A study on the mechanism of myocardial injury in myocarditis and dilated cardiomyopathy.

人们普遍认为心肌炎可能与扩张型心肌病的发病机制有关。然而，慢性心肌炎心肌损伤的机制尚不清楚。本实验采用注射猪心肌蛋白诱导Lewis大鼠心肌炎，分别于注射后第21天和第74天收获大鼠。第21天通过原位缺口末端标记法和DNA片段凝胶电泳证实凋亡细胞死亡，但第74天未发现凋亡细胞。第21天检测心肌中Fas mRNA和蛋白的表达。部分浸润淋巴细胞中检测到Fas配体。部分大鼠注射抗fas抗体或抗fas配体抗体后，第74天心肌损伤程度较未注射大鼠减轻。上述结果提示，抑制心肌炎急性期细胞凋亡现象可能与减轻心肌炎慢性期心肌损伤有关。

It has generally been recognized that myocarditis may be implicated in the pathogenesis of dilated cardiomyopathy. However, the mechanism of myocardial damage in the chronic stage of myocarditis is still unclear. In this study myocarditis was induced in Lewis rats by injection of porcine cardiac myosin and rats were harvested on day 21 or 74 after the initial injection. Apoptotic cell death was confirmed by in situ nick end labeling assay and gel-electrophoresis for DNA fragmentation on day 21, but none was disclosed on day 74. The expression of Fas mRNA and protein was detected on day 21 in the myocardium. In addition, Fas ligand was detected in some infiltrating lymphocytes. Some rats were injected with anti-Fas antibody or anti-Fas ligand antibody, and subsequently, myocardial damage was less severe than that in untreated rats on day 74. These results suggested that inhibition of apoptotic phenomenon in the acute stage may be related to the reduction of myocardial damage in the chronic stage of myocarditis.