摘要
目的 :探讨病毒性心肌炎心肌线粒体结构的功能变化。方法 :雄性Balb/c小鼠40只 ,随机分为柯萨奇B3 病毒 (CVB3)感染组和对照组 ,感染组分设感染后第7天、14天及28天3时相点 ;对照组 (10只 )只设28天一个时相点作总对照。电镜和形态计量学观察心肌线粒体形态、数量和膜磷脂定位 ,用酶细胞化学分析心肌线粒体细胞素氧化酶 (CCO)和琥珀酸脱氢酶 (SDH)活性。结果 :CVB3感染第7天心肌线粒体增生、肿胀 ,CCO和SDH活性明显降低 (P<0 05~0 01) ,膜磷脂定位无明显变化 ;第14天心肌线粒体高度肿胀 ,大量破坏 ,CCO和SDH活性进一步降低 ,膜磷脂严重缺失、定位改变SDH活性有所恢复 (P<0 05~0 01) ,但膜磷脂定位无明显改善 (P>0 05) ,所有指标与对照组比较差异有显著性 (P<0 01)。结论 :病毒性心肌炎心肌线粒体结构严重破坏 ,功能明显下降 ,心肌细胞存在产能障碍。
Objective:To explore the changes of myocardial mitochondrial structures and functions in viral myocarditis.Methods:The male Balb/c mice were randomly divided into coxsackie B3 virus(CVB3) infection group and control group.The myocardial samples of virus infection group were investigated on the 7th,14th,28th day.The morphology,membrane phospholipid as well as activities of cytochrome osidass(CCO) and succinate dehydromgenase(SDH) of mycardial mitochondria were studied by using transmission electron microscope,morphometry and enzyme cytothemical method respectivly.Results:On the 7th day after virus infection,the myocardial mitochondria swelled mildly,the mitochondrial number increased and the activities of CCO and SDH of mitochondria declined obviously(P<0.05~0.01),but the mitochondrial membrane phospholipid localization had no notable change.On the 14th day,myocardial mitochondria became mitochondria declined further,the mitochondrial membrane phospholipid apparent deletion and localization change were observed(P<0.01).On the 28th day,the number as well as the activities of CCO and SDH of myocardial mitochondria renewed to same extnet in comparison with those on the 14th day(P<0.05~0.01),but mitochondrial membrane phospholipid localization was no apparent improvement(P>0.05),all above were still significant as comparison with those of control group(P<0.01).Conclusion:the myocardial mitochondrial structures destroyed apparently and its funtions declined obviously in viral myocarditis.
出处
《现代医药卫生》
2004年第12期1075-1077,共3页
Journal of Modern Medicine & Health