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目的研究卡维地洛(CVD)、庚醇(HT)在缺血再灌注心肌损伤中作用。方法通过建立的心脏缺血再灌注模型,采用2%氯化三苯四唑(TTC)染色测量心肌梗死的重量,监测心肌型肌酸激酶同功酶(CK-MB)、乳酸脱氢酶(LDH)、丙二醛(MDA)和一氧化氮(NO)等的变化。观察CVD、HT对心肌梗死的影响。结果在缺血30min,再灌注6h后,CVD减少CK-MB、LDH及MDA的释放,稳定NO的分泌。HT组在一定程度上也减少了LDH、CK-MB的释放,但对NO、MDA的释放似乎没有太大影响。CVD组的大鼠梗死心肌仅占左心室心肌重量的(6.2±1.1)%,比对照组减少了51.6%。HT组梗死心肌占左心室心肌重量的(7.4±1.0)%,比对照组减少了42.2%。HE常规染色发现CVD组心肌细胞损伤程度明显减轻,粒细胞浸润也明显减少,大部分仅表现肌纤维肿胀和断裂。CVD可以防止内皮型一氧化氮合酶的减少。电镜下,CVD组和HT组心肌润盘肌丝、线粒体等损伤较轻。结论CVD通过β受体拮抗、抗氧化等方面的作用来保护心肌。HT可能是使缝隙连接可逆性解藕联产生心肌保护作用。
Objective To investigate the effects of carvedilol (CH) and heptanol (HT) on myocardial injury induced by ischemia-reperfusion. Methods The model of myocardial ischemia-reperfusion was established. The myocardial infarction weight was measured by 2% TTC staining. The levels of myocardial creatine kinase (CK-MB) and lactate dehydrogenase LDH), malondialdehyde (MDA) and nitric oxide (NO). To observe the effects of CVD and HT on myocardial infarction. Results After 30 min of ischemia and 6 h of reperfusion, CVD reduced the release of CK-MB, LDH and MDA and stabilized the secretion of NO. HT group also reduced the release of LDH and CK-MB to a certain extent, but it did not seem to have much effect on the release of NO and MDA. The infarcted myocardium in the CVD group only accounted for (6.2 ± 1.1)% of the left ventricular myocardium weight, 51.6% less than the control group. The infarcted myocardium in HT group accounted for (7.4 ± 1.0)% of the left ventricular myocardium weight, 42.2% less than the control group. The routine staining of HE in CVD group showed that the damage of cardiomyocytes was significantly reduced and the infiltration of granulocytes significantly decreased. Most of them showed only muscle fiber swelling and rupture. CVD can prevent the decrease of endothelial nitric oxide synthase. Electron microscopy, CVD group and HT group myocardial pericardial myofilament, mitochondria and other lesser damage. Conclusions CVD protects the myocardium through the effects of β-receptor antagonism and anti-oxidation. HT may be caused by reversible decoupling of gap junctions to produce myocardial protection.