Nagano M, Kato M, Nagai M, Yang J
Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan.
Basic Res Cardiol. 1991;86 Suppl 3:187-95. doi: 10.1007/978-3-662-30769-4_18.
Attempts at treating idiopathic cardiomyopathy have been made both clinically and experimentally using the cardiomyopathic Syrian hamster. In recent years, the angiotensin converting enzyme (ACE) inhibitor has attracted considerable attention as an agent to treat heart failure. We administered the ACE inhibitor captopril to the cardiomyopathic hamster. In this study, 15 mg/kg body weight of captopril was administered to the cardiomyopathic hamster J2N at 5 weeks of age for 10 weeks; age matched J2N hamsters were used as non-treated control animals. At the end of captopril administration, blood was collected from the ventral aorta. Serum malondialdehyde (MDA), serum CPK, aldolase and LDH were determined, and myosin isoenzyme patterns of the extirpated myocardium were compared. Additionally, ECGs were compared and the fibrotic ratio of both ventricles determined. Serum MDA, CPK, and aldolase increased significantly in the cardiomyopathic hamster, whereas these indices were significantly inhibited in the hamster treated with captopril. The pathological ECG findings and the ventricular V3 predominant myosin isoenzyme patterns of the J2N were also much improved in the captopril group. However, the improvement in these parameters by enalapril administration was less than that seen with captopril. These results suggested that the effect of captopril is not only due to decrease of the angiotensin II level, but also due to increase in tissue kinin and vasodilatory prostaglandin which play an important role in the beneficial effect of captopril.
临床上和实验中都已尝试使用患心肌病的叙利亚仓鼠来治疗特发性心肌病。近年来，血管紧张素转换酶（ACE）抑制剂作为一种治疗心力衰竭的药物引起了广泛关注。我们给患心肌病的仓鼠施用了ACE抑制剂卡托普利。在本研究中，对5周龄的患心肌病的J2N仓鼠施用15mg/kg体重的卡托普利，持续10周；将年龄匹配的J2N仓鼠用作未治疗的对照动物。在卡托普利给药结束时，从腹主动脉采集血液。测定血清丙二醛（MDA）、血清肌酸磷酸激酶（CPK）、醛缩酶和乳酸脱氢酶（LDH），并比较摘除心肌的肌球蛋白同工酶模式。此外，比较心电图并确定两个心室的纤维化比率。患心肌病的仓鼠血清MDA、CPK和醛缩酶显著升高，而在用卡托普利治疗的仓鼠中这些指标受到显著抑制。卡托普利组J2N的病理性心电图表现和心室V3为主的肌球蛋白同工酶模式也有很大改善。然而，依那普利给药对这些参数的改善小于卡托普利。这些结果表明，卡托普利的作用不仅归因于血管紧张素II水平的降低，还归因于组织激肽和血管舒张性前列腺素的增加，它们在卡托普利的有益作用中起重要作用。
