4℃高渗盐对心搏骤停复苏后大鼠脑组织作用的研究
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摘要
目的探讨4℃高渗盐(HTS)对心搏骤停(SCA)复苏后大鼠脑组织的作用。
方法54只雄性SD大鼠随机分为两大组,第一大组:假手术(A)组、生理盐水(NS)(B)组、4℃NS(C)组、HTS(D)组、4℃HTS(E)组,各组6只,除A组外,其余各组均于复苏即刻给药;第二大组:NS自主循环恢复(ROSC)后30分钟给药(B1)组、NS ROSC后60分钟给药(B2)组、4℃HTS ROSC后30分钟给药(E1)组、4℃HTS ROSC后60分钟给药(E2)组,各组6只。每组给药均按4ml/kg剂量,HTS浓度为7.5%。制作窒息致大鼠SCA模型。监测各组给药后60分钟内的平均动脉压(MAP)的变化;测定给药后60分钟各组大鼠血清Na+,并计算出各组血浆渗透压值;记录ROSC后6小时、12小时、24小时神经功能缺损评分(NDS);ROSC后24小时采静脉血检测各组血清S100蛋白浓度,处死大鼠取脑组织检测海马半胱氨酸天门冬氨酸蛋白酶-3(caspase-3)、胶质纤维酸性蛋白(GFAP)及髓鞘的表达,测定脑组织含水量。统计方法:多样本间均数多重比较用SNK-q检验。
结果第一大组:各组MAP的变化,血清Na+、血浆渗透压差异均无显著性(P>0.05)。各时间点NDS 4℃HTS组较NS组高(P<0.05),4℃NS组、HTS组、较NS组差异无显著性(P>0.05),4℃NS组、HTS组、4℃HTS组间比较差异无显著性(P>0.05)。各组血清S100蛋白浓度较假手术组明显升高(P<0.01), NS组、4℃NS组、HTS组、4℃HTS组间比较差异有显著性(P<0.01或P<0.05)。Caspases-3、GFAP阳性细胞数NS组、4℃NS组、HTS组较假手术组均明显增多(P<0.01),4℃HTS组较假手术组差异无显著性(P>0.05),NS组、4℃NS组、HTS组、4℃HTS组间比较差异有显著性(P<0.01或P<0.05)。各组脑组织含水量较假手术组均明显升高(P<0.01);4℃NS、HTS组、4℃HTS组较NS组差异有显著性(P<0.01或P<0.05),4℃NS组、HTS组、4℃HTS组间相比差异无显著性(P>0.05)。各组大鼠随鞘数差异无显著性(P>0.05)。第二大组:各组MAP的变化,Na+、血浆渗透压差异均无显著性(P>0.05)。各时间点NDS 4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组较NS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组高(P<0.05),4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组间比差异无显著性(P>0.05)。4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组血清S100蛋白浓度,脑组织Caspases-3、GFAP阳性细胞数及脑组织含水量较NS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组均明显降低减少(P<0.01);4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组组间比差异无显著性(P>0.05)。各组大鼠随鞘数差异无显著性(P>0.05)。
结论SCA后给予4℃HTS能能提高NDS,降低血清S100蛋白浓度,抑制脑海马组织Caspase-3、GFAP表达,减轻脑水肿及病理形态学损伤,对脑组织起保护作用;对机体血清Na+、渗透压、脑组织髓鞘影响不大;且复苏即刻、30分钟、60分钟给药均有效,且无差别。
Objective To investigate the effects of 4℃HTS in rat brain tissues after SCA and resuscitation .
Methods 54 Sprague-Dawley male rats were randomly divided into two groups:the first group included:shame-operated(A) group,NS-treated(B) group,4℃NS-treated(C) group,HTS-treated (D)group, 4℃HTS-treated (D) group.Each group included 6 tats. Except group A,the rest groups were administered at the onset of CPR. The second group included: NS-treated(B1) group at the 30 minutes after ROSC, NS-treated(B2) group at the 60 minutes after ROSC, 4℃HTS-treated(E1) group at the 30 minutes after ROSC, 4℃HTS-treated(E2) group at the 60 minutes after ROSC. Each group was administered in 4ml/kg.The concentration of HTS was 7.5%.SCA was induced on rats by asphyxia. We had a continuous monitoring on the change of MAP in 60 minutes after administration. We also determined the concentration of blood serum Na+ in each group at 60 minutes after administration,and then we calculated plasma osmotic pressure in each group. We recorded NDS at 6h,12h and 24h after ROSC. At 24h after ROSC, we got the venous blood to detcect the concentration of serum S100 protein in each group,and sacrificed the rats, got the brain tissues to compare the expression of caspase-3 ,GFAP and myelin staining in hippocampus, and calculated the brain water content.Statistical method: Comparison the mean of multiple samples used Student-Keuls(SNK-q).
Results The first group: There was no statistical difference in the change of MAP and Na+, plasma osmotic pressure in 60 minutes after administered in each group(P>0.05). Compared with NS-treated group, NDS in 4℃HTS-treated group at 6h,12h,24h after ROSC increased (P<0.05);that in 4℃NS-treated group and HTS-treated group was no statistical difference(P>0.05); also,there was no statistical difference among 4℃NS-treated group,HTS-treated group and 4℃HTS-treated group(P>0.05). Compared with group shame-operated group, the concentration of serum S100 protein in the rest group was much higher (P<0.01); There was statistical difference among NS-treated group, 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group(P<0.01 or P<0.05). Compared with group shame-operated group, the expression of caspase-3 and GFAP among NS-treated group, 4℃NS-treated group and HTS-treated group was much more(P<0.01), that in group 4℃HTS-treated group was no statistical difference(P>0.05); There was statistical difference among NS-treated group, 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group ( P<0.01or P<0.05).Compared with shame-operated group, the brain water content among NS-treated group, 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group was much higher(P<0.01); Compared with NS-treated group, there was statistical difference among 4℃NS-treated group,HTS-treated group and 4℃HTS-treated group(P<0.01 or P<0.05);there was no statistical difference in the brain water content among 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group (P>0.05). There was no statistical difference in numbers of myelin in each group(P>0.05). The second group: there was no statistical difference in the change of MAP and Na+, plasma osmotic pressure in 60 minutes after administered in each group(P>0.05). Compared with NS-treated group,NS-treated group at the 30 minutes after ROSC and NS-treated group at the 60 minutes after ROSC, NDS in group 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC at 6h,12h,24h after ROSC increased (P<0.05), but there was no statistical difference among 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC (P>0.05). Compared with NS-treated group,NS-treated group at the 30 minutes after ROSC and NS-treated group at the 60 minutes after ROSC , the concentration of serum S100 protein, the expression of caspase-3 and GFAP and the brain water content in group 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC at 24h after were much lower(P<0.01), but there was no statistical difference among 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC (P>0.05). There was no statistical difference in numbers of myelin in each group(P>0.05).
Conclusion 4℃HTS-treated after SCA can raise and NDS, decrease serum S100 protein level and the expression of caspase-3 and GFAP in hippocampus, reduce cerebral edema and histopathological damages,protect the brain tissius. There was no significant effect on serum Na+ and osmotic pressure as well as myelin in brain tissues after 4℃HTS treated. 4℃HTS-treated at the onset of CPR,at the 30 minutes after ROSC, at the 60 minutes after ROSC can all pretect brain tissues,and the effects were same.
方法54只雄性SD大鼠随机分为两大组,第一大组:假手术(A)组、生理盐水(NS)(B)组、4℃NS(C)组、HTS(D)组、4℃HTS(E)组,各组6只,除A组外,其余各组均于复苏即刻给药;第二大组:NS自主循环恢复(ROSC)后30分钟给药(B1)组、NS ROSC后60分钟给药(B2)组、4℃HTS ROSC后30分钟给药(E1)组、4℃HTS ROSC后60分钟给药(E2)组,各组6只。每组给药均按4ml/kg剂量,HTS浓度为7.5%。制作窒息致大鼠SCA模型。监测各组给药后60分钟内的平均动脉压(MAP)的变化;测定给药后60分钟各组大鼠血清Na+,并计算出各组血浆渗透压值;记录ROSC后6小时、12小时、24小时神经功能缺损评分(NDS);ROSC后24小时采静脉血检测各组血清S100蛋白浓度,处死大鼠取脑组织检测海马半胱氨酸天门冬氨酸蛋白酶-3(caspase-3)、胶质纤维酸性蛋白(GFAP)及髓鞘的表达,测定脑组织含水量。统计方法:多样本间均数多重比较用SNK-q检验。
结果第一大组:各组MAP的变化,血清Na+、血浆渗透压差异均无显著性(P>0.05)。各时间点NDS 4℃HTS组较NS组高(P<0.05),4℃NS组、HTS组、较NS组差异无显著性(P>0.05),4℃NS组、HTS组、4℃HTS组间比较差异无显著性(P>0.05)。各组血清S100蛋白浓度较假手术组明显升高(P<0.01), NS组、4℃NS组、HTS组、4℃HTS组间比较差异有显著性(P<0.01或P<0.05)。Caspases-3、GFAP阳性细胞数NS组、4℃NS组、HTS组较假手术组均明显增多(P<0.01),4℃HTS组较假手术组差异无显著性(P>0.05),NS组、4℃NS组、HTS组、4℃HTS组间比较差异有显著性(P<0.01或P<0.05)。各组脑组织含水量较假手术组均明显升高(P<0.01);4℃NS、HTS组、4℃HTS组较NS组差异有显著性(P<0.01或P<0.05),4℃NS组、HTS组、4℃HTS组间相比差异无显著性(P>0.05)。各组大鼠随鞘数差异无显著性(P>0.05)。第二大组:各组MAP的变化,Na+、血浆渗透压差异均无显著性(P>0.05)。各时间点NDS 4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组较NS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组高(P<0.05),4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组间比差异无显著性(P>0.05)。4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组血清S100蛋白浓度,脑组织Caspases-3、GFAP阳性细胞数及脑组织含水量较NS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组均明显降低减少(P<0.01);4℃HTS复苏即刻给药组、ROSC后30分钟给药组、ROSC后60分钟给药组组间比差异无显著性(P>0.05)。各组大鼠随鞘数差异无显著性(P>0.05)。
结论SCA后给予4℃HTS能能提高NDS,降低血清S100蛋白浓度,抑制脑海马组织Caspase-3、GFAP表达,减轻脑水肿及病理形态学损伤,对脑组织起保护作用;对机体血清Na+、渗透压、脑组织髓鞘影响不大;且复苏即刻、30分钟、60分钟给药均有效,且无差别。
Objective To investigate the effects of 4℃HTS in rat brain tissues after SCA and resuscitation .
Methods 54 Sprague-Dawley male rats were randomly divided into two groups:the first group included:shame-operated(A) group,NS-treated(B) group,4℃NS-treated(C) group,HTS-treated (D)group, 4℃HTS-treated (D) group.Each group included 6 tats. Except group A,the rest groups were administered at the onset of CPR. The second group included: NS-treated(B1) group at the 30 minutes after ROSC, NS-treated(B2) group at the 60 minutes after ROSC, 4℃HTS-treated(E1) group at the 30 minutes after ROSC, 4℃HTS-treated(E2) group at the 60 minutes after ROSC. Each group was administered in 4ml/kg.The concentration of HTS was 7.5%.SCA was induced on rats by asphyxia. We had a continuous monitoring on the change of MAP in 60 minutes after administration. We also determined the concentration of blood serum Na+ in each group at 60 minutes after administration,and then we calculated plasma osmotic pressure in each group. We recorded NDS at 6h,12h and 24h after ROSC. At 24h after ROSC, we got the venous blood to detcect the concentration of serum S100 protein in each group,and sacrificed the rats, got the brain tissues to compare the expression of caspase-3 ,GFAP and myelin staining in hippocampus, and calculated the brain water content.Statistical method: Comparison the mean of multiple samples used Student-Keuls(SNK-q).
Results The first group: There was no statistical difference in the change of MAP and Na+, plasma osmotic pressure in 60 minutes after administered in each group(P>0.05). Compared with NS-treated group, NDS in 4℃HTS-treated group at 6h,12h,24h after ROSC increased (P<0.05);that in 4℃NS-treated group and HTS-treated group was no statistical difference(P>0.05); also,there was no statistical difference among 4℃NS-treated group,HTS-treated group and 4℃HTS-treated group(P>0.05). Compared with group shame-operated group, the concentration of serum S100 protein in the rest group was much higher (P<0.01); There was statistical difference among NS-treated group, 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group(P<0.01 or P<0.05). Compared with group shame-operated group, the expression of caspase-3 and GFAP among NS-treated group, 4℃NS-treated group and HTS-treated group was much more(P<0.01), that in group 4℃HTS-treated group was no statistical difference(P>0.05); There was statistical difference among NS-treated group, 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group ( P<0.01or P<0.05).Compared with shame-operated group, the brain water content among NS-treated group, 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group was much higher(P<0.01); Compared with NS-treated group, there was statistical difference among 4℃NS-treated group,HTS-treated group and 4℃HTS-treated group(P<0.01 or P<0.05);there was no statistical difference in the brain water content among 4℃NS-treated group, HTS-treated group and 4℃HTS-treated group (P>0.05). There was no statistical difference in numbers of myelin in each group(P>0.05). The second group: there was no statistical difference in the change of MAP and Na+, plasma osmotic pressure in 60 minutes after administered in each group(P>0.05). Compared with NS-treated group,NS-treated group at the 30 minutes after ROSC and NS-treated group at the 60 minutes after ROSC, NDS in group 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC at 6h,12h,24h after ROSC increased (P<0.05), but there was no statistical difference among 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC (P>0.05). Compared with NS-treated group,NS-treated group at the 30 minutes after ROSC and NS-treated group at the 60 minutes after ROSC , the concentration of serum S100 protein, the expression of caspase-3 and GFAP and the brain water content in group 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC at 24h after were much lower(P<0.01), but there was no statistical difference among 4℃HTS-treated group, 4℃HTS-treated group at the 30 minutes after ROSC and 4℃HTS-treated group at the 60 minutes after ROSC (P>0.05). There was no statistical difference in numbers of myelin in each group(P>0.05).
Conclusion 4℃HTS-treated after SCA can raise and NDS, decrease serum S100 protein level and the expression of caspase-3 and GFAP in hippocampus, reduce cerebral edema and histopathological damages,protect the brain tissius. There was no significant effect on serum Na+ and osmotic pressure as well as myelin in brain tissues after 4℃HTS treated. 4℃HTS-treated at the onset of CPR,at the 30 minutes after ROSC, at the 60 minutes after ROSC can all pretect brain tissues,and the effects were same.
引文
[1]王姗姗,陈寿权,李章平,等.乌司他丁对心肺复苏后大鼠脑水肿和血脑屏障的作用[J].中华急诊医学杂志,2006,15(4):338-341.
[2] XiaoF,Zhang Z,Amold TC,et al.Mild hypothermia induced before cardiac arrest reduces brain edema formation in rats[J].Acad Emerg Med,2002,9(2):105-114.
[3] Reisinger J,H?llinger K,Lang W,et al.Prediction of neurological outcome after cardio- pulmonary resuscitation by serial determination of serum neuron-specific enolase[J]. Eur.Heart J,2007,28(1):52-58.
[4] Rosen H,Sunnerhagen KS,Herlitz J,et al.Serum levels of the brain-derived proteins S-100 and NSE predict long-term outcome after cardiac arrest[J].Resuscitation,2001,49(2):183 -191.
[5] Pike BR,Zhao X,Newcomb JK,et al.Stretch injury causes calpain and caspase-3 activation and necrotic and aimptotic cell death in septo-hippecamlml cell cu1tures[J]. J Neurotrauma, 2000,17 (4):283-298.
[6] ErecinskaM,ThoresenM,Silver IA,et al.Effects of hypothermia on energy metabolism in Mammalian central nervous system[J].J Cereb Blood Flow Metab,2003,23(5):513-530.
[7] Harada K,Maekawa T,Tsuruta R,et al.Hypothermia inhibitstranslocation of CaM kinase II and PKC- alpha,beta,gamma isoforms and fodrin proteolysis in rat brain synap tosome during ischemia- reperfusion[J].J Neurosci Res,2002,67(5):664-669.
[8] PrandiniMN,Neves Filho A,Lapa AJ,et al.Mild hypothermia reduces polymorphonuclear leukocytes infiltration in induced brain inflammation[J].Arq Neuropsiquiatr,2005,63(3B): 779-784.
[9] Busto R,Dietrich WD,Globus MY,et al.Small differences in intra-ischemic brain temperature critically determine the extent of ischemic neuronal injury[J].J Cereb Blood Flow Meta, 1987,7(6):729-738.
[10] Fay T.Early experiences with local and generalized refrigeration of the human brain[J].J Neurosurg,1959,16(3):239-260.
[11] Younes RN, Deutsch F,Itinoshe M,et al.Responsiveness to different volume therapies following hemodilution and hemorrhagic shock:a comparative experimental study in rats[J].Acta Cir Bras, 2007,22(5):355-360.
[12] Torg TJ,Hurn PD,Trayslman RJ,et a1.Global brain water increases after experimental focal cerebral ischemia:effect of hypertonic saline[J].Crit Care Med,2002,30(3):644-649
[13] Suarez JI,Qureshi AI,Bhardwaj A,et a1.Treatment of refractory intracranial hypertension with 23.4%saline[J].Crit Care med,1998,26(6):1118-1122.
[14] Schwarz S,Georgiadis D,Aschoff A,et a1.Effects of hypertonic(10%) saline in patients withraised intracranial pressure after stroke[J].Stroke,2002,33(1):136-l40.
[15] American Heart Association. Utstein-Style Guidelines for Uniform Reporting of Laboratory CPR Research[J].Circulation,1996,94(9):2324-2336.
[16] Geocadin RG,Ghodadra R,Kimura T,et al.A novel quantitative EEG injury measure of global cerebral ischemia[J].Clin Neurophysiol,2000,111(10):1779-1787.
[17]曾春,马中富.心肺复苏的方法学进展[J].中华急诊医学杂志,2001,10(6):418-420.
[18] Walraven CV,Stiell LC,Wells GA,et al.Do advanced cardiac life support during increase resuscita- tion rate from in hospital cardiac[J].Br J Anasth,1999,82(5):738.
[19] Rubertsson.Cardiopulmonary cerebral resuscitation-present and future perspective[J]. Acta Anaesthesiol Scand,1999,43(5):526-535.
[20]周彬,孟力.心肺复苏后的脑损害及预后评价[J].中华急诊医学杂志,1996,5(2):119-122.
[21] El-Menyar AA.Pathophysiology and hemodynamic of postresuscitation syndrome[J].Saudi Med J,2006 Apr;27(4):441-445.
[22] Padosch SA,Vogel P,Bottiger BW.Neuronal apoptosis following cerebral ischemia[J]. Basis,physio- pathology and treatment strategies Anaesthesist,2001,50(12):905-920.
[23] Tsuchiya D,Hong S,Matsumori Y,et al.Overexpression of rat heat shock protein 70 reduces neuronal injury after transient focal ischemia, transient global ischemia,or kainic acid- induced seiz- ures[J]. Neurosurgery,2003,53(5):1179 -1187;discussion 1187-1188.
[24] Torregrosa G,Barberu MD,Orti M,et al.Temporospatial expression of HSP72 and c-JUN, and DNA fragmentation in goat hippocampus after global cerebral ischemia[J]. ischemia [J].Hippocampus,2001,11(2): 146-156.
[25] Yamaguchi T,Miyata K,Shibasaki F,et al.Effect of cyclosporin a on immediate early gene in rat global ischemia and its neuroprotection[J].J Pharmacol Sci,2006,100(1):73-81.
[26] Qi JP,Wu AP,Wang DS,et al.Correlation between neuronal injury and Caspase-3 after focal ischemia in human hippocampus[J].Chin Med J(Engl),2004,117(10):1507-1512.
[27] D'Cruz BJ,Fertig KC,Filiano AJ,et al.Hypothermic reperfusion after cardiac arrest augments brain -derived neurotrophicfactor activation[J].J Cereb Blood FlowMetab, 2002,22(7):848-851.
[28] Hicks SD,DeFranco DB,Callaway CW.Hypothermia during reperfusion after saphyxial cardiac arrest improves functional recovery and selectively alters stress -induced protein expression[J].J Cereb Blood Flow Metab,2000,20(3):520-530.
[29] Li LX,Jiang T,Liu EZ, et a1. Effect of intraischemic mild hypothermia on interleukin-1beta and monocyte chemoattractant protein-1 contents in ischemic core of rat cortex after transient focal cerebral ischemia[J].Zhonghua Yi Xue Za Zhi,2003,10;83(7):541-543.
[30] Zhan RZ,Fujiwara N,Endoh H,et al. Thiopental inhibits increases in [Ca2+]i induced by membrane depolarization, NMDA receptor activation, and ischemia in rat hippocampal and cortical slices[J]. Anesthesiology,1998,89(2): 456-466.
[31] Harris OA,Colford JM Jr,Good MC,et al.The role of hypothermia in the management of severe brain injury : a meta-analysis. [J].Arch Neurol,2002,59(7):1077-1088.
[32] Kimura A,Sakurada S,Ohkami H,et a1.Moderate hypothermia delays proinflammatory cytokine production of Human peripheral blood mononuclear cells[J].Crit Care Med,2002,30(7):l499-l502.
[33] Soukup J,Zauner A,Doppenberg EM,et a1.Relationship between brain temperature,brain chemistry and oxygen delivery after severe human head injury:the effect of mild hypothermia[J].Neurol Res,2002,24(2):161-168.
[34] Kimura T,Sako K,Tanaka K,et a1.Effect of mild hypothermia on energy state recovery following transient forebrain ischemia in the gerbil[J].Exp Brain Res,2002,145(1):83-90.
[35] Xu L,Yenail MA,Steinberg GK,et a1.Mild hypothermia reduces apoptosis of mouse neurons in vitro early in the cascade[J].J Cereb Blood F1ow Metab,2002,22(1):2l-28.
[36] Bedell EA,DeWitt DS,Uchida T,et al. Cerebral pressure autoregulation is intact and is not influenced by hypothermia after traumatic brain injury in rats[J].J Neurotrauma,2004,21(9): 1212-1222.
[37] Tokutomi T,Morimoto K,Miyagi T,et al. Optimal temperature for the management of severe traumatic brain injury: Effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism[J].Neurosurgery,2003,52(1):102-111.
[38] Bernard S , Buist M, Monteiro O,et al.Induced hypothermia using large volume ,ice-cold intravenous fluid in comatose survivors of out-of hospital cardiac arrest:a preliminary report[J]. Resusci- tation, 2003,56(1):9-13.
[39] Weed LH,MeKibben PS.Experimental alteration of brain bulk[J].Am J Physiol,1919, 48(5):531-558.
[40] Zhou QQ,Liu FY,Gao YQ.et al.Effects of liquids with different osmotic pressure and different oxygen concentration on resuscitation of hemorrhagic shock at high altitude in rat[J].Zhongguo Wei Zhong Bing Ji Jiu Yi Xue,2008 ,20(7):393-396.
[41] Qin W,Yu YH,Sheng C.Protective effect of hypotensive fluid resuscitation against lung ischmia -reperfusion injury in pregnant rabbits with uncontrolled hemorrhagic shock[J].Nan Fang Yi Ke Da Xue Xue Bao.2008,28(6):1042-1044.
[42] Suarez JI.Hypertonic saline for cerebral edema and elevated intracranial pressure[J].Cleve Clin J Med,2004,71(1):S9-13.
[43] Huang SJ,Chang L,Han YY,et al.Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury[J].Surg Neurol,2006,65(6):539-546;discussion 546.
[44] Sidi A,Muehlschleqel JD,Kirby DS,et al.Treating ischemic left ventricular dysfunction with hypertonic saline administered after coronary occlusion in pigs[J].J Cardiothorac Vasc Anesth, 2007,21(3): 400-405.
[45] Doyle JA,Davis DP,Hoyt DB.The use of hypertonic saline in the treatment of traumatic brain injury[J].J Trauma,2001,50(2):367-383.
[46] Chang Y,Chen TY,Chen CH,et al.Plasma arginine-vasopressin following experimental stroke: effect of osmotherapy[J].J Appl Physiol,2006,100(5):1445-1451.
[47] Thiel M,Imendorffer S,Chouker A,et al.Expression of adhesion molecules on circulatingpolymorphonuclear leukocytes during orthotopic liver transplantation[J]. Hepatology,1998, 28(6): 1538–1550.
[48] Ciesla DJ,Moore EE,Gonzalez RJ.Hypertonic saline inhibits neutrophil (PMN) priming via attenuation of p38 MAPK signaling[J].Shock,2000,14(3):265-269; discussion 269-270.
[49] Loomis William H,Sachiko Namiki,David B,et al.Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators[J].Am J Physiol Cell Physiol,2001,281(3):C480 -848.
[50] Horton JW,Maass DL,White DJ.Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis[J].Am J Physiol Heart Circ physiol,2006, 290(4):H1642-1650.
[51]黄唯佳,李章平,陈寿权.心肺脑复苏动物模型[J].中华急诊医学杂志.2002,11(6):419-420.
[52] von PlantaI,Weil MH,von Planta M,et al.Cardiopulmonary resuscitation in the rat[J].J Appl Physiol,1988,65(6):2641-2647.
[53] Bottiger BW,Krumnikl JJ,Gass P,et al.The cerebral“no-reflow”phenomenon after cardiac arrest in rats:influence of low-flow reperfusion[J]. Resuscitation,1997,34(1):79-87.
[54] Hendrickx HH,Rao GR,Safar P,et al.Asphyxia,cardiac arrest and resuscitation in rats.Ⅰ.Short term recovery[J].Resuscitation,1984,12(2):97-116.
[55] Hendrickx HH,Safar P,Miller A.Asphyxia,cardiac arrest and resuscitation in rats.ⅡLong term behavioral changes[J].Resuscitation,1984,12(2):117-128.
[56]陈寿权,李章平,王姗姗,等.窒息法致大鼠SCA模型复苏的影响因素[J].中华急诊医学,2005,14(10): 814-8 17.
[57] Ajito T,Suzuki K,Iwabuchi S.Effect of Intravenous Infusion of a 7.2% Hypertonic Saline Solution on Serum Electrolytes and Osmotic Pressure in Healthy Beagles[J].J Vet Med Sci,1999,61(6): 637-641.
[58] Harutjunyan L,Holz C,Rieger A,et al.Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients-a randomized clinical trial[J].Crit Care,2005,9(5):R530–540.
[59] Doshi VS,Say JH,Young SH,et al.Complications in Stroke Patients:A Study Carried out at The Rehabilitation Medcine Service,Changgi General Hospital[J].Singapore Med J, 2003;44(12): 643-652.
[60] Wassertheil-Smoller S,Shumaker S,Ockene J,et al.Depression and cardiovascular sequeae in postmenopausal women:The Women,s Health Initiative(WHI)[J].Arch Intern Med, 2004; 164(3): 289-298.
[61] Picavet MT,Gasthuys FM,Laevens HH,et al.Cardiopumonary effects of combined xylazine-guaiph- enesin- ketamine infusion and extradural(inter-coccygeal lidocaine) Anaesthesia in calves[J]. Vet Anaesth Analg,2004;31(1):11-9.
[62] Rothermundt M,Peters M,Prehn JH,et al.S100βin brain damage and neurodegeneration [J].Microsc Res Tech,2003,60(6):614-632.
[63] Muramatsu Y,Kurosaki R,Kato H,et al.Effect of pitavastatin against expression of S100 beta protein in the gerbil hippocampus after transient cerebral ischemia[J].Acta Physiol Scand, 2004,182(1):95-107.
[64] Wainwright MS,Craft JM,Griffin WS,et al.Increased susceptibility of S100B transgenic mice to perinatal hypoxia-ischemia[J].Ann Neurol,2004,56(1):61-67.
[65] Love S.Oxidative stress in brain ischemia[J].Brain Pathol,1999,9(1):119-131.
[66] Ali MS , Harmer M ,Vaughan R. Serum S100 protein as a marker of cerebral damage during cardiac surgery [ J ] . B r J A naesth ,2000 ,85 (2) : 287-298.
[67] Boat right KM,Salvesen GS.Mechanisms of caspase activation[J].Curr Opin Cell Biol,2003,15(6): 725-731.
[68] Daniel PT.Dissecting the pathways to death[J].Leukemia,2000,14(12):2035-2044.
[69] Love S,Barber R,Srinivasan A ,et al.Activation of caspase-3 in permanent and transient brain ischaemia in man[J].Neuroreport,2000,11(11):2495.
[70] Gill R,Soriano M,Blomgren K,et al.Role of caspase-3 activation in cerebral ischemia- induced neurodegeneration in adult and neonatal brain[J].J Cereb Blood Flow Metab, 2002,22(4):420.
[71] Iwal T,Niwa M,Hara A.DNA fragmentation in the CA2 sector of gerbil hippoeampus following transient forebrain ischemia[J].Brain Res,2000,857(1-2):275-278.
[72] Sharma AB,Barlow MA,Yang SH,et al.Pyruvate enhances neurological recovery following cardiopul- monary arrest and resuscitation[J].Resuscitation,2008,76(1):108-119.
[73] Yuan GQ, Wu YL, Jia ZH. Experimental study on effect of tongxinluo on nerve cell apoptosis after cerebral ischemia in middle cerebral arterial obstructive model rats[J]. Zhongguo Zhong Xi Yi Jie He Za Zhi, 2007;27(8):720-723.
[74] He X,Mo X,Gu H,et al.Neuroprotective effect of diazoxide on brain injury induced by cerebral ischemia/reperfusion during deep hypothermia[J].J Neurol Sci,2008,15; 268 (1-2):18-27.
[75] Lok J,Martin LJ.Rapid subcellular redistribution of Bax precedes caspase-3 and endonuclease activation during excitotoxic neuronal apoptosis in rat brain[J].J Neurotrauma,2002,19(7): 815-828.
[76] Cernak I,Chapman SM,Hamlin GP,et al.Temporal characterization of pro-and anti-apoptotic mechanisms following diffuse traumatic brain injury in rats[J].J Clin Neurosci,2002,9(5): 565-572.
[77] Mammen EF,Barnhart MI,Selik NR ,et al“.Sticky platelet syndrome”:A congenital platelet abnormality predisposing to thrombosis?[J].Folia Haematol,1998,115(3):361-365.
[78] Chaturvedi S,Dzieczkowski JS.Protein S deficiency,activated protein C resistance and platelet syndrome in a young women with bilateral strokes[J].Cerebrovasc Dis,1999, 9(2): 127-130.
[79] Fields RD,Stevens-Graham B.New insights into neuron-glia communication[J].Science, 2002,298 (5593):556-562.
[80] Hansson E,Ronnback L.Glial neuronal signaling in the central nervous system[J].FASEB J,2003, 17(3):341-348.
[81] Sasaki T,Hamada J,ShibataM,et al.Inhibition of nitric oxide production during global ischemia ameliorates ischemic damage of pyramidal neurons in the hippocampus[J].Keio JMed,2001,50(3): 182-187.
[82] Yasuda Y, Tateishi N, Shimoda T, et al. Relationship between S100beta and GFAP expression in astrocytes during infarction and glial scar formation after mild transient ischemia [J].Brain Res,2004,1021(1): 20-31.
[83] Kimelberg HK,Nestor NB,Feustel PJ.Inhibition of release of taurine and excitatory amino acids in ischemia and neuroprotection[J].Neurochem Res,2004,29(1):267-274.
[84] Waxweiler R J, Thurman D, Smeiezek J. Monitoring the impact of traumatic brain injury, a review and update [ J ]. J Neurotrauma, 1995, 12 (4) : 509 - 516.
[85] Kofler J, Hattori K, Sawada Met al. Histopathological and behavioral characterization of a novel model of cardiac arrest and cardiopulmonary resuscitation in mice[J].J Neurosci Methords 2004,15;136 (1):33-44.
[86] Baker CJ, Onesti ST, Solomon RA. Reduction by delayed hypothermia of cerebral infarction followingmiddle cerebral artery occlusion in the rat: a time course study[ J ]. J Neurosurg, 1992, 77(3): 438-444.
[87] Miyazawa T , Tamura A , Fukhui S , et al. Effect of mild hypothermia on focal cerebral ischemia review of experimental studies[ J ]. Neurol Res ,2003 ,25 (5):457- 464.
[88] Xiao F,Zhang S,Amold TC,et al.Mild hypothermia induced before cardiac arrest rduces brain edema formation in rats[J].Acad Emerg Med,2002,9(2):105-114.
1 Pascual JM,Solivera J,Prieto R,et al.Time course of early metabolic changes following diffuse traumatic brain injury in rats as detected by (1)H NMR spectroscopy[J].J Neurotrauma,2007 ,24(6):944-959.
2 Boulard G,Marguinaud E,Sesay M.Osmotic cerebral edema: the role of plasma osmolarity and blood brain barrier[J].Ann Fr Anesth Reanim,2003,22(3):215-219.
3 Qureshi AI,Suarez JI.Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension[J]. Crit Care Me,2000,28(9):3301-3313.
4 Huang SJ,Chang L,Han YY,et al.Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury[J].Surg Neurol,2006,65(6):539-546; discussion 546.
5 Harutjunyan L,Holz C,Rieger A,et al.Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients-a randomized clinical trial[J].Crit Care,2005,9(5):R530–540.
6 Younes RN, Deutsch F,Itinoshe M,et al.Responsiveness to different volume therapies following hemodilution and hemorrhagic shock: a comparative experimental study in rats[J].Acta Cir Bras, 2007,22(5):355-360.
7 Sidi A,Muehlschleqel JD,Kirby DS,et al.Treating ischemic left ventricular dysfunction with hypertonic saline administered after coronary occlusion in pigs[J]. J Cardiothorac Vasc Anesth, 2007,21(3):400-405.
8 Doyle JA,Davis DP,Hoyt DB.The use of hypertonic saline in the treatment of traumatic brain injury[J].J Trauma,2001,50(2):367-383.
9 Oertel M, Boscardin WJ, Obrist WD,et al. Posttraumatic vasospasm: the epidemiology, severity,and time course of an underestimated phenomenon: a prospective study performed in 299 patients[J].J Neurosurg,2005,103(5):812-824.
10 ELena K,Marta L,Carmine M.Glutamine synthetase activity and glutamine content in brain: modulation by NMDA receptors and nitric oxide[J]. Neurochemist,2003,43(4-5):493-499.
11 Small DL,Morley P,Buchan AM.Biology of ischemsic cerebral cell death[J].Prog Cardiovasc Dis,1999,42(3):185-207.
12 Franceschini R,Tenconi GL,Zoppoli F,et al.Endocrine abnormalities and outcome of ischaemic stroke[J]. Biomed Pharmacother,2001,55(8):458–465.
13 Szmydynger-Chodobska J,Chung I,Kozniewska E,et al.Increased expression of vasopressin V1a receptors after traumatic brain injury[J]. J Neurotrauma,2004,21(8):1090-1102.
14 Chang Y,Chen TY,Chen CH,et al.Plasma arginine-vasopressin following experimental stroke: effect of osmotherapy[J]. J Appl Physiol,2006,100(5):1445-1451.
15 LU Yuan qiang,CAI Xiu jun,GU Lin hui,et al.Hypertonic saline resuscitation maintains a more balanced profile of T-lymphocyte subpopulations in a rat model of hemorrhagic shock[J]. J Zhejiang Univ Sci B,2007,8(1):70-75.
16 Thiel M,Imendorffer S,Chouker A,et al.Expression of adhesion molecules on circulating polymorphonuclear leukocytes during orthotopic liver transplantation[J].Hepatology ,1998,28(6): 1538–1550.
17 Ciesla DJ,Moore EE,Gonzalez RJ.Hypertonic saline inhibits neutrophil (PMN) priming via attenuation of p38 MAPK signaling[J].Shock, 2000,14(3):265-269; discussion 269-270.
18 Chen Yu,Naoyuki Hashiguchi,Linda Yip,et al.Hypertonic saline enhances neutrophil elastase release through activation of P2 and A3 receptors[J].Am J Physiol Cell Physiol,2006,290(4): C1051-1059.
19 Loomis William H,Sachiko Namiki,David B,et al.Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators[J].Am J Physiol Cell Physiol,2001,281(3):C480 -848.
20 Horton JW,Maass DL,White DJ.Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis[J].Am J Physiol Heart Circ physiol, 2006, 290(4):H1642-1650.
21 Xiao F,Zhang S,Amold TC,et al.Mild hypothermia induced before cardiac arrest rduces brain edema formation in rats[J].Acad Emerg Med,2002,9(2):105-114.
22 Khanna S,Davis D,Peterson B,et al.Use of hypertonic saline in the treatment of severe refractory posttraumatic intracranial hypertension in pediatric traumatic brain injury[J].Crit Care Med, 2000,28(4):1144–1151.
23 Schwarz S,Georgiadis D,Aschoff A,et al.Effects of hypertonic (10%) saline in patients with raised intracranial pressure after stroke[J].Stroke,2002,33(1):136–140.
[2] XiaoF,Zhang Z,Amold TC,et al.Mild hypothermia induced before cardiac arrest reduces brain edema formation in rats[J].Acad Emerg Med,2002,9(2):105-114.
[3] Reisinger J,H?llinger K,Lang W,et al.Prediction of neurological outcome after cardio- pulmonary resuscitation by serial determination of serum neuron-specific enolase[J]. Eur.Heart J,2007,28(1):52-58.
[4] Rosen H,Sunnerhagen KS,Herlitz J,et al.Serum levels of the brain-derived proteins S-100 and NSE predict long-term outcome after cardiac arrest[J].Resuscitation,2001,49(2):183 -191.
[5] Pike BR,Zhao X,Newcomb JK,et al.Stretch injury causes calpain and caspase-3 activation and necrotic and aimptotic cell death in septo-hippecamlml cell cu1tures[J]. J Neurotrauma, 2000,17 (4):283-298.
[6] ErecinskaM,ThoresenM,Silver IA,et al.Effects of hypothermia on energy metabolism in Mammalian central nervous system[J].J Cereb Blood Flow Metab,2003,23(5):513-530.
[7] Harada K,Maekawa T,Tsuruta R,et al.Hypothermia inhibitstranslocation of CaM kinase II and PKC- alpha,beta,gamma isoforms and fodrin proteolysis in rat brain synap tosome during ischemia- reperfusion[J].J Neurosci Res,2002,67(5):664-669.
[8] PrandiniMN,Neves Filho A,Lapa AJ,et al.Mild hypothermia reduces polymorphonuclear leukocytes infiltration in induced brain inflammation[J].Arq Neuropsiquiatr,2005,63(3B): 779-784.
[9] Busto R,Dietrich WD,Globus MY,et al.Small differences in intra-ischemic brain temperature critically determine the extent of ischemic neuronal injury[J].J Cereb Blood Flow Meta, 1987,7(6):729-738.
[10] Fay T.Early experiences with local and generalized refrigeration of the human brain[J].J Neurosurg,1959,16(3):239-260.
[11] Younes RN, Deutsch F,Itinoshe M,et al.Responsiveness to different volume therapies following hemodilution and hemorrhagic shock:a comparative experimental study in rats[J].Acta Cir Bras, 2007,22(5):355-360.
[12] Torg TJ,Hurn PD,Trayslman RJ,et a1.Global brain water increases after experimental focal cerebral ischemia:effect of hypertonic saline[J].Crit Care Med,2002,30(3):644-649
[13] Suarez JI,Qureshi AI,Bhardwaj A,et a1.Treatment of refractory intracranial hypertension with 23.4%saline[J].Crit Care med,1998,26(6):1118-1122.
[14] Schwarz S,Georgiadis D,Aschoff A,et a1.Effects of hypertonic(10%) saline in patients withraised intracranial pressure after stroke[J].Stroke,2002,33(1):136-l40.
[15] American Heart Association. Utstein-Style Guidelines for Uniform Reporting of Laboratory CPR Research[J].Circulation,1996,94(9):2324-2336.
[16] Geocadin RG,Ghodadra R,Kimura T,et al.A novel quantitative EEG injury measure of global cerebral ischemia[J].Clin Neurophysiol,2000,111(10):1779-1787.
[17]曾春,马中富.心肺复苏的方法学进展[J].中华急诊医学杂志,2001,10(6):418-420.
[18] Walraven CV,Stiell LC,Wells GA,et al.Do advanced cardiac life support during increase resuscita- tion rate from in hospital cardiac[J].Br J Anasth,1999,82(5):738.
[19] Rubertsson.Cardiopulmonary cerebral resuscitation-present and future perspective[J]. Acta Anaesthesiol Scand,1999,43(5):526-535.
[20]周彬,孟力.心肺复苏后的脑损害及预后评价[J].中华急诊医学杂志,1996,5(2):119-122.
[21] El-Menyar AA.Pathophysiology and hemodynamic of postresuscitation syndrome[J].Saudi Med J,2006 Apr;27(4):441-445.
[22] Padosch SA,Vogel P,Bottiger BW.Neuronal apoptosis following cerebral ischemia[J]. Basis,physio- pathology and treatment strategies Anaesthesist,2001,50(12):905-920.
[23] Tsuchiya D,Hong S,Matsumori Y,et al.Overexpression of rat heat shock protein 70 reduces neuronal injury after transient focal ischemia, transient global ischemia,or kainic acid- induced seiz- ures[J]. Neurosurgery,2003,53(5):1179 -1187;discussion 1187-1188.
[24] Torregrosa G,Barberu MD,Orti M,et al.Temporospatial expression of HSP72 and c-JUN, and DNA fragmentation in goat hippocampus after global cerebral ischemia[J]. ischemia [J].Hippocampus,2001,11(2): 146-156.
[25] Yamaguchi T,Miyata K,Shibasaki F,et al.Effect of cyclosporin a on immediate early gene in rat global ischemia and its neuroprotection[J].J Pharmacol Sci,2006,100(1):73-81.
[26] Qi JP,Wu AP,Wang DS,et al.Correlation between neuronal injury and Caspase-3 after focal ischemia in human hippocampus[J].Chin Med J(Engl),2004,117(10):1507-1512.
[27] D'Cruz BJ,Fertig KC,Filiano AJ,et al.Hypothermic reperfusion after cardiac arrest augments brain -derived neurotrophicfactor activation[J].J Cereb Blood FlowMetab, 2002,22(7):848-851.
[28] Hicks SD,DeFranco DB,Callaway CW.Hypothermia during reperfusion after saphyxial cardiac arrest improves functional recovery and selectively alters stress -induced protein expression[J].J Cereb Blood Flow Metab,2000,20(3):520-530.
[29] Li LX,Jiang T,Liu EZ, et a1. Effect of intraischemic mild hypothermia on interleukin-1beta and monocyte chemoattractant protein-1 contents in ischemic core of rat cortex after transient focal cerebral ischemia[J].Zhonghua Yi Xue Za Zhi,2003,10;83(7):541-543.
[30] Zhan RZ,Fujiwara N,Endoh H,et al. Thiopental inhibits increases in [Ca2+]i induced by membrane depolarization, NMDA receptor activation, and ischemia in rat hippocampal and cortical slices[J]. Anesthesiology,1998,89(2): 456-466.
[31] Harris OA,Colford JM Jr,Good MC,et al.The role of hypothermia in the management of severe brain injury : a meta-analysis. [J].Arch Neurol,2002,59(7):1077-1088.
[32] Kimura A,Sakurada S,Ohkami H,et a1.Moderate hypothermia delays proinflammatory cytokine production of Human peripheral blood mononuclear cells[J].Crit Care Med,2002,30(7):l499-l502.
[33] Soukup J,Zauner A,Doppenberg EM,et a1.Relationship between brain temperature,brain chemistry and oxygen delivery after severe human head injury:the effect of mild hypothermia[J].Neurol Res,2002,24(2):161-168.
[34] Kimura T,Sako K,Tanaka K,et a1.Effect of mild hypothermia on energy state recovery following transient forebrain ischemia in the gerbil[J].Exp Brain Res,2002,145(1):83-90.
[35] Xu L,Yenail MA,Steinberg GK,et a1.Mild hypothermia reduces apoptosis of mouse neurons in vitro early in the cascade[J].J Cereb Blood F1ow Metab,2002,22(1):2l-28.
[36] Bedell EA,DeWitt DS,Uchida T,et al. Cerebral pressure autoregulation is intact and is not influenced by hypothermia after traumatic brain injury in rats[J].J Neurotrauma,2004,21(9): 1212-1222.
[37] Tokutomi T,Morimoto K,Miyagi T,et al. Optimal temperature for the management of severe traumatic brain injury: Effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism[J].Neurosurgery,2003,52(1):102-111.
[38] Bernard S , Buist M, Monteiro O,et al.Induced hypothermia using large volume ,ice-cold intravenous fluid in comatose survivors of out-of hospital cardiac arrest:a preliminary report[J]. Resusci- tation, 2003,56(1):9-13.
[39] Weed LH,MeKibben PS.Experimental alteration of brain bulk[J].Am J Physiol,1919, 48(5):531-558.
[40] Zhou QQ,Liu FY,Gao YQ.et al.Effects of liquids with different osmotic pressure and different oxygen concentration on resuscitation of hemorrhagic shock at high altitude in rat[J].Zhongguo Wei Zhong Bing Ji Jiu Yi Xue,2008 ,20(7):393-396.
[41] Qin W,Yu YH,Sheng C.Protective effect of hypotensive fluid resuscitation against lung ischmia -reperfusion injury in pregnant rabbits with uncontrolled hemorrhagic shock[J].Nan Fang Yi Ke Da Xue Xue Bao.2008,28(6):1042-1044.
[42] Suarez JI.Hypertonic saline for cerebral edema and elevated intracranial pressure[J].Cleve Clin J Med,2004,71(1):S9-13.
[43] Huang SJ,Chang L,Han YY,et al.Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury[J].Surg Neurol,2006,65(6):539-546;discussion 546.
[44] Sidi A,Muehlschleqel JD,Kirby DS,et al.Treating ischemic left ventricular dysfunction with hypertonic saline administered after coronary occlusion in pigs[J].J Cardiothorac Vasc Anesth, 2007,21(3): 400-405.
[45] Doyle JA,Davis DP,Hoyt DB.The use of hypertonic saline in the treatment of traumatic brain injury[J].J Trauma,2001,50(2):367-383.
[46] Chang Y,Chen TY,Chen CH,et al.Plasma arginine-vasopressin following experimental stroke: effect of osmotherapy[J].J Appl Physiol,2006,100(5):1445-1451.
[47] Thiel M,Imendorffer S,Chouker A,et al.Expression of adhesion molecules on circulatingpolymorphonuclear leukocytes during orthotopic liver transplantation[J]. Hepatology,1998, 28(6): 1538–1550.
[48] Ciesla DJ,Moore EE,Gonzalez RJ.Hypertonic saline inhibits neutrophil (PMN) priming via attenuation of p38 MAPK signaling[J].Shock,2000,14(3):265-269; discussion 269-270.
[49] Loomis William H,Sachiko Namiki,David B,et al.Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators[J].Am J Physiol Cell Physiol,2001,281(3):C480 -848.
[50] Horton JW,Maass DL,White DJ.Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis[J].Am J Physiol Heart Circ physiol,2006, 290(4):H1642-1650.
[51]黄唯佳,李章平,陈寿权.心肺脑复苏动物模型[J].中华急诊医学杂志.2002,11(6):419-420.
[52] von PlantaI,Weil MH,von Planta M,et al.Cardiopulmonary resuscitation in the rat[J].J Appl Physiol,1988,65(6):2641-2647.
[53] Bottiger BW,Krumnikl JJ,Gass P,et al.The cerebral“no-reflow”phenomenon after cardiac arrest in rats:influence of low-flow reperfusion[J]. Resuscitation,1997,34(1):79-87.
[54] Hendrickx HH,Rao GR,Safar P,et al.Asphyxia,cardiac arrest and resuscitation in rats.Ⅰ.Short term recovery[J].Resuscitation,1984,12(2):97-116.
[55] Hendrickx HH,Safar P,Miller A.Asphyxia,cardiac arrest and resuscitation in rats.ⅡLong term behavioral changes[J].Resuscitation,1984,12(2):117-128.
[56]陈寿权,李章平,王姗姗,等.窒息法致大鼠SCA模型复苏的影响因素[J].中华急诊医学,2005,14(10): 814-8 17.
[57] Ajito T,Suzuki K,Iwabuchi S.Effect of Intravenous Infusion of a 7.2% Hypertonic Saline Solution on Serum Electrolytes and Osmotic Pressure in Healthy Beagles[J].J Vet Med Sci,1999,61(6): 637-641.
[58] Harutjunyan L,Holz C,Rieger A,et al.Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients-a randomized clinical trial[J].Crit Care,2005,9(5):R530–540.
[59] Doshi VS,Say JH,Young SH,et al.Complications in Stroke Patients:A Study Carried out at The Rehabilitation Medcine Service,Changgi General Hospital[J].Singapore Med J, 2003;44(12): 643-652.
[60] Wassertheil-Smoller S,Shumaker S,Ockene J,et al.Depression and cardiovascular sequeae in postmenopausal women:The Women,s Health Initiative(WHI)[J].Arch Intern Med, 2004; 164(3): 289-298.
[61] Picavet MT,Gasthuys FM,Laevens HH,et al.Cardiopumonary effects of combined xylazine-guaiph- enesin- ketamine infusion and extradural(inter-coccygeal lidocaine) Anaesthesia in calves[J]. Vet Anaesth Analg,2004;31(1):11-9.
[62] Rothermundt M,Peters M,Prehn JH,et al.S100βin brain damage and neurodegeneration [J].Microsc Res Tech,2003,60(6):614-632.
[63] Muramatsu Y,Kurosaki R,Kato H,et al.Effect of pitavastatin against expression of S100 beta protein in the gerbil hippocampus after transient cerebral ischemia[J].Acta Physiol Scand, 2004,182(1):95-107.
[64] Wainwright MS,Craft JM,Griffin WS,et al.Increased susceptibility of S100B transgenic mice to perinatal hypoxia-ischemia[J].Ann Neurol,2004,56(1):61-67.
[65] Love S.Oxidative stress in brain ischemia[J].Brain Pathol,1999,9(1):119-131.
[66] Ali MS , Harmer M ,Vaughan R. Serum S100 protein as a marker of cerebral damage during cardiac surgery [ J ] . B r J A naesth ,2000 ,85 (2) : 287-298.
[67] Boat right KM,Salvesen GS.Mechanisms of caspase activation[J].Curr Opin Cell Biol,2003,15(6): 725-731.
[68] Daniel PT.Dissecting the pathways to death[J].Leukemia,2000,14(12):2035-2044.
[69] Love S,Barber R,Srinivasan A ,et al.Activation of caspase-3 in permanent and transient brain ischaemia in man[J].Neuroreport,2000,11(11):2495.
[70] Gill R,Soriano M,Blomgren K,et al.Role of caspase-3 activation in cerebral ischemia- induced neurodegeneration in adult and neonatal brain[J].J Cereb Blood Flow Metab, 2002,22(4):420.
[71] Iwal T,Niwa M,Hara A.DNA fragmentation in the CA2 sector of gerbil hippoeampus following transient forebrain ischemia[J].Brain Res,2000,857(1-2):275-278.
[72] Sharma AB,Barlow MA,Yang SH,et al.Pyruvate enhances neurological recovery following cardiopul- monary arrest and resuscitation[J].Resuscitation,2008,76(1):108-119.
[73] Yuan GQ, Wu YL, Jia ZH. Experimental study on effect of tongxinluo on nerve cell apoptosis after cerebral ischemia in middle cerebral arterial obstructive model rats[J]. Zhongguo Zhong Xi Yi Jie He Za Zhi, 2007;27(8):720-723.
[74] He X,Mo X,Gu H,et al.Neuroprotective effect of diazoxide on brain injury induced by cerebral ischemia/reperfusion during deep hypothermia[J].J Neurol Sci,2008,15; 268 (1-2):18-27.
[75] Lok J,Martin LJ.Rapid subcellular redistribution of Bax precedes caspase-3 and endonuclease activation during excitotoxic neuronal apoptosis in rat brain[J].J Neurotrauma,2002,19(7): 815-828.
[76] Cernak I,Chapman SM,Hamlin GP,et al.Temporal characterization of pro-and anti-apoptotic mechanisms following diffuse traumatic brain injury in rats[J].J Clin Neurosci,2002,9(5): 565-572.
[77] Mammen EF,Barnhart MI,Selik NR ,et al“.Sticky platelet syndrome”:A congenital platelet abnormality predisposing to thrombosis?[J].Folia Haematol,1998,115(3):361-365.
[78] Chaturvedi S,Dzieczkowski JS.Protein S deficiency,activated protein C resistance and platelet syndrome in a young women with bilateral strokes[J].Cerebrovasc Dis,1999, 9(2): 127-130.
[79] Fields RD,Stevens-Graham B.New insights into neuron-glia communication[J].Science, 2002,298 (5593):556-562.
[80] Hansson E,Ronnback L.Glial neuronal signaling in the central nervous system[J].FASEB J,2003, 17(3):341-348.
[81] Sasaki T,Hamada J,ShibataM,et al.Inhibition of nitric oxide production during global ischemia ameliorates ischemic damage of pyramidal neurons in the hippocampus[J].Keio JMed,2001,50(3): 182-187.
[82] Yasuda Y, Tateishi N, Shimoda T, et al. Relationship between S100beta and GFAP expression in astrocytes during infarction and glial scar formation after mild transient ischemia [J].Brain Res,2004,1021(1): 20-31.
[83] Kimelberg HK,Nestor NB,Feustel PJ.Inhibition of release of taurine and excitatory amino acids in ischemia and neuroprotection[J].Neurochem Res,2004,29(1):267-274.
[84] Waxweiler R J, Thurman D, Smeiezek J. Monitoring the impact of traumatic brain injury, a review and update [ J ]. J Neurotrauma, 1995, 12 (4) : 509 - 516.
[85] Kofler J, Hattori K, Sawada Met al. Histopathological and behavioral characterization of a novel model of cardiac arrest and cardiopulmonary resuscitation in mice[J].J Neurosci Methords 2004,15;136 (1):33-44.
[86] Baker CJ, Onesti ST, Solomon RA. Reduction by delayed hypothermia of cerebral infarction followingmiddle cerebral artery occlusion in the rat: a time course study[ J ]. J Neurosurg, 1992, 77(3): 438-444.
[87] Miyazawa T , Tamura A , Fukhui S , et al. Effect of mild hypothermia on focal cerebral ischemia review of experimental studies[ J ]. Neurol Res ,2003 ,25 (5):457- 464.
[88] Xiao F,Zhang S,Amold TC,et al.Mild hypothermia induced before cardiac arrest rduces brain edema formation in rats[J].Acad Emerg Med,2002,9(2):105-114.
1 Pascual JM,Solivera J,Prieto R,et al.Time course of early metabolic changes following diffuse traumatic brain injury in rats as detected by (1)H NMR spectroscopy[J].J Neurotrauma,2007 ,24(6):944-959.
2 Boulard G,Marguinaud E,Sesay M.Osmotic cerebral edema: the role of plasma osmolarity and blood brain barrier[J].Ann Fr Anesth Reanim,2003,22(3):215-219.
3 Qureshi AI,Suarez JI.Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension[J]. Crit Care Me,2000,28(9):3301-3313.
4 Huang SJ,Chang L,Han YY,et al.Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury[J].Surg Neurol,2006,65(6):539-546; discussion 546.
5 Harutjunyan L,Holz C,Rieger A,et al.Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients-a randomized clinical trial[J].Crit Care,2005,9(5):R530–540.
6 Younes RN, Deutsch F,Itinoshe M,et al.Responsiveness to different volume therapies following hemodilution and hemorrhagic shock: a comparative experimental study in rats[J].Acta Cir Bras, 2007,22(5):355-360.
7 Sidi A,Muehlschleqel JD,Kirby DS,et al.Treating ischemic left ventricular dysfunction with hypertonic saline administered after coronary occlusion in pigs[J]. J Cardiothorac Vasc Anesth, 2007,21(3):400-405.
8 Doyle JA,Davis DP,Hoyt DB.The use of hypertonic saline in the treatment of traumatic brain injury[J].J Trauma,2001,50(2):367-383.
9 Oertel M, Boscardin WJ, Obrist WD,et al. Posttraumatic vasospasm: the epidemiology, severity,and time course of an underestimated phenomenon: a prospective study performed in 299 patients[J].J Neurosurg,2005,103(5):812-824.
10 ELena K,Marta L,Carmine M.Glutamine synthetase activity and glutamine content in brain: modulation by NMDA receptors and nitric oxide[J]. Neurochemist,2003,43(4-5):493-499.
11 Small DL,Morley P,Buchan AM.Biology of ischemsic cerebral cell death[J].Prog Cardiovasc Dis,1999,42(3):185-207.
12 Franceschini R,Tenconi GL,Zoppoli F,et al.Endocrine abnormalities and outcome of ischaemic stroke[J]. Biomed Pharmacother,2001,55(8):458–465.
13 Szmydynger-Chodobska J,Chung I,Kozniewska E,et al.Increased expression of vasopressin V1a receptors after traumatic brain injury[J]. J Neurotrauma,2004,21(8):1090-1102.
14 Chang Y,Chen TY,Chen CH,et al.Plasma arginine-vasopressin following experimental stroke: effect of osmotherapy[J]. J Appl Physiol,2006,100(5):1445-1451.
15 LU Yuan qiang,CAI Xiu jun,GU Lin hui,et al.Hypertonic saline resuscitation maintains a more balanced profile of T-lymphocyte subpopulations in a rat model of hemorrhagic shock[J]. J Zhejiang Univ Sci B,2007,8(1):70-75.
16 Thiel M,Imendorffer S,Chouker A,et al.Expression of adhesion molecules on circulating polymorphonuclear leukocytes during orthotopic liver transplantation[J].Hepatology ,1998,28(6): 1538–1550.
17 Ciesla DJ,Moore EE,Gonzalez RJ.Hypertonic saline inhibits neutrophil (PMN) priming via attenuation of p38 MAPK signaling[J].Shock, 2000,14(3):265-269; discussion 269-270.
18 Chen Yu,Naoyuki Hashiguchi,Linda Yip,et al.Hypertonic saline enhances neutrophil elastase release through activation of P2 and A3 receptors[J].Am J Physiol Cell Physiol,2006,290(4): C1051-1059.
19 Loomis William H,Sachiko Namiki,David B,et al.Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators[J].Am J Physiol Cell Physiol,2001,281(3):C480 -848.
20 Horton JW,Maass DL,White DJ.Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis[J].Am J Physiol Heart Circ physiol, 2006, 290(4):H1642-1650.
21 Xiao F,Zhang S,Amold TC,et al.Mild hypothermia induced before cardiac arrest rduces brain edema formation in rats[J].Acad Emerg Med,2002,9(2):105-114.
22 Khanna S,Davis D,Peterson B,et al.Use of hypertonic saline in the treatment of severe refractory posttraumatic intracranial hypertension in pediatric traumatic brain injury[J].Crit Care Med, 2000,28(4):1144–1151.
23 Schwarz S,Georgiadis D,Aschoff A,et al.Effects of hypertonic (10%) saline in patients with raised intracranial pressure after stroke[J].Stroke,2002,33(1):136–140.