Kodama M, Hanawa H, Saeki M, Hosono H, Inomata T, Suzuki K, Shibata A
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Circ Res. 1994 Aug;75(2):278-84. doi: 10.1161/01.res.75.2.278.
One of the possible causes of dilated cardiomyopathy is considered to be a sequel to myocarditis. Two mechanisms have been proposed in the process of progression of myocarditis into dilated cardiomyopathy: one is a persistent viral infection, and the other is an autoimmune myocardial injury. To clarify the possible part played by the autoimmune mechanism in the process, using an animal model, we investigated whether autoimmune myocarditis, exclusively not related to viral infection, might develop into dilated cardiomyopathy. Experimental autoimmune myocarditis was elicited in Lewis rats by immunization with cardiac myosin fraction. Rats of the control group were immunized with ovalbumin. The clinical course was observed over 4 months. Six rats from the myosin-immunized group died during the acute phase and the healing phase, and all those rats had severe myocarditis. All rats that survived until the end of the study showed enlarged and discolored hearts. Aneurysmal changes were observed in the right ventricle during thoracotomy. The ratio of heart weight to body weight of the myosin-immunized group was significantly higher than that of the control group (3.36 +/- 0.49 versus 2.69 +/- 0.06 g/kg, respectively; P < .005). The lengths of the anterior interventricular fissure and the posterior interventricular fissure of the hearts of the myosin-immunized group were significantly longer than those of the control group. The external diameter of the left ventricle of the myosin-immunized group was also significantly larger than that of the control group. Diffuse myocardial muscle loss and replacement fibrosis were the prominent histological findings of the rats of the myosin-immunized group.(ABSTRACT TRUNCATED AT 250 WORDS)
扩张型心肌病的可能病因之一被认为是心肌炎的后遗症。在心肌炎进展为扩张型心肌病的过程中，已提出两种机制：一种是持续性病毒感染，另一种是自身免疫性心肌损伤。为了阐明自身免疫机制在这一过程中可能发挥的作用，我们使用动物模型研究了与病毒感染无关的自身免疫性心肌炎是否会发展为扩张型心肌病。通过用心肌肌球蛋白组分免疫Lewis大鼠诱发实验性自身免疫性心肌炎。对照组大鼠用卵清蛋白免疫。观察4个月的临床过程。肌球蛋白免疫组的6只大鼠在急性期和愈合期死亡，所有这些大鼠都有严重的心肌炎。所有存活至研究结束的大鼠心脏均增大且颜色改变。开胸时在右心室观察到动脉瘤样改变。肌球蛋白免疫组的心脏重量与体重之比显著高于对照组（分别为3.36±0.49与2.69±0.06 g/kg；P<0.005）。肌球蛋白免疫组心脏的前室间沟和后室间沟长度显著长于对照组。肌球蛋白免疫组左心室的外径也显著大于对照组。弥漫性心肌肌肉丢失和替代性纤维化是肌球蛋白免疫组大鼠突出的组织学表现。（摘要截短至250字）
