较均有统计学意义(P<0.05),且T3与T0比较有显著统计学意义(P<0.01)。
2 HVHF治疗前后ALI/ARDS患者APACHEⅡ评分、LIS评分的变化: HVHF治疗后APACHEⅡ评分逐渐降低,具有统计学意义(P<0.05)。LIS评分亦呈降低趋势,具有统计学意义(P<0.05或P<0.01)。
3 ALI/ARDS患者与健康志愿者比较:与健康志愿者比较,ALI/ARDS患者HVHF治疗前血浆NE和VEGF水平较健康志愿者均显著升高(P<0.01)。
4 HVHF治疗前后ALI/ARDS患者血浆NE和VEGF水平变化: HVHF治疗后所有患者血浆NE和VEGF水平均显著降低,与T0比较,各时间点差异均有统计学意义(P<0.05或P<0.01)。存活组患者血浆NE和VEGF水平呈下降趋势,T3与T0时间点相比差异有统计学意义(P<0.05);VEGF经HVHF干预后T3较T0时间点相比有显著统计学意义(P<0.01)。死亡组患者血浆NE和VEGF经治疗后48小时内有统计学意义(P<0.05),但72小时后均无统计学意义。超滤液中均检出NE和VEGF。
结论:
1 ALI/ARDS患者经过HVHF治疗后降低了肺血管通透性,减少了血管外肺水,改善了氧合状态。
2 ALI/ARDS患者血浆NE和VEGF水平增高,肺血管通透性增高,引起肺水肿,且持续高水平NE和VEGF的ALI/ARDS患者预后差。
3 HVHF治疗可通过清除ALI/ARDS患者血浆部分NE和VEGF,减轻炎症反应,改善肺血管通透性,减少血管外肺水,减轻肺水肿,从而改善氧合状态。
4 HVHF治疗可降低ALI/ARDS患者死亡率,改善预后,可作为治疗ALI/ARDS的重要手段之一。
Objective: ALI/ARDS (acute lung injury/acute respiratory distress syndrome) is the common diseases of critically ill patients in ICU (Intensive Care Unit), which with a high fatality rate. Permeability pulmonary edema was an important feature of the ALI/ARDS patients. Pulse indicator contious cadiac output (PICCO) technology can measured Pulmonary Vascular Permeability Index (PVPI) and Extravascular Lung Water Index (EVLWI) which are to determine the type of pulmonary edema and evaluation indicators. Dynamic monitoring of EVIWI can be helped to identify pulmonary edema, and to beneficial for clinical prevention and treatment of pulmonary edema. There are pulmonary capillary endothelial cells and alveolar epithelial cells barrier permeability, alveolar and interstitial pulmonary edema in ALI/ARDS patients. The accumulation of a large number of fluid, which is rich in protein such as Neutrophil Elastase (NE) and with a variety of neutrophil-based inflammatory cells is also found. In addition, the alveolar epithelial cells and fibroblasts can produce much inflammatory cytokines cytokines such as Vascular Endothelial Growth Factor (VEGF), and thus exacerbate inflammatory reactions. NE and VEGF which has a potent pro-inflammatory role of systemic inflammatory response are considered to lead to lung epithelial and pulmonary capillary endothelial permeability and contribute to pulmonary edema. With the development of the pathogenesis of ARDS and the mechanism of Continuous Blood Purification (CBP), people began to treat ARDS with CBP in 20th century. High Volume Hemofiltration (HVHF) is considered to increase the replacement fluid input and to improve the large and medium sized solutes removal. In this study, 15 patients with ALI/ARDS, were choosed before and after treatment with HVHF. PICCO technique was used to observe state of oxygen and the changes of EVLWI., while the changes of NE and VEGF were also detected before and after treatment with HVHF. The purpose of this study was to explore the role of plasma NE and VEGF in the pathophysiology of ALI/ARDS, the effects of extravascular lung water after treatment with HVHF.
Methods:
Fifteen patients,which were diagnosed as ALI/ARDS according to American-European Consensus Conference (AECC) criteria in 1994, were selected in this study. All the patients treated with HVHF and apply the PiCCO monitor (single-instruction agent through the lung-heat dilution technique). Records were enrolled at the following time points: pre-HVHF (T0) and after treatment with HVHF 24h (T1), 48h (T2), 72h (T3). The parameters included extravascular lung water index (EVLWI), pulmonary vascular permeability permeability index (PVPI), Oxygenation ratio (PaO2/FiO2 ratio), Intra-thoracic Blood Volume Index (ITBVI) ,central venous pressure (CVP), acute lung injury score (LIS) and acute physiology and chronic Health (APACHEⅡ) score. At the same time, venous blood samples were measured in plasma neutrophil elastase (NE) and vascular endothelial growth factor (VEGF) by enzyme linked immunosorbent assay (ELISA). According to the prognosis, the patients were divided into the survival group and death group. Twenty healthy volunteers were as a control for VEGF and NE levels.
Results:
1 The hemodynamic indexes and PaO2/FiO2 changes after HVHF treatment:
In 15 patients, compared with T3 and T0 point, CVP changes in pre-HVHF and pro-HVHF, were statistically significant difference (P<0.05). As for ITBVI, there were no statistically significant differences among all time points. EVLEI had downward trend, and T2 and T3 compared with T0 point were statistically significant difference (P<0.05). For PVPI, there are significant differences betewen T2 and T0 point (P<0.01). So did in T3 compared with T0 point (P<0.05). PaO2/FiO2 were increased, and T1, T2 compared with T0 time point were statistically significant difference (P<0.05), but the difference of T3 compared with T0 was significantly (P<0.01).
2 The APACHEⅡscore, LIS score changes before and after HVHF treatment :
APACHEⅡscore after treatment HVHF gradually reduced, with statistical significance (P<0.05). LIS score was also trend lower, with statistically significant (P<0.05 or P<0.01).
3 The comparison between ALI / ARDS patients and healthy volunteers: Compared with the healthy volunteers, the plasma NE, and VEGF in ALI /ARDS patients were significantly higher before HVHF treatment (P<0.01).
4 The VEGF and NE levels before and after HVHF treatment : After HVHF treatment, the NE and VEGF levels of all patients were significantly lower. Compared with the T0 point, each time point differences were statistically significant (P<0.05 or P<0.01). In survival group, the VEGF and NE levels showed a downward trend. Compared with T3 and T0 time Points, the difference was statistically significant (P<0.05). Compared with T0 point, The VEGF levels after HVHF treatment time point in T3 had significantly statistically difference (P<0.01). In death cases, treated within 48 hours, the NE, and VEGF had statistically significant difference (P<0.05), but there was no statistical difference after 72 hours. Ultrafiltrate were detected in both the NE and VEGF.
Conclusion:
1 For all the ALI/ARDS patients after HVHF treatment, pulmonary vascular permeability were reduced, and extravascular lung water decreased, and oxygen were improved.
2 For all the ALI/ARDS patients, neutrophil elastase and vascular endothelial growth factor levels were significantly higher compared with healthy people, and continuing high levels of NE and VEGF had poor prognosis.
3 HVHF treatment had the effects of clearing part of the NE and VEGF, reducing their concentrations, reducing inflammation and improving blood vessel permeability, and reducing extravascular lung water, and then reducing pulmonary edema, thereby improving the oxygen and status.
4 HVHF treatment can reduce the mortality of ALI/ARDS patients, improve the prognosis, which may be a useful treatment for ALI/ARDS.
方法:按1994年欧美联合会议(American-European Consensus Coference, AECC)定义的诊断标准选择ALI/ARDS患者15例,且这些患者具有应用HVHF治疗指征,给予HVHF治疗,并应用PiCCO监测仪(单指示剂经肺热稀释技术)记录患者入选时(T0)和HVHF治疗后24h(T1)、48h(T2)、72h(T3)的血管外肺水指数(EVLWI)、肺血管通透性指数(Pulmonary Vascular Permeability Index, PVPI)、胸腔内血容积指数(Intrathoracic Blood Volume Index,ITBVI)及氧合指数(Oxygenation ratio, PaO2/FiO2 ratio),中心静脉压(Central Venous Pressure, CVP),急性肺损伤评分(Lung Injury Score, LIS)和急性生理和慢性健康( Acute Physiology and Chronic Health Evaluation ,APACHEⅡ)评分,同时抽静脉血用酶联免疫吸附法(Enzyme Linked Immunosorbent Assay, ELISA)的方法测定患者血浆中性粒细胞弹性蛋白酶(NE)和血管内皮生长因子(VEGF)。根据患者预后分为存活组及死亡组,以及20名健康体检的志愿者作为血浆NE和VEGF水平的健康对照。
结果:
1 HVHF治疗后ALI/ARDS患者PICCO监测指标及PaO2/FiO2的变化:所有患者HVHF治疗过程后CVP,T3与T0时间点相比有统计学意义(P<0.05)。ITBVI各时间点没有统计学差异。EVLWI呈下降趋势,T2和T3与T0时间点相比均有统计学意义(P<0.05),比较PVPI发现T2与T0时间点差异有统计学意义(P<0.05),T3与T0时间点比较有显著统计学意义(P<0.01)。PaO2/FiO2升高,T1、T2与T0时间点比较均有统计学意义(P<0.05),且T3与T0比较有显著统计学意义(P<0.01)。
2 HVHF治疗前后ALI/ARDS患者APACHEⅡ评分、LIS评分的变化: HVHF治疗后APACHEⅡ评分逐渐降低,具有统计学意义(P<0.05)。LIS评分亦呈降低趋势,具有统计学意义(P<0.05或P<0.01)。
3 ALI/ARDS患者与健康志愿者比较:与健康志愿者比较,ALI/ARDS患者HVHF治疗前血浆NE和VEGF水平较健康志愿者均显著升高(P<0.01)。
4 HVHF治疗前后ALI/ARDS患者血浆NE和VEGF水平变化: HVHF治疗后所有患者血浆NE和VEGF水平均显著降低,与T0比较,各时间点差异均有统计学意义(P<0.05或P<0.01)。存活组患者血浆NE和VEGF水平呈下降趋势,T3与T0时间点相比差异有统计学意义(P<0.05);VEGF经HVHF干预后T3较T0时间点相比有显著统计学意义(P<0.01)。死亡组患者血浆NE和VEGF经治疗后48小时内有统计学意义(P<0.05),但72小时后均无统计学意义。超滤液中均检出NE和VEGF。
结论:
1 ALI/ARDS患者经过HVHF治疗后降低了肺血管通透性,减少了血管外肺水,改善了氧合状态。
2 ALI/ARDS患者血浆NE和VEGF水平增高,肺血管通透性增高,引起肺水肿,且持续高水平NE和VEGF的ALI/ARDS患者预后差。
3 HVHF治疗可通过清除ALI/ARDS患者血浆部分NE和VEGF,减轻炎症反应,改善肺血管通透性,减少血管外肺水,减轻肺水肿,从而改善氧合状态。
4 HVHF治疗可降低ALI/ARDS患者死亡率,改善预后,可作为治疗ALI/ARDS的重要手段之一。
Objective: ALI/ARDS (acute lung injury/acute respiratory distress syndrome) is the common diseases of critically ill patients in ICU (Intensive Care Unit), which with a high fatality rate. Permeability pulmonary edema was an important feature of the ALI/ARDS patients. Pulse indicator contious cadiac output (PICCO) technology can measured Pulmonary Vascular Permeability Index (PVPI) and Extravascular Lung Water Index (EVLWI) which are to determine the type of pulmonary edema and evaluation indicators. Dynamic monitoring of EVIWI can be helped to identify pulmonary edema, and to beneficial for clinical prevention and treatment of pulmonary edema. There are pulmonary capillary endothelial cells and alveolar epithelial cells barrier permeability, alveolar and interstitial pulmonary edema in ALI/ARDS patients. The accumulation of a large number of fluid, which is rich in protein such as Neutrophil Elastase (NE) and with a variety of neutrophil-based inflammatory cells is also found. In addition, the alveolar epithelial cells and fibroblasts can produce much inflammatory cytokines cytokines such as Vascular Endothelial Growth Factor (VEGF), and thus exacerbate inflammatory reactions. NE and VEGF which has a potent pro-inflammatory role of systemic inflammatory response are considered to lead to lung epithelial and pulmonary capillary endothelial permeability and contribute to pulmonary edema. With the development of the pathogenesis of ARDS and the mechanism of Continuous Blood Purification (CBP), people began to treat ARDS with CBP in 20th century. High Volume Hemofiltration (HVHF) is considered to increase the replacement fluid input and to improve the large and medium sized solutes removal. In this study, 15 patients with ALI/ARDS, were choosed before and after treatment with HVHF. PICCO technique was used to observe state of oxygen and the changes of EVLWI., while the changes of NE and VEGF were also detected before and after treatment with HVHF. The purpose of this study was to explore the role of plasma NE and VEGF in the pathophysiology of ALI/ARDS, the effects of extravascular lung water after treatment with HVHF.
Methods:
Fifteen patients,which were diagnosed as ALI/ARDS according to American-European Consensus Conference (AECC) criteria in 1994, were selected in this study. All the patients treated with HVHF and apply the PiCCO monitor (single-instruction agent through the lung-heat dilution technique). Records were enrolled at the following time points: pre-HVHF (T0) and after treatment with HVHF 24h (T1), 48h (T2), 72h (T3). The parameters included extravascular lung water index (EVLWI), pulmonary vascular permeability permeability index (PVPI), Oxygenation ratio (PaO2/FiO2 ratio), Intra-thoracic Blood Volume Index (ITBVI) ,central venous pressure (CVP), acute lung injury score (LIS) and acute physiology and chronic Health (APACHEⅡ) score. At the same time, venous blood samples were measured in plasma neutrophil elastase (NE) and vascular endothelial growth factor (VEGF) by enzyme linked immunosorbent assay (ELISA). According to the prognosis, the patients were divided into the survival group and death group. Twenty healthy volunteers were as a control for VEGF and NE levels.
Results:
1 The hemodynamic indexes and PaO2/FiO2 changes after HVHF treatment:
In 15 patients, compared with T3 and T0 point, CVP changes in pre-HVHF and pro-HVHF, were statistically significant difference (P<0.05). As for ITBVI, there were no statistically significant differences among all time points. EVLEI had downward trend, and T2 and T3 compared with T0 point were statistically significant difference (P<0.05). For PVPI, there are significant differences betewen T2 and T0 point (P<0.01). So did in T3 compared with T0 point (P<0.05). PaO2/FiO2 were increased, and T1, T2 compared with T0 time point were statistically significant difference (P<0.05), but the difference of T3 compared with T0 was significantly (P<0.01).
2 The APACHEⅡscore, LIS score changes before and after HVHF treatment :
APACHEⅡscore after treatment HVHF gradually reduced, with statistical significance (P<0.05). LIS score was also trend lower, with statistically significant (P<0.05 or P<0.01).
3 The comparison between ALI / ARDS patients and healthy volunteers: Compared with the healthy volunteers, the plasma NE, and VEGF in ALI /ARDS patients were significantly higher before HVHF treatment (P<0.01).
4 The VEGF and NE levels before and after HVHF treatment : After HVHF treatment, the NE and VEGF levels of all patients were significantly lower. Compared with the T0 point, each time point differences were statistically significant (P<0.05 or P<0.01). In survival group, the VEGF and NE levels showed a downward trend. Compared with T3 and T0 time Points, the difference was statistically significant (P<0.05). Compared with T0 point, The VEGF levels after HVHF treatment time point in T3 had significantly statistically difference (P<0.01). In death cases, treated within 48 hours, the NE, and VEGF had statistically significant difference (P<0.05), but there was no statistical difference after 72 hours. Ultrafiltrate were detected in both the NE and VEGF.
Conclusion:
1 For all the ALI/ARDS patients after HVHF treatment, pulmonary vascular permeability were reduced, and extravascular lung water decreased, and oxygen were improved.
2 For all the ALI/ARDS patients, neutrophil elastase and vascular endothelial growth factor levels were significantly higher compared with healthy people, and continuing high levels of NE and VEGF had poor prognosis.
3 HVHF treatment had the effects of clearing part of the NE and VEGF, reducing their concentrations, reducing inflammation and improving blood vessel permeability, and reducing extravascular lung water, and then reducing pulmonary edema, thereby improving the oxygen and status.
4 HVHF treatment can reduce the mortality of ALI/ARDS patients, improve the prognosis, which may be a useful treatment for ALI/ARDS.
引文
1 Eisenberg PR, Hansbrough JR, Anderson D, et al. A prospective study of lung water measurements during patient management in an intensive care unit. Am Rev Respir Dis, 1987, 136: 662-668
2 Matthay MA. Clinical measurement of pulmonary edema. Chest, 2002,122: 1877-1879
3 Luce JM. Acute lung injury and the acute respiratory distress syndrome. Crit Care Med ,1998, 26: 369-376
4 Huang H, Yao T, Wanq W, et al. Continuous ultrafiltration attrnuates the pulmonary injury that follows open heart surgery with cardiopulmonary bypass. Ann Thorac Surg. 2003, 76(1): 136-140
5 Koperna T, Voql SE, Poschl GP, et al. Cytokine patterns in patients in patients who undergo hemofiltration for treatment of multiple organ failur. World Journal of Surgery.1998, 22(5): 443-448
6 Su X, Bai C, Hong Q, Zhu D, et al. Effect of continuous hemofiltration on hemodynamics , lung inflammation and pulmonary edema in a canine model of acute lung injury. Intensive Care Med, 2003, 29(11): 2034-2042
7吴坚平,顾勇,丁峰,等.高容量血液滤过在犬急性肺损伤中的作用.中华肾脏病杂志, 2001, 17(5): 301-304
8 Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous hemofiltration on outcomes of acute renal failure: A prospective randomized trial. Lancet, 2000, 356: 26-30
9 Ware LB, Matthay MA: The acute respiratory distress syndrome. N Engl J Med, 2000, 342: 1334-1349
10 Piantadosi CA, Schwartz DA: The acute respiratory distress syndrome. Ann Intern Med, 2004, 141: 460-470
11 Wheeler AP, Bernard GR: Acute lung injury and the acute respiratory distress syndrome: A clinical review. Lancet, 2007, 369: 1553-1564
12 Katzenstein AL, Bloor CM, Leibow AA: Diffuse alveolar damage—the role of oxygen, shock, and related factors. A review. Am J Pathol, 1976, 85: 209-228
13 Schuster DP: What is acute lung injury? What is ARDS? Chest, 1995, 107: 1721-1726
14 Abraham E, Matthay MA, Dinarello CA, et al. Consensus conference definitions for sepsis, septic shock, acute lung injury, and acute respiratory distress syndrome: time for a reevaluation. Crit Care Med,2000, 28: 232-235
15 Menezes SL, Bozza PT, Neto HC, et al. Pulmonary and extrapulmonary acute lung injury: inflammatory and ultrastructural analyses. J Appl Physiol, 2005, 98: 1777-1783
16 Steinberg KP, Hudson LD, Goodman RB, et al. Efficacy and safety of corticosterPaO2/FiO2ds for persistent acute respiratory distress syndrome. N Engl J Med, 2006, 354: 1671-1684
17 Meduri GU, Headley AS, Golden E, et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: A randomized controlled trial. JAMA, 1998, 280: 159-165
18 Grasso S, Mascia L, Del Turco M, et al. Effects of recruiting maneuvers in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology, 2002, 96: 795-802
19 Monchi M, Bellenfant F, Cariou A, et al. Early predictive factors of survival in the acute respiratory distress syndrome. A multivariate analysis. Am J Respir Crit Care Med, 1998, 158: 1076-1081
20 Ferguson ND, Frutos-Vivar F, Esteban A, et al. Airway pressures, tidal volumes, and mortality in patients with acute respire- atory distress syndrome. Crit Care Med, 2005, 33: 21-30
21 Esteban A, Anzueto A, Frutos F, et al. Characteristics and outcomes in adult patients receiving mechanical ventilation: A 28-day international study. JAMA, 2002, 287: 345-355
22 Croce MA, Fabian TC, Davis KA, et al. Early and late acute respiratory distress syndrome: Two distinct clinical entities. J Trauma, 1999, 46: 361-366
23 Ware LB, Eisner MD, Thompson BT, et al. Significance of von Wille- brand factor in septic and nonseptic patients with acute lung injury. Am J Respir Crit Care Med, 2004, 170: 766-772
24 Clark JG, Milberg JA, Steinberg KP, et al. Type III procollagen peptide in the adult respiratory distress syndrome. Association of increased peptide levels in bronchoalveolar lavage fluid with increased risk for death. AnnIntern Med, 1995, 122: 17-23
25 Elings VB, Lewis FR. A single indicator technique to estimate extravascular lung water. J Surg Res, 1982, 33: 375-385
26 Sakka SG, Klein M, Reinhart K, et al. Prognostic value of extravascular lung water in Critically ill patients. Chest, 2002, 122 (6): 2080-2086
27 Ferna’ndez-Monde’jar E, Rivera-Ferna’ndez R,Garci’a-Delgado M,et al. Small increases in extravascular lung water are accurately detected by transpulmonary thermodilution.J Trauma 2005, 59:1420-1424
28 Honore PM, Jamez J, Wauthier M, et al. Prospective valuation of short-term high-volume isovolemicpatients with intractable circulatory failure resulting from septic shock. Crit Care Med, 2000, 28 (11): 3581-3587
29刘卫江,谢长江,熊旭明.连续血液净化在感染性休克中的应用.中国血液净化, 2005, 4(4): 205-207
30 Tetta C, Bellomo R, Inguaggiato P, et al. Endotoxin and cytokine removal in sepsis. Ther Apher, 2002, 6(2): 109-115
31 Carlile PV, Lowery DD, Gray BA. Effect of PEEP and type of injury on thermal-dye estimation of pulmonary edema. J Appl Physiol, 1986, 60: 22-31
32 Michard F, Schachtrupp A, Toens C. Factors influencing the estimation of extravascular lung water by transpulmonary thermodilution in critically ill patients. Crit Care Med, 2005 Jun, 33(6): 1243-1247
33 Demling RH, Staub NC, Edmunds LH Jr. Effect of end-expiratory airway pressure on accumulation of extravascular lung water. J Appl Physiol, 1975,38: 907-912
34王殿华,刘旭,凌亦凌.中性粒细胞弹性蛋白酶与急性肺损伤.国外医学呼吸系统分册, 2004, 24 (6): 368-370
35黄晓军,王选锭.急性肺损伤抗氧化治疗的研究进展.临床内科杂志, 2004, 21 (10): 652-654
36 Donnelly SC, MacGregor I, Zamani A et al. Plasma elastase levels and the development of the adult respiratory distress syndrome. Am J RespirCrit Care Med, 1995, 151: 1428-1433
37 Greneveld AB, Raijmakers PG, Haik CE et al. Interleukin 8-related neutrophil elastase and the severity of the adult respiratory distress syndrome. Cytokine, 1995, 7 (7): 746-752
38 Berse B, Brown LF, Van de Water L, et al. Vascular permeability factor(vascular endothelial growth factor) gene is expressed differentially in normal tissues, macrophages, and tumours. Mol Biol Cell 1992, 3: 211-220
39 Boussat S, Eddahibi S, Coste A, et al. Expression and regulation of vascular endothelial growth factor in human pulmonary epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2000, 279: L371-378
40 Koyama S, Sato E, Tsukadaira A, et al. Vascular endothelial growth factor mRNA and protein expression in airway epithelial cell lines in vitro. Eur Respir J. 2002, 20: 1449-1456
41 Armstrong L, Millar AB, Thickett DR, et al. A role for vascular endothelial growth factor in acute and resolving lung injury. Am J Respir Crit Care Med 2002, 166: 1332-1337
42 Maniscalco WM, Watkins RH, Finkelstein JN, et al. Vascular endothelial growth factor mRNA increases in alveolar eptithelial cells during recove- ry from oxygen injury. Am J Respir Cell Mol Biol 1995, 13: 377-386
43 Thieme H,Aiello LP, Takagi H ,et al. Comparative analysis of vascular en dothelial growth factor receptors on retinal and aortic vascular endotheli- al cells. Diabetes.1995, 44: 98-103
44 Seko Y, Takahashi N , Shibuya M ,et al. Pulsatile stretch stimulartes vasc- ular endothelial growth factor(VEGF)secretion by cultured rat cardiac myocytes. Biochem Biophys Res Commun.1999 Jan 19, 254(2): 462-465
45 Ancelin M, Chollet-Martin S, HervéMA,et alVascular endothelial growth factor VEGF189 induces human neuteophil chemotaxis in extravascular tissue via an autocrine amplification mechanism. Lab Invest, 2004, 84(4): 502-512
46 Dvorak HF, Brown LF, Deteman M ,et al. Vascular permeability factor/vascular endothelial growth factor microvascular hypermeability and angiogenesis. Am JP athol. 1995, 146: 1029
47 TiltonR G, Chang KC, Lejeune WS, et al. Role for nitric oxide in the hyperpermeability and hemodynamic changes induced by intravenous VEGF. Invest Ophthalmol Vis Sci. 1999 Mar, 40(3): 689-696
48 Murielle G, Dlivier B,Valerie A, et al. Intracellular pool of vascularEndothelial Growth Factor in Human Neutrophils.J.Blood, 1997, 90(10): 4153-4161
49 Nimah M, Brilli RJ. Coagulation dysfunction in sepsis and multiple organ system failure. Crit Care Clin, 2003, 19(3): 441-458
50 Murray MJ ,Matthay MA ,Luce JM ,et al. An expanded definition of the adult repiratory distress syndrome. J Am Rev Respir Dis , 1988,138: 720 -730
51 Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, orthe response to volume infusion in normal subjects. Crit CareMed, 2004, 32 (3): 691-699
52 Connors AF Jr, Speroff T, Dawson NV, et al. The efectiveness of right heart catheterization in the initial care of critically ill patients. JAMA, 1996, 276 (11): 889-897
53肖秋生,张斌,潘永等. PICCO技术在多发伤患者指导液体复苏中的临床应用.四川医学, 2010, 31(1): 42-44
54 Krebs J, Pelos P, Tsagogiorgas C, et al. Effects of positive end-expiratory pressure on respiratory function and hemodynamics in patients with acute respiratory failure with and without intra-abdominal hypertension: a pilot study. Crit Care, 2009,13(5): 199
55 Xie J, Yang J, et al. Effect of continuous high-volume hemofiltration on patients with acute respiratory distress syndrome and multiple organ dysfunction syndrome. Zhongguuo Wei Zhong Bing Ji Jiu Yi Xue, 2009 Jul, 21(7): 402-404
1聂晓红,周向东.蛋白酶抑制剂对肺炎性损伤的保护作用.临床肺科杂志,2004,9 (6): 665-667
2王殿华,刘旭,凌亦凌.中性粒细胞弹性蛋白酶与急性肺损伤.国外医学呼吸系统分册, 2004,24 (6): 368-370
3 Lee WL, Downey GP. Leukocyte elastase: physiological functions and role in acute lung injury. AM J Respir Crit Care Med, 2001, 164: 896-904
4 Kazuhito Kawabata, Tetsuya Hagio, Shigeru Matsumoto, et al. Delayed neutrophil elastase inhibition prevents subsequent progression of acute lung injury induced by endotoxin inhalation in hamsters. Am J Respir Crit Care Med, 2000, 161 (6): 2013-2018
5徐晓艳,周向东.中性粒细胞弹性蛋白酶与黏蛋白.中国药物与临床, 2004, 4(10): 741-744
6 Donnelly SC, MacGregor I, Zamani A et al. Plasma elastase levels and the development of the adult respiratory distress syndrome. Am J Respir Crit Care Med, 1995, 151: 1428-1433
7 Greneveld AB, Raijmakers PG, Hack CE et al. Interleukin 8-related neutrophil elastase and the severity of the adult respiratory distress syndrome. Cytokine, 1995, 7 (7): 746-752
8 Taniguchi H, Koncloh Y, Ikuta N et al. Diagnosis of acute respiratory distress syndrome: analysis of bronchoalveolar lavage fluid. Nihon Kyobu Shikkan Gakkai Zasshi, 1995, 33 (Suppl): 251-256
9 Kawabata K, Hagio T, Matsuoka S. The role of neu- trophil elastase in acute lung injury. European Journal of Pharmacology, 2002, 451(1):1-10
10 Takashige Kuraki, Masayoshi Ishibashi, Masanori Takayama, et al. A novel oral neutrophil elastase inhibitor (ONO-6818) Inhibits human neutrophil elastase-induced emphysema in rats. Am J Respir Crit Care Med, 2002, 166: 496-500
11 Tetsuya Hagio, Shigeru Matsumoto, Shintaro Nakao, et al. Elastase inhibition reduced death associated with acid aspiration-induced lunginjury in hamsters. European Journal of Pharmacology, 2004, 488:173- 180
12 Hagio T, Matsumoto S Nakao S, et al. Sivelestat, a specific neutrophil elastase inhibitor, prevented phorbol myristate acetate-induced acute lung injury in conscious rabbits. Pulm Pharmacol Ther, 2005, 18: 285-290
13揭志军,罗勇,徐卫国等.急性肺损伤患者血清中中性粒细胞弹性蛋白酶活性的变化.中华急诊医学杂志, 2005, 14(6):497-499
14 Lee WL, Downey GP. Leukocyte elastase physiological functions and role in acute lung injury. AM J Respir Crit Care Med, 2001, 164: 896-904
15 Palmgren MS, Deshazo RD, Carter RM et al. Mechanisms of neutrophil damage to human alveolar extracellular matrix: the role of serine and metalloproteases.J Allergy Clin Immunol, 1992, 89: 905-915
16黄晓军,王选锭.急性肺损伤抗氧化治疗的研究进展.临床内科杂志, 2004, 21(10): 652- 654
17 Peter A Henriksena, Andrew Devitt, Yuri Kotelevtsev, et al. Gene delivery of the elastase inhibitor elafin protects macrophages from neutrophil elastase-mediated impairment of apoptotic cell recognition. J Federation of European Biochemical Societies, 2004, 574: 80-84
18 Kapui Z, Varga M, Urban-Szabo K, et al. Biochemical and pharma- cological characterization of 2-(9-(2-piperidinoethoxy)-4-oxo-4H-pyrido [1,2-a]pyrimidin-2-yloxymethyl)-4-(1-methylethyl)-6-methoxy-1,2-benzisothiazol-3 (2H)-one-1, 1-dioxide (SSR69071), a novel, orally active elastase inhibitor. J Pharmacol Exp Ther, 2003, 305(2): 451-459
19 Daudi I, Gudewicz PW, Saba TM et al. Proteolysis of gelatin-bound fibronectin by activated leukocytes: a role for leukocyte elastase. J Leukocyte Biol, 1991, 50: 33-340
20 Bedard M, McClured CD, Schiller NL et al. Release of interleukin-8, interleukin-6, and colony-stimulating factors by upper airway epithelial cells: implications for cystic fibrosis. Am J Respir Cell Mol Biol, 1993, 9: 455-462
21 Liau DF, Yin NX, Huang J et al. Effects of human polymorphonuclearleukocyte elastase upon surfactant proteins in vitro. Biochim Biophys Acta, 1996, 1302 (2): 117-128
22 Holter JF, Weiland JE, Pacht ER et al. Protein permeability in the adult respiratory distress syndrome. Loss of size selectivity of the alveolar epithelium. J Clin Invest, 1986, 78: 1513-1522
23 Wewers MD, Casolaro MA, Sellers SE, et al. Replacement therapy for alpha 1-antitrypsin deficiency associated with emphysema. N Engl J Med. 1987 Apr 23, 316(17): 1055-1062
24 Gossage JR, Kuratomi Y, Davidson JM et al. Neutrophil elastase inhibitors, SC-37698 and SC-39026, reduce endotoxin-induced lung dysfunction in awake sheep. Am Rev Respir Dis, 1993, 147: 1371-1379
25 Mikawa K, Nishina K, Takao Y, et al. Attenuation of cardiovascular responses to tracheal extubation: comparison of verapamil, lidocaine, and verapamil-lidocaine combination. Anesth Analg, 1997, 84: 1097-1103
26 Crystal RG, Bast A, Roshan-Ali Y et al. Oxidants and respiratory tract epithelial injury: pathogenesis and strategies for therapeutic intervention. AmJ Med, 1991, 91(Suppl 3C): 39-44
27 Wallaert B, Gressier B, Gosset P et al. Oxidative inactivation of alpha 1-proteinase inhibitor by alveolar epithelial type II cells. J Appl Physiol. 1993 Dec, 5(6): 2376-2382
28 Bunnell E, Pacht ER. Oxidized glutathione is increased in the alveolar fluid of patients with the adult respiratory distress syndrome. Am Rev Respir Dis, 1993, 148: 1174-1178
29 Suter PM, Domenighetti G, Schaller MD et al. N-acetylcysteine enhances recovery from acute lung injury in man. A randomized, double-blind, placebo-controlled clinical study. Chest, 1994, 105: 190-194
30 Gregory TJ, Berman PW, Wilkes DM et al. Comparison of the immune response to recombinant gp120 in humans and chimpanzees. AIDS, 1994, 8: 591-601
31 Miyazaki Y, Inoue T, Kyi M et al. Effects of a neutrophil elastase inh- ibitor (ONO-5046) on acute pulmenary injury induced by tumor necrosisfactor alpha (TNF alpha) an activated neutrophils in isolated perfused rabbit lungs. Am J Resp ir crit CareMed, 1998, 157: 89-94
32 Hagio T, Matsumoto S, Nakao S, et al. Elastase inhibition reduced death associated with acid aspiration-induced lung injury in hamsters. Eur J Pharmacol, 2004, 488: 173-180
33郑修艳,曹立莉,杜冠华.新型弹性蛋白酶抑制剂西维来司钠临床前药理及机制研究.中国新药杂志, 2004, 13: 292-295
34杜冠华,吴松,冯文化.西维来司钠治疗急性肺损伤研究现状.中国药学杂志, 2004, 39(5): 321-324
35徐凌,蔡柏蔷,单渊东等.弹性蛋白酶抑制剂对严重急性呼吸综合征急性肺损伤有效性和安全性随机开放、平行对照、多中心临床研究.中华内科杂志,2005, 44: 147-148
36 Kuraki T, Ishibashi M, Takayama M, et al. A novel oral neutrophil elastase inhibitor (ONO-6818) inhibits human neutrophil elastase -induced emphysema in rats. Am J Respir Crit Care Med, 2002, 166: 496-500
37 Tamakuma S, Ogawa M, Aikawa N et al. Relationship between neutrophil elastase and acute lung injury in humans. Pulm. Pharmacol. Ther. 2004, 17: 271-279
38 Miura M, Ito S, Baba E et al. A neutrophil elastase inhibitor; Clinical pharmacology of ONO-5046-Na in systemic inflammatory syndrome. Rinsho Iyaku 1998, 14: 379-395
39 Aikawa N, Fujishima S, Kobayashi M et al. Cost-minimisation analysis of sivelestat for acute lung injury associated with systemic inflammatory response syndrome. Pharmacoeconomics 2005, 23: 169-181
40 Koperna T, Voql SE, Poschl GP, et al. Cytokine patterns in patients in patients who undergo hemofiltration for treatment of multiple organ failur. World Journal of Surgery.1998, 22(5): 443-448
41吴坚平,顾勇,丁峰,等.高容量血液滤过在犬急性肺损伤中的作用.中华肾脏病杂志, 2001, 17(5): 301-304
2 Matthay MA. Clinical measurement of pulmonary edema. Chest, 2002,122: 1877-1879
3 Luce JM. Acute lung injury and the acute respiratory distress syndrome. Crit Care Med ,1998, 26: 369-376
4 Huang H, Yao T, Wanq W, et al. Continuous ultrafiltration attrnuates the pulmonary injury that follows open heart surgery with cardiopulmonary bypass. Ann Thorac Surg. 2003, 76(1): 136-140
5 Koperna T, Voql SE, Poschl GP, et al. Cytokine patterns in patients in patients who undergo hemofiltration for treatment of multiple organ failur. World Journal of Surgery.1998, 22(5): 443-448
6 Su X, Bai C, Hong Q, Zhu D, et al. Effect of continuous hemofiltration on hemodynamics , lung inflammation and pulmonary edema in a canine model of acute lung injury. Intensive Care Med, 2003, 29(11): 2034-2042
7吴坚平,顾勇,丁峰,等.高容量血液滤过在犬急性肺损伤中的作用.中华肾脏病杂志, 2001, 17(5): 301-304
8 Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous hemofiltration on outcomes of acute renal failure: A prospective randomized trial. Lancet, 2000, 356: 26-30
9 Ware LB, Matthay MA: The acute respiratory distress syndrome. N Engl J Med, 2000, 342: 1334-1349
10 Piantadosi CA, Schwartz DA: The acute respiratory distress syndrome. Ann Intern Med, 2004, 141: 460-470
11 Wheeler AP, Bernard GR: Acute lung injury and the acute respiratory distress syndrome: A clinical review. Lancet, 2007, 369: 1553-1564
12 Katzenstein AL, Bloor CM, Leibow AA: Diffuse alveolar damage—the role of oxygen, shock, and related factors. A review. Am J Pathol, 1976, 85: 209-228
13 Schuster DP: What is acute lung injury? What is ARDS? Chest, 1995, 107: 1721-1726
14 Abraham E, Matthay MA, Dinarello CA, et al. Consensus conference definitions for sepsis, septic shock, acute lung injury, and acute respiratory distress syndrome: time for a reevaluation. Crit Care Med,2000, 28: 232-235
15 Menezes SL, Bozza PT, Neto HC, et al. Pulmonary and extrapulmonary acute lung injury: inflammatory and ultrastructural analyses. J Appl Physiol, 2005, 98: 1777-1783
16 Steinberg KP, Hudson LD, Goodman RB, et al. Efficacy and safety of corticosterPaO2/FiO2ds for persistent acute respiratory distress syndrome. N Engl J Med, 2006, 354: 1671-1684
17 Meduri GU, Headley AS, Golden E, et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: A randomized controlled trial. JAMA, 1998, 280: 159-165
18 Grasso S, Mascia L, Del Turco M, et al. Effects of recruiting maneuvers in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology, 2002, 96: 795-802
19 Monchi M, Bellenfant F, Cariou A, et al. Early predictive factors of survival in the acute respiratory distress syndrome. A multivariate analysis. Am J Respir Crit Care Med, 1998, 158: 1076-1081
20 Ferguson ND, Frutos-Vivar F, Esteban A, et al. Airway pressures, tidal volumes, and mortality in patients with acute respire- atory distress syndrome. Crit Care Med, 2005, 33: 21-30
21 Esteban A, Anzueto A, Frutos F, et al. Characteristics and outcomes in adult patients receiving mechanical ventilation: A 28-day international study. JAMA, 2002, 287: 345-355
22 Croce MA, Fabian TC, Davis KA, et al. Early and late acute respiratory distress syndrome: Two distinct clinical entities. J Trauma, 1999, 46: 361-366
23 Ware LB, Eisner MD, Thompson BT, et al. Significance of von Wille- brand factor in septic and nonseptic patients with acute lung injury. Am J Respir Crit Care Med, 2004, 170: 766-772
24 Clark JG, Milberg JA, Steinberg KP, et al. Type III procollagen peptide in the adult respiratory distress syndrome. Association of increased peptide levels in bronchoalveolar lavage fluid with increased risk for death. AnnIntern Med, 1995, 122: 17-23
25 Elings VB, Lewis FR. A single indicator technique to estimate extravascular lung water. J Surg Res, 1982, 33: 375-385
26 Sakka SG, Klein M, Reinhart K, et al. Prognostic value of extravascular lung water in Critically ill patients. Chest, 2002, 122 (6): 2080-2086
27 Ferna’ndez-Monde’jar E, Rivera-Ferna’ndez R,Garci’a-Delgado M,et al. Small increases in extravascular lung water are accurately detected by transpulmonary thermodilution.J Trauma 2005, 59:1420-1424
28 Honore PM, Jamez J, Wauthier M, et al. Prospective valuation of short-term high-volume isovolemicpatients with intractable circulatory failure resulting from septic shock. Crit Care Med, 2000, 28 (11): 3581-3587
29刘卫江,谢长江,熊旭明.连续血液净化在感染性休克中的应用.中国血液净化, 2005, 4(4): 205-207
30 Tetta C, Bellomo R, Inguaggiato P, et al. Endotoxin and cytokine removal in sepsis. Ther Apher, 2002, 6(2): 109-115
31 Carlile PV, Lowery DD, Gray BA. Effect of PEEP and type of injury on thermal-dye estimation of pulmonary edema. J Appl Physiol, 1986, 60: 22-31
32 Michard F, Schachtrupp A, Toens C. Factors influencing the estimation of extravascular lung water by transpulmonary thermodilution in critically ill patients. Crit Care Med, 2005 Jun, 33(6): 1243-1247
33 Demling RH, Staub NC, Edmunds LH Jr. Effect of end-expiratory airway pressure on accumulation of extravascular lung water. J Appl Physiol, 1975,38: 907-912
34王殿华,刘旭,凌亦凌.中性粒细胞弹性蛋白酶与急性肺损伤.国外医学呼吸系统分册, 2004, 24 (6): 368-370
35黄晓军,王选锭.急性肺损伤抗氧化治疗的研究进展.临床内科杂志, 2004, 21 (10): 652-654
36 Donnelly SC, MacGregor I, Zamani A et al. Plasma elastase levels and the development of the adult respiratory distress syndrome. Am J RespirCrit Care Med, 1995, 151: 1428-1433
37 Greneveld AB, Raijmakers PG, Haik CE et al. Interleukin 8-related neutrophil elastase and the severity of the adult respiratory distress syndrome. Cytokine, 1995, 7 (7): 746-752
38 Berse B, Brown LF, Van de Water L, et al. Vascular permeability factor(vascular endothelial growth factor) gene is expressed differentially in normal tissues, macrophages, and tumours. Mol Biol Cell 1992, 3: 211-220
39 Boussat S, Eddahibi S, Coste A, et al. Expression and regulation of vascular endothelial growth factor in human pulmonary epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2000, 279: L371-378
40 Koyama S, Sato E, Tsukadaira A, et al. Vascular endothelial growth factor mRNA and protein expression in airway epithelial cell lines in vitro. Eur Respir J. 2002, 20: 1449-1456
41 Armstrong L, Millar AB, Thickett DR, et al. A role for vascular endothelial growth factor in acute and resolving lung injury. Am J Respir Crit Care Med 2002, 166: 1332-1337
42 Maniscalco WM, Watkins RH, Finkelstein JN, et al. Vascular endothelial growth factor mRNA increases in alveolar eptithelial cells during recove- ry from oxygen injury. Am J Respir Cell Mol Biol 1995, 13: 377-386
43 Thieme H,Aiello LP, Takagi H ,et al. Comparative analysis of vascular en dothelial growth factor receptors on retinal and aortic vascular endotheli- al cells. Diabetes.1995, 44: 98-103
44 Seko Y, Takahashi N , Shibuya M ,et al. Pulsatile stretch stimulartes vasc- ular endothelial growth factor(VEGF)secretion by cultured rat cardiac myocytes. Biochem Biophys Res Commun.1999 Jan 19, 254(2): 462-465
45 Ancelin M, Chollet-Martin S, HervéMA,et alVascular endothelial growth factor VEGF189 induces human neuteophil chemotaxis in extravascular tissue via an autocrine amplification mechanism. Lab Invest, 2004, 84(4): 502-512
46 Dvorak HF, Brown LF, Deteman M ,et al. Vascular permeability factor/vascular endothelial growth factor microvascular hypermeability and angiogenesis. Am JP athol. 1995, 146: 1029
47 TiltonR G, Chang KC, Lejeune WS, et al. Role for nitric oxide in the hyperpermeability and hemodynamic changes induced by intravenous VEGF. Invest Ophthalmol Vis Sci. 1999 Mar, 40(3): 689-696
48 Murielle G, Dlivier B,Valerie A, et al. Intracellular pool of vascularEndothelial Growth Factor in Human Neutrophils.J.Blood, 1997, 90(10): 4153-4161
49 Nimah M, Brilli RJ. Coagulation dysfunction in sepsis and multiple organ system failure. Crit Care Clin, 2003, 19(3): 441-458
50 Murray MJ ,Matthay MA ,Luce JM ,et al. An expanded definition of the adult repiratory distress syndrome. J Am Rev Respir Dis , 1988,138: 720 -730
51 Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, orthe response to volume infusion in normal subjects. Crit CareMed, 2004, 32 (3): 691-699
52 Connors AF Jr, Speroff T, Dawson NV, et al. The efectiveness of right heart catheterization in the initial care of critically ill patients. JAMA, 1996, 276 (11): 889-897
53肖秋生,张斌,潘永等. PICCO技术在多发伤患者指导液体复苏中的临床应用.四川医学, 2010, 31(1): 42-44
54 Krebs J, Pelos P, Tsagogiorgas C, et al. Effects of positive end-expiratory pressure on respiratory function and hemodynamics in patients with acute respiratory failure with and without intra-abdominal hypertension: a pilot study. Crit Care, 2009,13(5): 199
55 Xie J, Yang J, et al. Effect of continuous high-volume hemofiltration on patients with acute respiratory distress syndrome and multiple organ dysfunction syndrome. Zhongguuo Wei Zhong Bing Ji Jiu Yi Xue, 2009 Jul, 21(7): 402-404
1聂晓红,周向东.蛋白酶抑制剂对肺炎性损伤的保护作用.临床肺科杂志,2004,9 (6): 665-667
2王殿华,刘旭,凌亦凌.中性粒细胞弹性蛋白酶与急性肺损伤.国外医学呼吸系统分册, 2004,24 (6): 368-370
3 Lee WL, Downey GP. Leukocyte elastase: physiological functions and role in acute lung injury. AM J Respir Crit Care Med, 2001, 164: 896-904
4 Kazuhito Kawabata, Tetsuya Hagio, Shigeru Matsumoto, et al. Delayed neutrophil elastase inhibition prevents subsequent progression of acute lung injury induced by endotoxin inhalation in hamsters. Am J Respir Crit Care Med, 2000, 161 (6): 2013-2018
5徐晓艳,周向东.中性粒细胞弹性蛋白酶与黏蛋白.中国药物与临床, 2004, 4(10): 741-744
6 Donnelly SC, MacGregor I, Zamani A et al. Plasma elastase levels and the development of the adult respiratory distress syndrome. Am J Respir Crit Care Med, 1995, 151: 1428-1433
7 Greneveld AB, Raijmakers PG, Hack CE et al. Interleukin 8-related neutrophil elastase and the severity of the adult respiratory distress syndrome. Cytokine, 1995, 7 (7): 746-752
8 Taniguchi H, Koncloh Y, Ikuta N et al. Diagnosis of acute respiratory distress syndrome: analysis of bronchoalveolar lavage fluid. Nihon Kyobu Shikkan Gakkai Zasshi, 1995, 33 (Suppl): 251-256
9 Kawabata K, Hagio T, Matsuoka S. The role of neu- trophil elastase in acute lung injury. European Journal of Pharmacology, 2002, 451(1):1-10
10 Takashige Kuraki, Masayoshi Ishibashi, Masanori Takayama, et al. A novel oral neutrophil elastase inhibitor (ONO-6818) Inhibits human neutrophil elastase-induced emphysema in rats. Am J Respir Crit Care Med, 2002, 166: 496-500
11 Tetsuya Hagio, Shigeru Matsumoto, Shintaro Nakao, et al. Elastase inhibition reduced death associated with acid aspiration-induced lunginjury in hamsters. European Journal of Pharmacology, 2004, 488:173- 180
12 Hagio T, Matsumoto S Nakao S, et al. Sivelestat, a specific neutrophil elastase inhibitor, prevented phorbol myristate acetate-induced acute lung injury in conscious rabbits. Pulm Pharmacol Ther, 2005, 18: 285-290
13揭志军,罗勇,徐卫国等.急性肺损伤患者血清中中性粒细胞弹性蛋白酶活性的变化.中华急诊医学杂志, 2005, 14(6):497-499
14 Lee WL, Downey GP. Leukocyte elastase physiological functions and role in acute lung injury. AM J Respir Crit Care Med, 2001, 164: 896-904
15 Palmgren MS, Deshazo RD, Carter RM et al. Mechanisms of neutrophil damage to human alveolar extracellular matrix: the role of serine and metalloproteases.J Allergy Clin Immunol, 1992, 89: 905-915
16黄晓军,王选锭.急性肺损伤抗氧化治疗的研究进展.临床内科杂志, 2004, 21(10): 652- 654
17 Peter A Henriksena, Andrew Devitt, Yuri Kotelevtsev, et al. Gene delivery of the elastase inhibitor elafin protects macrophages from neutrophil elastase-mediated impairment of apoptotic cell recognition. J Federation of European Biochemical Societies, 2004, 574: 80-84
18 Kapui Z, Varga M, Urban-Szabo K, et al. Biochemical and pharma- cological characterization of 2-(9-(2-piperidinoethoxy)-4-oxo-4H-pyrido [1,2-a]pyrimidin-2-yloxymethyl)-4-(1-methylethyl)-6-methoxy-1,2-benzisothiazol-3 (2H)-one-1, 1-dioxide (SSR69071), a novel, orally active elastase inhibitor. J Pharmacol Exp Ther, 2003, 305(2): 451-459
19 Daudi I, Gudewicz PW, Saba TM et al. Proteolysis of gelatin-bound fibronectin by activated leukocytes: a role for leukocyte elastase. J Leukocyte Biol, 1991, 50: 33-340
20 Bedard M, McClured CD, Schiller NL et al. Release of interleukin-8, interleukin-6, and colony-stimulating factors by upper airway epithelial cells: implications for cystic fibrosis. Am J Respir Cell Mol Biol, 1993, 9: 455-462
21 Liau DF, Yin NX, Huang J et al. Effects of human polymorphonuclearleukocyte elastase upon surfactant proteins in vitro. Biochim Biophys Acta, 1996, 1302 (2): 117-128
22 Holter JF, Weiland JE, Pacht ER et al. Protein permeability in the adult respiratory distress syndrome. Loss of size selectivity of the alveolar epithelium. J Clin Invest, 1986, 78: 1513-1522
23 Wewers MD, Casolaro MA, Sellers SE, et al. Replacement therapy for alpha 1-antitrypsin deficiency associated with emphysema. N Engl J Med. 1987 Apr 23, 316(17): 1055-1062
24 Gossage JR, Kuratomi Y, Davidson JM et al. Neutrophil elastase inhibitors, SC-37698 and SC-39026, reduce endotoxin-induced lung dysfunction in awake sheep. Am Rev Respir Dis, 1993, 147: 1371-1379
25 Mikawa K, Nishina K, Takao Y, et al. Attenuation of cardiovascular responses to tracheal extubation: comparison of verapamil, lidocaine, and verapamil-lidocaine combination. Anesth Analg, 1997, 84: 1097-1103
26 Crystal RG, Bast A, Roshan-Ali Y et al. Oxidants and respiratory tract epithelial injury: pathogenesis and strategies for therapeutic intervention. AmJ Med, 1991, 91(Suppl 3C): 39-44
27 Wallaert B, Gressier B, Gosset P et al. Oxidative inactivation of alpha 1-proteinase inhibitor by alveolar epithelial type II cells. J Appl Physiol. 1993 Dec, 5(6): 2376-2382
28 Bunnell E, Pacht ER. Oxidized glutathione is increased in the alveolar fluid of patients with the adult respiratory distress syndrome. Am Rev Respir Dis, 1993, 148: 1174-1178
29 Suter PM, Domenighetti G, Schaller MD et al. N-acetylcysteine enhances recovery from acute lung injury in man. A randomized, double-blind, placebo-controlled clinical study. Chest, 1994, 105: 190-194
30 Gregory TJ, Berman PW, Wilkes DM et al. Comparison of the immune response to recombinant gp120 in humans and chimpanzees. AIDS, 1994, 8: 591-601
31 Miyazaki Y, Inoue T, Kyi M et al. Effects of a neutrophil elastase inh- ibitor (ONO-5046) on acute pulmenary injury induced by tumor necrosisfactor alpha (TNF alpha) an activated neutrophils in isolated perfused rabbit lungs. Am J Resp ir crit CareMed, 1998, 157: 89-94
32 Hagio T, Matsumoto S, Nakao S, et al. Elastase inhibition reduced death associated with acid aspiration-induced lung injury in hamsters. Eur J Pharmacol, 2004, 488: 173-180
33郑修艳,曹立莉,杜冠华.新型弹性蛋白酶抑制剂西维来司钠临床前药理及机制研究.中国新药杂志, 2004, 13: 292-295
34杜冠华,吴松,冯文化.西维来司钠治疗急性肺损伤研究现状.中国药学杂志, 2004, 39(5): 321-324
35徐凌,蔡柏蔷,单渊东等.弹性蛋白酶抑制剂对严重急性呼吸综合征急性肺损伤有效性和安全性随机开放、平行对照、多中心临床研究.中华内科杂志,2005, 44: 147-148
36 Kuraki T, Ishibashi M, Takayama M, et al. A novel oral neutrophil elastase inhibitor (ONO-6818) inhibits human neutrophil elastase -induced emphysema in rats. Am J Respir Crit Care Med, 2002, 166: 496-500
37 Tamakuma S, Ogawa M, Aikawa N et al. Relationship between neutrophil elastase and acute lung injury in humans. Pulm. Pharmacol. Ther. 2004, 17: 271-279
38 Miura M, Ito S, Baba E et al. A neutrophil elastase inhibitor; Clinical pharmacology of ONO-5046-Na in systemic inflammatory syndrome. Rinsho Iyaku 1998, 14: 379-395
39 Aikawa N, Fujishima S, Kobayashi M et al. Cost-minimisation analysis of sivelestat for acute lung injury associated with systemic inflammatory response syndrome. Pharmacoeconomics 2005, 23: 169-181
40 Koperna T, Voql SE, Poschl GP, et al. Cytokine patterns in patients in patients who undergo hemofiltration for treatment of multiple organ failur. World Journal of Surgery.1998, 22(5): 443-448
41吴坚平,顾勇,丁峰,等.高容量血液滤过在犬急性肺损伤中的作用.中华肾脏病杂志, 2001, 17(5): 301-304
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