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缺血后适应减轻大鼠肢体缺血再灌注后的心肌损伤 被引量:7

Ischemic postconditioning reduces myocardial damage in rats suffering from limb ischemia-reperfusion
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摘要 目的:探讨肢体缺血后适应(LIPostC)对大鼠肢体缺血再灌注(LIR)后心肌的保护作用。方法:Wistar大鼠随机分为对照组(C组)、缺血再灌注组(IR组)和缺血再灌注+缺血后适应组(IR+IPostC组)。制作大鼠LIR模型,IR+IPostC组在缺血后,实施肢体松解-结扎各5 min,反复5次,即缺血后适应,然后再进入持续的血流再灌注阶段。生物化学方法测定血清肌酸激酶(CK)及其MB同工酶(CK-MB)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、α-羟丁酸脱氢酶(α-HBDH)及心肌肌钙蛋白I(cTnI)水平,测定血清及心肌组织中超氧化物歧化酶(SOD)、黄嘌呤氧化酶(XOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)水平。电镜下观察心肌组织超微结构变化。结果:与对照组比较,IR组及IR+IPostC组血清CK、CK-MB、AST、LDH、α-HBDH及cTnI水平均升高,心肌组织及血清MDA及XOD水平升高(P<0.05),而SOD活性降低(P<0.05)。与IR组比较,IR+IPostC组血清CK、CK-MB、AST、LDH、a-HBDH及cTnI水平均降低(P<0.05),血浆及心肌组织的MDA及XOD有所降低而SOD水平升高(P<0.05)。电镜下可见C组心肌肌原纤维排列整齐,明暗带清晰,线粒体基质致密,嵴排列紧密整齐。IR组可见肌丝排列紊乱或消失,基质明显水肿,线粒体大部分或全部的嵴和膜融合或消失,空泡化明显,糖原数量明显减少。IR+IPostC组心肌上述病理改变有所减轻。结论:LIPostC可减轻LIR对心肌的损伤作用。 AIM: To investigate the protective effect of limb ischemic postconditioning on the myocardial damage in the rats suffering from limb ischemia -reperfusion (LIR). METHODS: Wistar rats were randomly divided into control group ( C group), ischemia - reperfusion group ( IR group) and ischemic post - conditioning group ( IR + IPostC group). For conducting ischemic postconditioning, the rats in IR + IPostC group underwent 5 min of ischemia and 5 min of reperfusion on their hind limbs repeatedly after 4 h of ischemia, and then, 4 h of reperfusion was applied. The activity of superoxide dismutase ( SOD), xanthine oxidase (XOD) and myeloperoxidase (MPO) was measured. The levels of malon-aldehyde (MDA) in plasma and myocardial tissues, the levels of creatine kinase (CK), creatine kinase MB (CK- MB), aspartate aminotransferase ( AST), lactate dehydrogenase ( LDH), α - hydroxybutyrate dehydrogenase ( α - HBDH) and myocardial troponin I (cTnI) were also detected. The changes of uhrastructure in the myocardium were observed under electron microscope. RESULTS : Compared with C group, the levels of CK - MB, AST, LDH,α - HBDH and cTnI were all increased in IR and IR + IPostC groups. The levels of MDA and XOD also increased (P 〈 0. 05 ), but the activity of SOD decreased (P 〈 0. 05). However, compared with group IR, the levels of CK - MB, AST, LDH, α - HBDH and cTnI decreased (P 〈 0. 05 ) in IR + IPostC group. The levels of MDA and XOD also decreased (P 〈 0. 05 ), but the activity of SOD increased (P 〈 0. 05 ). Under electron microscope, the cardiac myofibrils arranged neatly, light and dark bands were clear, the mitochondrial cristae arranged closely and neatly, and the mitochondrial matrix densification was observed in C group. However, the cardiac fiber arrangement was disordered or disappeared, stromal edema was obvious, most or all mitochondrial cristae and membrane became fusion or disappeared, mitochondrial vacuolization and decrease in glycogen were obvious in IR group. In IR + IPostC group, the pathological changes mentioned above were attenuated somewhat than those in IR group. CONCLUSION: Ischemic postconditioning protects rat myocardium under limb ischemia - reperfusion.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2012年第10期1892-1894,1900,共4页 Chinese Journal of Pathophysiology
基金 唐山市科技局资助项目(No.10150204A-17)
关键词 缺血后适应 再灌注 大鼠 心肌 Ischemic postconditioning Reperfusion Rats Myocardium
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