儿茶酚胺心肌病：发病机制的综述与分析
Catecholamine cardiomyopathy: review and analysis of pathogenetic mechanisms.
作者信息
Jiang J P, Downing S E
机构信息
Department of Pathology, Yale University School of Medicine, New Haven, CT 06510.
出版信息
Yale J Biol Med. 1990 Nov-Dec;63(6):581-91.
Abstract
Catecholamines given in high concentrations produce myocardial damage in several mammalian species. The histological changes are similar to those found in patients given large amounts of pressor agents and in those who develop pheochromocytomas. They include myofiber necrosis, myofibrillar degeneration, and mononuclear leukocytic infiltration. Cardiac function is significantly impaired. Endogenous release of catecholamines can also induce myocardial injury in rabbits infused with tyramine. Anatomic and functional abnormalities described in various models of catecholamine cardiomyopathy are summarized. The several major theories regarding pathogenesis are reviewed. Recent data suggesting that O2-derived free radical generation is involved are discussed.
摘要
高浓度给予的儿茶酚胺会在几种哺乳动物物种中造成心肌损伤。组织学变化类似于接受大量升压药的患者以及患有嗜铬细胞瘤的患者中发现的变化。这些变化包括肌纤维坏死、肌原纤维变性和单核白细胞浸润。心脏功能会受到显著损害。内源性儿茶酚胺的释放也可在输注酪胺的兔子中诱发心肌损伤。总结了儿茶酚胺心肌病各种模型中描述的解剖学和功能异常。回顾了关于发病机制的几种主要理论。讨论了近期表明涉及氧衍生自由基生成的数据。
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