Koyama S, Kodama M, Izumi T, Shibata A
Division of Cardiology, Tachikawa General Hospital, Nagaoka, Japan.
Cardiovasc Drugs Ther. 1995 Oct;9(5):701-7. doi: 10.1007/BF00878553.
The most important clinical manifestation of myocarditis is congestive heart failure. The precise mechanisms of heart failure during myocarditis have not been elucidated because no animal model that would permit in vivo study of hemodynamics in severe active myocarditis has been available. We monitored hemodynamics and left ventricular function in a rat model of experimental autoimmune myocarditis to determine if this model could be useful for the study of in vivo hemodynamics in severe active myocarditis. Lewis rats were immunized with human cardiac myosin suspended in complete Freund's adjuvant. Baseline hemodynamics were measured using an ultraminiature catheter pressure transducer via the right internal carotid artery, 4 weeks after immunization in one group of rats (acute phase) and 3 months after immunization in another group (chronic phase). Untreated rats served as the control group. Hemodynamic measurements were also obtained after infusion of dobutamine in the acute-phase and chronic-phase groups. The heart weight-to-body weight ratios were significantly higher in both the acute-phase group and the chronic-phase group compared with normal control rats. The baseline left ventricular systolic pressure was significantly lower in the chronic phase group than in the control group. Peak dP/dt and peak -dP/dt were significantly lower in both the acute-phase group and the chronic-phase group compared with the control group. Dobutamine significantly increased left ventricular systolic pressure, peak dP/dt, and peak -dP/dt in the chronic-phase group but caused only minor changes in hemodynamic variables in the acute-phase group. In vivo measurements of hemodynamic variables indicated the presence of left ventricular dysfunction in rats with experimental autoimmune myocarditis. This animal model may be useful for the study of both acute heart failure related to acute myocarditis and chronic heart failure due to diffuse myocardial fibrosis.
心肌炎最重要的临床表现是充血性心力衰竭。由于尚无能够在体内研究严重活动性心肌炎血流动力学的动物模型，因此心肌炎期间心力衰竭的确切机制尚未阐明。我们监测了实验性自身免疫性心肌炎大鼠模型的血流动力学和左心室功能，以确定该模型是否可用于研究严重活动性心肌炎的体内血流动力学。将Lewis大鼠用悬浮于完全弗氏佐剂中的人心脏肌球蛋白进行免疫。一组大鼠在免疫后4周（急性期）和另一组大鼠在免疫后3个月（慢性期），通过右颈内动脉使用超小型导管压力传感器测量基线血流动力学。未治疗的大鼠作为对照组。在急性期和慢性期组中输注多巴酚丁胺后也获得了血流动力学测量值。与正常对照大鼠相比，急性期组和慢性期组的心脏重量与体重之比均显著更高。慢性期组的基线左心室收缩压显著低于对照组。与对照组相比，急性期组和慢性期组的dP/dt峰值和 -dP/dt峰值均显著更低。多巴酚丁胺显著增加了慢性期组的左心室收缩压、dP/dt峰值和 -dP/dt峰值，但在急性期组中仅引起血流动力学变量的微小变化。体内血流动力学变量测量表明实验性自身免疫性心肌炎大鼠存在左心室功能障碍。该动物模型可能有助于研究与急性心肌炎相关的急性心力衰竭以及由弥漫性心肌纤维化引起的慢性心力衰竭。
