缺血再灌注损伤心肌电镜细胞化学的定性与定量分析（二）──琥珀酸脱氢酶和细胞色素氧化酶

Qualitative and Quantitative Studies on Cytochemistry of Ischemia Reperfusion Injury of Myocardium by Electronic Microscope.Ⅱ.Succinate Dehydrogenase and Cytochrome Oxidase.

本研究选择心脏瓣膜病患者２０例，随机分为两组，每组１０例，在瓣膜置换术中，一组采用低温体外循环加冷晶体停跳液（Ｓｔ．Ｔｈｏｍａｓ医院液）间断灌注的心肌保护方法（简称低温组），另一组采用常温体外循环加温血停跳液持续灌注的心肌保护方法（简称常温组）。两组缺血期和再灌注期心肌琥珀酸脱氢酶（ＳＤＨ）和细胞色素氧化酶（ＣＣＯ）染色定性分析结果均为阳性，计算机图像分析结果表明，低温组再灌注期ＳＤＨ酶活力灰度值高于低温组缺血期（１４３．０７±１．３８，１１５．２５±０．１５，Ｐ＜０．０５）．两组再灌注期ＳＤＨ酶活力灰度值相差极为显著，低温组大于常温组（１４３．０７±１．３８，１２９．０６±４．６３，Ｐ＜０．０１）。常温组缺血期ＣＣＯ酶活力灰度值显著高于低温组缺血期（１４５．５４±６．９０，１２８．４０±５．４３，Ｐ＜０．０５），常温组再灌注期ＣＣＯ活力显著高于低温组再灌注期（１４８．６２±４．８２，１２３．６０＋４．８２，Ｐ＜０．０５）。表明低温组缺血期心肌线粒体酶系可发生代偿，低温组再灌注期心肌线粒体损伤较重，而常温组可减轻缺血再灌注损伤，无需代偿。同时也表明温血停跳液可提供ＣＣＯ以适宜的相对高氧代谢环境，在该代谢环节?

Twenty patients undergoing open-heart valvular surgical procedures were divided randomly into two groups in this study.Instermittent perfusion of cold crystalloid (St.Thomas Hospital solution) with hypothermic cardioplmonary bypass(CPB)(hypothermic group)and continuous administration of warm blood cardioplegia with normothermic CPB(normothermic group)were utilized respectively.The results of qualitative analysis of both myocardial succinate dehydrogenase(SDH)and cytochrome oxidase(CCO)all showed positive in the two groups.The quantitative results of SDH by computerizing the micmphotographs were higher in reperfusion period than in ischemic period in the hypothermic group(143.07±1.38vs.115.25±0.15,P<0.05).It was also much higher in the reperfusion period in the hypothermic group than in the normothermic group(143.07±1.38 vs.129.06 ± 4.63,P<0.01).The activity of CCO by computerizing the electronic microscopic photographa was siguificantly promoted in the normothermic group in both ischemic and reperfusion period(145.54±6.90vs.128.40±5.43,P<0.05;148. 62±4.82 vs.123.60±4.82,P<0.05).It showed that compensative reaction would occur in mitochondrial enzymes in the hypothermic group during ischemia,and more severe mitochondrial damage could be noted in reperfusion period in the cold group.Nevertheless,compensation would not occur in the normothermic group because of the alleviation of the ischemia-reperfusion injury.It also illustrated that warm blood cardioplegia could provide CCO with appropriate environment of metabolism, and this would be of beneficial effect on myocardial protection in this point.