早期心肌梗死与冠状动脉痉挛致心肌肌红蛋白缺失的实验研究  

Experimental study of myocardial myoglobin depletion induced by early myocardial infarction and coronary artery spasm

作　　者：周伟[1] 王斐[2] 秦启生[3] 胡俊[3] 黄光照[3] 

机构地区：[1]中山医科大学法医学系,广东510089 [2]上海市劳动卫生职业病研究所,上海200003 [3]同济医科大学法医病理教研室,武汉430030

出　　处：《法医学杂志》1997年第3期133-134,137,共3页Journal of Forensic Medicine

摘　　要：本实验按Selye法结扎Wistar大鼠冠状动脉左前降支复制早期心肌梗死模型；又经颈外静脉注射垂体后叶素复制冠状动脉痉挛模型。按心肌不同缺血时间（25min、1h、3h）及对照组将以上各模型均分成四组．每组均取心关部及其相邻组织块制成石蜡切片，进行HE染色、链霉菌素-生物素-肌红蛋白免疫组化染色（LSAN－Mb染色）。结果表明：心肌梗死25min即可见左心室前壁心内膜下心肌条片状Mb缺失，随着梗死时间的延长，条片状缺染区向外层心肌扩展；冠状动脉痉挛组呈多发性、小灶性Mb缺失，右心室Mb缺染灶多于左心室，且Mb缺染灶多围绕冠状动脉周围，或沿一支冠状动脉之各分枝是葡萄串样分布。可见大鼠早期心肌梗死与冠状动脉痉挛所致心肌Mb缺失具有不同的形态学特点．故LSAB－Mb法可望为冠状动脉痉挛所致心肌缺血提供客观形态学证据．In this study, the model of early myocardialinfarction(EMI) was Produce by legation of leftanterior descending artery in rat.The artery spasm(CAS) was produced by extermal jugular veininjection of vasopressin (VP). Myocardium of apex and adjoining slice was used to make paraffinsections, then HE and LSAB-Mb staining wereperformed. Results showed: Ih 25 min aftermyocardial infarction, stretch-shape Mb depletionwas obsered in subendocardial myocardium ofaortic ventricle′s frontal wall. As the time of EMIprolonged, stretch-shape Mb depletion extended toepicardial layer. In CAS group, multiply, spotty Mbdepletion was detected. There were more Mbdepletion zones in right heart than that in left heart.The Mb dapletion zones surrounded the CA or werelike grape-clusters along the branches of one largeCA. Thus, Thus,myocardial Mb depletion induced by EMIand CAS had different morphologic peculiarity.LSAB-Mb method could be hoped for the use ofsupplying objectively morphologic evidence tomyocardial ischemia induced by CAS.

关 键 词：早期心肌梗死 冠状动脉痉挛 肌红蛋白 免疫组织化学 

分 类 号：R542.22[医药卫生—心血管疾病]