Pathogenesis of myocardial injury in myocarditis and cardiomyopathy.
Pathogenesis of myocardial injury in myocarditis and cardiomyopathy.
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心肌炎和心肌病中心肌损伤的发病机制。
DOI：
10.1253/jcj.55.1132
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
C. Kawai
中科院分区：
文献类型：
--
作者：
A. Matsumori;I. Okada;T. Yamada;S. Maruyama;C. Kawai
研究了心肌炎和心肌病中心肌细胞损伤的发病机制。使用 5' 端序列的 32P 标记 cDNA 探针，通过 Northern 印迹分析研究了实验性柯萨奇病毒 B3 心肌炎中小鼠心脏中病毒基因组的存在。阳性放射自显影图的最强信号始终位于约 7.4 kb，对应于病毒完整基因组的大小。连续感染柯萨奇病毒和脑心肌炎（EMC）病毒感染，同时出现急性心肌炎和已治愈的心肌炎，结果提示连续病毒感染会造成额外的心肌损伤，并出现类似于慢性心肌炎或扩张型心肌病的病变。 EMC病毒感染期间诱导的抗心脏自身抗体主要与肌球蛋白反应。部分心肌病患者中Indium-111抗肌球蛋白闪烁显像呈阳性，且其摄取量与左心室功能呈负相关。当小鼠注射抗肌球蛋白抗体时，在EMC病毒性心肌炎慢性期的心脏中、纤维化和钙化周围的肌细胞中检测到小鼠免疫球蛋白G，表明抗肌球蛋白抗体沉积。尽管需要进一步研究来阐明心肌病中抗肌球蛋白的摄取机制，但抗肌球蛋白抗体可能在持续变性和坏死的存活肌细胞中积聚。
The pathogenesis of myocardial cell injury in myocarditis and cardiomyopathy was investigated. The presence of viral genomes in the murine heart in experimental coxsackievirus B3 myocarditis was studied by Northern blotting analysis using a 32P-labeled cDNA probe from the 5' end sequence. The strongest signal of positive autoradiograms was always at about 7.4 kilobases, corresponding to the size of the complete genome of the virus. Successive infections with coxsackievirus and encephalomyocarditis (EMC) virus infection showed simultaneous acute myocarditis and healed myocarditis, and the results suggest that successive virus infections cause additional myocardial damage, and develop lesions similar to chronic myocarditis or dilated cardiomyopathy. Anti-heart auto-antibody, induced during EMC virus infection, reacted predominantly with myosin. Indium-111 antimyosin scintigraphy showed positive in some of the patients with cardiomyopathy, and the uptake was inversely correlated with left ventricular function. When mice were injected with antimyosin antibody, mouse immunoglobulin G was detected in hearts in the chronic stage of EMC virus myocarditis, in myocytes surrounding fibrosis and calcification, suggesting deposition of antimyosin antibody. Although further study is necessary to clarify the mechanism of uptake of antimyosin in cardiomyopathy, antimyosin antibody may accumulate in viable myocytes with ongoing degeneration as well as in necrosis.