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为探讨缺氧和缺血预处理对心肌细胞的保护作用 ,分别在培养的乳鼠心肌细胞缺氧 复氧模型、离体大鼠灌注和在体大鼠心肌缺血 再灌注模型中 ,观察缺血和缺氧预处理对心肌细胞再次长时间缺氧 复氧或缺血 再灌注损伤的保护作用。结果发现 ,在培养的乳鼠心肌细胞中 ,缺氧预处理组细胞存活率和超氧化物歧化酶含量较缺氧 复氧组增加 (P <0 .0 1) ,乳酸脱氢酶的释放和丙二醛含量则减少 (P <0 .0 1)。对离体或在体大鼠心脏的缺血预处理也可减少长时间缺血 再灌注对心肌细胞的损伤。离体大鼠缺血预处理组冠状动脉流出液中乳酸脱氢酶的释放和组织丙二醛的含量较非预处理组减少 (P <0 .0 1) ,心脏的湿干重比和组织超氧化物歧化酶含量则增加 (P <0 .0 1)。在体大鼠心肌缺血预处理组梗死范围和血清乳酸脱氢酶较缺血 再灌注组减少 (P <0 .0 1) ,无论是再次缺血还是再灌注期室性心律失常的发生率在预处理组明显低于非预处理组 (P <0 .0 1)。结果提示 ,缺血或缺氧预处理对心肌具有保护作用 ,预处理可以减少再次长时间的缺氧 复氧或缺血 再灌注对心肌细胞的损伤
To investigate the protective effects of hypoxia and ischemic preconditioning on cardiomyocytes, the effects of hypoxia-reoxygenation on cultured neonatal rat cardiomyocytes, in vitro and in vivo myocardial ischemia-reperfusion models were observed respectively Protective effects of blood and hypoxic preconditioning on cardiomyocytes against prolonged hypoxia / reoxygenation injury or ischemia / reperfusion injury. The results showed that in the cultured neonatal rat cardiomyocytes, the cell survival rate and superoxide dismutase content in hypoxic preconditioning group were higher than those in hypoxia-reoxygenation group (P <0.01), and the release of lactate dehydrogenase MDA content decreased (P <0.01). Ischemic preconditioning of isolated and in vivo rat hearts can also reduce myocardial damage caused by prolonged ischemia and reperfusion. The release of lactate dehydrogenase and the content of malondialdehyde in coronary effluent of isolated rat ischemic preconditioning group were lower than those of non-preconditioned group (P <0.01), and the ratio of wet to dry weight and tissue The content of superoxide dismutase increased (P <0.01). The extent of infarction and serum lactate dehydrogenase in ischemic preconditioning group were lower than those in ischemia-reperfusion group (P <0.01), and the incidence of ventricular arrhythmia in either ischemic or reperfused groups The pretreatment group was significantly lower than the non-pretreatment group (P <0. 01). The results suggest that ischemic or hypoxic preconditioning has a protective effect on myocardium, and preconditioning can reduce the damage of myocardial cells caused by prolonged hypoxia-reoxygenation or ischemia-reperfusion