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低温闭胸心肺转流对缺血再灌注损伤血浆和组织中SOD、MDA、NO的影响

Influence to Levels of SOD,MDA,NO in Plasma and Tissues by Closed Chest Hypothermia Cardiopulmonary Bypass(CPB)during Reperfusion Injury
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摘要 目的:了解狗心脏停搏15分钟后,用浅低温和深低温闭胸心肺转流(CPB)时,对血浆和组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)的影响。方法:10只实验狗,用10%氯化钾静注致心脏停搏15分钟后,行闭胸CPB复苏,浅低温组(33℃~34℃)(N=5),深低温组(26℃~27℃)(N=5),15分钟后复温。于停搏前、停搏15分钟、CPB开始后1小时、3小时抽血,并于3小时取心、肺、脑组织,行血浆和组织SOD、MDA和NO测定。结果:在停搏15分钟时,两组血浆SOD活性均明显高于停搏前;CPB后1小时,二组均明显低于停搏前(P<0.05),但至3小时,二组均上升接近停搏前水平(P>0.05)。两组血浆MDA和NO含量于停搏15分钟和CPB后1小时、3小时均明显低于停搏前(P<0.05)。浅低温组脑组织和肺组织中SOD明显低于深低温组(P<0.05),MDA明显高于深低温组(P<0.05);而心肌组织中NO含量明显低于深低温组(P<0.05),MDA也明显低于深低温组(P<0.05)。结论:狗心脏停搏15分钟后,用低温闭胸CPB复苏,血浆SOD代偿性升高,MDA和NO下降,即低温复苏有助于减轻氧自由基和NO造成的再灌注损伤。组织中的指标测定,表明深低温闭胸CPB复苏对脑和肺的再灌注损伤较轻,浅低温闭胸CPB复苏则对心肌的再灌注损伤较轻。 Objective: To observe levels of SOD, MDA, and NO by mild or deep hypothermia after cardiac arrest of 15 minutes in dogs. Methods: With our established dog CPR model, cardiac arrest of 15 minutes was followed by reperfusion with closed chest CPB. Group 1(n=5) was received mild hypothermia(33℃~34℃), group 2(n=5) was deep hypothermia (26℃~27℃), and the levels of SOD, MDA, NO in plasma and tissues were measured during CPR. Results: After cardiac arrest of 15minutes, concentrations of SOD in plasma in-group 1(2615.84±57.64u/ml) was significantly higher than pre-arrest (2586.36±61.78u/ml) (P<0.05), and in-group 2(2690.48±35.50u/ml) was also higher than pre-arrest. The concentration of SOD in plasma at 1 hr CPB were lower than pre-arrest (P<0.05) and nearly pre-arrest (P>0.05)at 3 hrs CPB. The levels of MDA and NO were lower than pre-arrest after cardiac arrest of 15 minutes, at 1 hr, and 3 his CPB. There was no difference in two groups. After three hrs CPB in the cerebral tissues, the concentrations of SOD in group 2(1075.6±11.15u/g) was significantly higher than in group 1(1057.2±11.80u/ml) (P<0.05). In the pulmonary tissues, the concentration of SOD in group 2(690.6±8.7u/g) was also significantly higher than in group 1(626.67±23.50u/g),(P<0.01),and the levels of MDA(4.72±1.5u/ml) was lower than in-group 1(7.32±1.54nmol/g)(P<0.05).In the cardiac tissues the levels of MDA and NO in group 1 were significantly lower than group 2(P<0.05).Conclusion: Resuscitation by closed chest hypothermia CPB may decrease free-radical-induced reperfusion injury after cardiac arrest of 15 minutes in dogs. The cerebral and pulmonary reperfusion injury during deep hypothermia CPB was more slightly than during mild hypothermia, whereas the cardiac reperfusion injury during mild hypothermia CPB was more slightly than during deep hypothermia.
出处 《岭南急诊医学杂志》 2002年第4期321-323,332,共4页 Lingnan Journal of Emergency Medicine
关键词 闭胸心肺转流 再灌注损伤 心肺复苏 自由基 CPB CPR reperfusion injury free radical
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参考文献9

  • 1[1]Jask BE,Lingle RJ,Overlie P,et al. Long- term survival with use of percutanaeous extracorporeal life support in- patients presenting with acute myocardial infraction and cardiovascular collapse. ASAIO J,1999,45(6):615.
  • 2[2]Becker LB. Minimizing hypoxic injures during cardiac arrest. NEW Horiz,1997,5(2):145.
  • 3[3]Chan PH. Role of oxidants in ischemic brain damage. Stroke,1996,27(6):1124.
  • 4[4]Siragusa P,Javazzi B,Lazzarino G,et al. Experimental model of asymmetric brain ischemia and reperfusion in the rat. J Neurosurg Sci, 1997,41(3):249.
  • 5[5]Kinodin H,Kamii H,Mikawa S,et al. Role of superoxide dismutase in ischemic brain injure:a study using SOD- 1 transgenic mice. Cell Mol Neurobiol,1998,18(6):609.
  • 6[6]Liu.SL observations on the compensatory effects of superoxide dismutase under hypoxic or ischemic stress in rats and rabbits. Med Sci Res,1998,26(11):741.
  • 7[7]Baumgar WA,Redmond M,Brock M,et al. Pathophysiology of cerebral injury and future management. J Card Surg,1997,12(2 supple):300.
  • 8[8]Kumara E,Yoshimine T,Kubu S,et al. Effects of superoxide dismutase on nitric oxide production during reperfusion after focal cerebral ischemia in rats. Neurosci Lett,1995,200(2):137.
  • 9[9]O' Neil BJ,McLean JR,Disgrace DJ,et al. Cell death calcium mobilization, and immunostraining for phosphorylated eukaryotic initiation factor 2- alpa (eIF 2 alpha) in neuronal differentiated NB- 104 cells:arachidonate and medical- mediated injure mechanisms. Resuscitation,1999,41(1):71.

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