Rózycka Z, Lewicki Z, Wutzen J
Pol Tyg Lek. 1989 Apr 10;44(10-11):247-52.
Dynamics of changes in the myocardium of rabbits subjected to food hypercholesterolemia lasting from 6 to 16 weeks was investigated. An intensification of coronary atheromatosis was proportional to the duration of the high-cholesterol diet. There were observed focal and growing in time damages of cardiomyocytes. They were sharply outlined in atherosclerotically changed coronary arteries. The following morphological and histochemical changes have been observed: increased acidophilia and fuchsinophilia in the single and grouped muscle fibres, foci of infiltrations by mononuclear cells, contraction bands, and outlines of myocardial fibres, separation of myofibrils, granular disintegration of cardiomyocytes, healed infarcts, depletion and excessive accumulation of glycogen in muscle fibres, presence of neutral fats, cholesterol and its esters in atheromatous plaques of coronary arteries, presence of neutral fats in some cardiomyocytes: focal acid phosphates, loss of activity of Mg- and Ca-dependent ATPases and SDH: oedema of mitochondria with disorganization of cristae, disorganisation of fibres and lysis of myofilaments, margination of chromatin in cardiomyocyte nuclei, increased number of lysosomes, intensified symptoms of egzocytosis, widening of channels of sarcoplasmatic reticulum, oedema of endothelium of capillary vessels and increased number of the collagenous fibres in the interstitial space. The results of histological, histochemical and microscopic-electron investigations correlated with each other. It may be considered that the observed damages of cardiomyocytes precede myocardial infarction and result from progressive and increasing ischemia, hypoxia and accumulation of fat substances and cholesterol and its esters in intima of coronary arterioles as well as in cardiomyocytes.
研究了持续6至16周的食物性高胆固醇血症家兔心肌的变化动态。冠状动脉粥样硬化的加剧与高胆固醇饮食的持续时间成正比。观察到心肌细胞有局灶性且随时间发展的损伤。在动脉粥样硬化改变的冠状动脉中,这些损伤界限清晰。观察到以下形态学和组织化学变化:单个和成群的肌纤维嗜酸性和嗜品红性增加、单核细胞浸润灶、收缩带以及心肌纤维轮廓、肌原纤维分离、心肌细胞颗粒状崩解、愈合的梗死灶、肌纤维中糖原的消耗和过度积累、冠状动脉粥样斑块中存在中性脂肪、胆固醇及其酯类,一些心肌细胞中存在中性脂肪:局灶性酸性磷酸酶、镁和钙依赖性ATP酶及琥珀酸脱氢酶活性丧失;线粒体水肿伴嵴紊乱、纤维紊乱和肌丝溶解、心肌细胞核染色质边缘化、溶酶体数量增加、胞吐症状加剧、肌浆网通道增宽、毛细血管内皮水肿以及间质空间胶原纤维数量增加。组织学、组织化学和微观电子研究结果相互关联。可以认为,观察到的心肌细胞损伤先于心肌梗死,是由冠状动脉小动脉内膜以及心肌细胞中进行性增加的缺血、缺氧以及脂肪物质、胆固醇及其酯类的积累所致。