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儿茶酚胺诱导的实验性心肌病——一项组织病理学、组织化学和超微结构研究。

Catecholamine-induced experimental cardiomyopathy--a histopathological, histochemical and ultrastructural study.

作者信息

Khullar M, Datta B N, Wahi P L, Chakravarti R N

出版信息

Indian Heart J. 1989 Sep-Oct;41(5):307-13.

PMID:2599540
Abstract

An experimental model of myocardiopathy was induced in rhesus monkeys following noradrenaline (NA) infusion (20 ug/kg body wt/minute), for a period of 2 hours daily for three consecutive days. The animals were sacrificed after two hours (acute phase), forty-eight hours (sub-acute phase) and twenty-one days (chronic phase). Focal depletion of succinic dehydrogenase, increase in adenosine triphosphatase, acid phosphatase and appearance of large fat droplets in myocardial muscle was noted in the acute phase. Histopathological examination revealed focal edema, opacity and fuchsinorrhagia of the muscle fibres distributed in both the ventricles. Myofibrillar degeneration, myocytolysis and vacuolization with aggregation of lymphomononuclear cells were the significant features in the acute phase. During sub-acute and chronic phases, these features became less prominent and reparative changes with proliferation of fibroblasts became more marked. By the twenty-first day, irregular, focal scars replaced the necrosed myocardium. Ultrastructurally, heart muscle showed myofibrillar disorganisation, distortion of Z and A bands, dilatation of sarcoplasmic reticulum and swelling and rupture of mitochondria. Altered membrane permeability was evidenced by the presence of reaction products of horseradish peroxidase within the cardiac cells. In the reparative phase, however, myocytolytic changes regressed and collagen deposition was the prominent feature. This experimental study has several histological features simulating human cases of myocardial infarction without coronary occlusion.

摘要

连续三天,每天以20微克/千克体重/分钟的剂量给恒河猴输注去甲肾上腺素(NA),诱导出心肌病实验模型。分别在两小时(急性期)、四十八小时(亚急性期)和二十一天(慢性期)后处死动物。急性期可见琥珀酸脱氢酶局灶性缺失、三磷酸腺苷酶、酸性磷酸酶增加以及心肌中出现大量脂肪滴。组织病理学检查显示,两心室肌纤维局灶性水肿、浑浊及品红出血。急性期的显著特征为肌原纤维变性、肌细胞溶解和空泡化以及淋巴单核细胞聚集。在亚急性期和慢性期,这些特征变得不那么突出,而成纤维细胞增殖的修复性改变更为明显。到第21天,不规则的局灶性瘢痕取代了坏死的心肌。超微结构上,心肌显示肌原纤维紊乱、Z带和A带扭曲、肌浆网扩张以及线粒体肿胀和破裂。心肌细胞内存在辣根过氧化物酶反应产物,证明膜通透性改变。然而,在修复期,肌细胞溶解变化消退,胶原沉积成为突出特征。这项实验研究具有一些模拟无冠状动脉闭塞的人类心肌梗死病例的组织学特征。

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