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通过褪黑素（MT）对大鼠心肌缺血/再灌注损伤（IRI）的影响的研究,证实了MT能抗心肌缺血/再灌注损伤,并探讨其作用机制。实验采用在体大鼠心肌缺血再灌注损伤的模型,观察了MT对此模型大鼠缺血期、再灌注期心律失常发生的抑制作用及再灌注结束后心肌超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量及血浆乳酸脱氢酶（LDH）、肌酸激酶（CK）活性的影响,同时用酶组织化学染色法观察琥珀酸脱氢酶（SDH）的改变。结果表明MT能明显降低缺血和再灌注后室速（VT）和室颤（VF）的发生率,显著缩短其持续时间,明显提高心肌SOD活性,显著减少MDA含量,减少血浆LDH,CK的含量,明显减轻SDH损伤性反应,从而证实它对心肌的保护作用与增强机体内源性抗氧化能力,清除氧自由基,减少脂质过氧化以及保护线粒体有关。
The study of the effect of melatonin (MT) on myocardial ischemia / reperfusion injury (IRI) in rats demonstrates that MT can prevent myocardial ischemia / reperfusion injury and to explore its mechanism. The model of ischemia-reperfusion injury in vivo was used to observe the inhibitory effect of MT on ischemia-reperfusion arrhythmias and the changes of superoxide dismutase (SOD) Activity, malondialdehyde (MDA) content and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activity were measured. Meanwhile, the changes of succinate dehydrogenase (SDH) were observed by enzyme histochemical staining. The results showed that MT can significantly reduce the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) after ischemia and reperfusion, significantly shorten the duration, significantly increase myocardial SOD activity, significantly reduce the MDA content and reduce the plasma LDH, CK content , Significantly reduce the SDH injury response, thus confirming its protective effect on myocardial and enhance the body’s endogenous antioxidant capacity, scavenging oxygen free radicals, reduce lipid peroxidation and mitochondria related.