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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?
In this study, 20 patients with valvular heart disease were randomly divided into two groups, 10 in each. During valve replacement, a group of patients with intermittent perfusion of myocardial perfusion by hypothermic cardiopulmonary bypass plus cold crystalloid cardioplegia (St. Thomas Hospital fluid) Protection method (referred to as the low temperature group), another group of cardioprotective methods using ambient cardiopulmonary bypass plus warm blood cardioplegia continuous perfusion (referred to as room temperature group). The results of qualitative analysis of myocardial succinate dehydrogenase (SDH) and cytochrome oxidase (CCO) staining in both groups during ischemia and reperfusion were all positive. The results of computer image analysis showed that SDH activity gray level Value higher than hypothermia group (143.07 ± 1.38,115.25 ± 0.15, P <0.05). There was a significant difference in the gray value of SDH activity between the two groups during reperfusion. The hypothermia group was larger than the normal temperature group (143.07 ± 1.38, 129.06 ± 4.63, P <0.01). The gray value of CCO activity in ischemia group at room temperature was significantly higher than that in hypothermia group (145.54 ± 6.90,128.40 ± 5.43, P <0.05). CCO activity at reperfusion stage Which was significantly higher than that in hypothermia group (148.62 ± 4.82, 123.60 + 4.82, P <0.05). It showed that mitochondrial enzymes could be compensated during hypothermic ischemia, and myocardial mitochondria were more damaged during hypothermia reperfusion. However, normal temperature group could reduce ischemia-reperfusion injury without compensatory. At the same time also shows that warm blood cardioplegia can provide CCO suitable for relatively high oxygen metabolism environment, in the metabolic link?