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双下肢缺血后处理对大鼠心肌缺血再灌注损伤的保护作用 被引量:9

An Experimental Study on Protective Effects of Non-wound IschemicPostconditioning to Ischemia/Reperfusion Myocardial Injury of Rats
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摘要 目的 :探讨在体条件下 ,非创伤性双下肢缺血后处理 (N WIPTC)是否具有减轻心肌缺血再灌注 (I/R)损伤的作用。方法 :采用SD大鼠心肌I/R模型 ,应用Evan蓝、TTC染色 ,观察N WIPTC对心肌梗死面积的影响 ;并应用生化检测及免疫组织化学技术 ,研究N WIPTC、丙二醛 (MDA)、超氧化物歧化酶 (SOD)对大鼠心肌I/R损伤的作用。结果 :与I/R组比较 ,N WIPTC组的心肌梗死面积减少 ,MDA含量显著降低 (P <0 .0 1 ) ,而SOD含量明显升高 (P <0 .0 1 )。结论 :N WIPTC能有效降低心肌I/R梗塞面积 ,其机制可能与减少自由基损伤和抗氧化作用加强有关。 Objective: To observe if there would be protective effects of ischemic postconditioning in non wound legs (N WIPTC) on ischemia/reperfusion (I/R) caused mycocardia injury of rats in vivo. Methods: 30 Sprague Dawley rats were divided randomly into four groups and the model of I/R myocardial injury were produced. The influence of N WIPTC on infarction sizes (IS) was measured with Evan’s and TTC dye. The effects of N WIPTC, malondialehyde (MDA) and superoxide dismutase (SOD) on the I/R caused mycocardia injury were tested with biochemistry and immunohistochemistry techniques. Results: Compared with those of I/R group, the IS and the concentration of MDA in plasma of N WIPTC group were lower (P<0 01), and the concentration of SOD in plasma of N WIPTC group was higher. Comparing with that of the ischemic preconditioning (IPC) group, the IS and the concentrations of MDA and SOD in plasma were not significantly different between IPC group and N WIPTC group (P>0 05). Conclusion: N WIPTC has the same protective effects as IPC through decreasing the IS. The potential mechanism might be decreasing of the injury caused by oxygen free radical and strengthening the action of antioxidization.
出处 《贵阳医学院学报》 CAS 2004年第1期7-9,共3页 Journal of Guiyang Medical College
关键词 心肌再灌注损伤 心肌梗塞 大鼠 myocardial reperfusion injury myocardial infarction rat
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参考文献9

  • 1刘兴德,陈运贞.蛋白激酶C和蛋白酪氨酸激酶活性对缺血再灌注心肌细胞凋亡影响的实验研究[J].重庆医科大学学报,2000,25(1):20-22. 被引量:11
  • 2Nakano A,Liu GS,Heusch G,et al.Exogenous nitric oxide can trigger a preconditioned state through a free radical mechanism,but endogenous nitric oxide is not a trigger of classical ischemic precoditioning[J].J Mol Cell Cardiol,2000,32:1 159-1 167.
  • 3Murry CE,Richard VJ,Reimer KA,et al.Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained is-chemic episode[J].Circ Res,1990,66:913-931.
  • 4Li GC,Vasquez JA,Gallagher KP,et al.Myocardial Protection with preco-nditioning[J].Circulation,1990,82:609-619.
  • 5Gross GJ,Auchampach JA.Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs[J].Circ Res,1992,70:223-233.
  • 6Thompson JA,Hess ML.The oxygen free radical system:a fundamental mechanism in the production of myocardial necrosis[J].Prog Cardiovasc Dis,1986,28:499-512.
  • 7McCord JM.Oxygen derived free radical in postischemic injury[J].New Engl Med,1985,312:159-163.
  • 8Mitchell MB,Meng XZ,Ao L,et al.Preconditioning of isolated rat heart is mediated by protein kinase C[J].Circ Res,1995,76(l):73-81.
  • 9Pain T,Yang XM,Critz SD,et al.Opening of mitochondrial KATP channels triggers the preconditioned state by generating free radicals[J].Circ Res,2000,87:460-466.

二级参考文献5

  • 1Bines C P,J Mol Cell Cardiol,1998年,30卷,383页
  • 2Maulik N,FEBS Lett,1996年,396期,233页
  • 3Khalil R A,Circulation Research,1995年,76卷,1101页
  • 4Bhat N R,J Cell Phys,1995年,165卷,417页
  • 5Ytrehus K,Am J Physiol,1994年,266期,1145页

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