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为探讨铬对实验性心肌损伤的保护作用机制，选用Ｗｉｓｔａｒ大鼠腹肢内注射铬，尾静脉注射阿霉素，复制动物模型，用荧光偏振法测定心肌线粒体膜流动性，低温电子自旋共振技术测定心肌及肝脏自由基含量，同时观察抗氧化酶及心肌酶活性变化。结果表明单纯注射阿霉素大鼠心肌线粒体膜流动性降低，血清ＬＤＨ及ＣＰＫ活性增强，心肌及肝脏自由基含量升高，全血、心肌及肝脏ＧＳＨ－Ｐｘ活性降低，血清ＳＯＤ活性增强，心肌及肝脏ＳＯＤ活性降低。铬保护的大鼠心肌线粒体膜流动性改善，ＬＤＨ及ＣＰＫ释放减少，心肌及肝脏自由基含量降低，ＧＳＨ－Ｐｘ活性增强。维持膜的稳定性，增强抗氧化功能。可能是铬抗心肌损伤的重要机制。
In order to explore the protective mechanism of chromium on experimental myocardial injury, Wistar rats were injected intraperitoneally with chrome and adriamycin in the tail vein to replicate the animal model. The mitochondrial membrane fluidity was measured by fluorescence polarization method. Low temperature electron spin resonance The contents of free radicals in myocardium and liver were determined by the technique. At the same time, the changes of antioxidant enzymes and myocardial enzymes were observed. The results showed that the myocardial mitochondrial membrane flux decreased, LDH and CPK activity increased, the content of free radicals in myocardium and liver increased, the activity of GSH-Px in whole blood, myocardium and liver decreased, the activity of SOD in serum increased, And liver SOD activity decreased. Chromium-protected rat myocardial mitochondrial membrane fluidity improved, LDH and CPK release decreased, heart and liver free radicals decreased, GSH-Px activity increased. Maintains membrane stability and enhances anti-oxidant function. Chromium may be an important mechanism of myocardial injury.