CATECHOLAMINE-INDUCED CARDIOMYOPATHY IN MULTIPLE ENDOCRINE NEOPLASIA - A HISTOLOGIC, ULTRASTRUCTURAL, AND BIOCHEMICAL-STUDY
CATECHOLAMINE-INDUCED CARDIOMYOPATHY IN MULTIPLE ENDOCRINE NEOPLASIA - A HISTOLOGIC, ULTRASTRUCTURAL, AND BIOCHEMICAL-STUDY
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DOI：
10.1378/chest.99.2.382
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发表时间：
1991-02-01
期刊：
影响因子：
9.6
通讯作者：
RUSSO, MA
中科院分区：
文献类型：
--
作者：
FRUSTACI, A;LOPERFIDO, F;RUSSO, MA
儿茶酚胺诱导的扩张性心肌病报告了一例多发性内分泌瘤，3型。对心脏活检样本进行了组织学和超微结构研究，并测定了心肌钙++和细胞膜脂肪酸。心肌细胞收缩带坏死伴肌节过度收缩进展为肌纤维溶解，心肌ca++水平升高分别为形态学和生化异常。在这项研究中，没有发现细胞膜脂质过氧化或α -肾上腺素能介导的冠状动脉供应减少。我们指出，受体介导的细胞内钙离子超载是导致心肌损害的主要异常。
A catecholamine-induced dilated cardiomyopathy is reported in a patient with multiple endocrine neoplasia, type 3. A histologic and ultrastructural study has been undertaken in cardiac biopsy samples, together with determination of myocardial Ca++ and cellular membrane fatty acids. Contraction band necrosis of cardiocytes with supercontraction of sarcomeres progressing to myofibrolysis and increased levels of myocardial Ca++ have been found as morphologic and biochemical abnormalities, respectively. No lipoperoxidation of cellular membranes or an alpha-adrenergic mediated reduction of coronary supply could be recognized in the study. We indicate a receptor-mediated intracellular Ca++ overload as the main abnormality responsible for myocardial impairment.