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链脲佐菌素诱导的糖尿病大鼠的心肌机械和肌球蛋白同工酶改变

Myocardial mechanical and myosin isoenzyme alterations in streptozotocin-diabetic rats.

作者信息

Takeda N, Nakamura I, Hatanaka T, Ohkubo T, Nagano M

机构信息

Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan.

出版信息

Jpn Heart J. 1988 Jul;29(4):455-63. doi: 10.1536/ihj.29.455.

Abstract

Fifteen week old male Wistar rats (n = 7) were made diabetic by intravenous injection of streptozotocin (50 mg/kg). Age-matched, untreated male Wistar rats (n = 9) served as controls. Hearts were removed after 5-6 weeks of diabetes, and the isometric developed tension (T) of isolated left ventricular papillary muscles and its first derivative (dT/dt) were measured at a frequency of 0.2 Hz. During testing, the muscles were perfused with Tyrode's solution (Ca2+ concentration was half of normal Tyrode's solution, pH 7.4, 32 degrees C, bubbled with 95% O2 and 5% CO2). In addition, the left ventricular isoenzyme pattern, which is related to myocardial energetics, was determined by pyrophosphate gel electrophoresis. There was no significant difference in isometric developed tension between diabetic and control rats (DM: 2.90 +/- 0.89 vs controls: 2.87 +/- 0.85 g/mm2, mean +/- SD), but in diabetic rats, dT/dtmax decreased significantly as compared with controls (DM: 23.5 +/- 4.2 vs controls: 31.9 +/- 7.9 g/mm2.s, p less than 0.05). Myocardial mechanical responses to isoproterenol (10(-7)M) and dibutyryl cyclic AMP (10(-5)M) also decreased in diabetic rats. The left ventricular myosin isoenzyme pattern shifted toward VM-3 in diabetic rats (VM-3: DM: 74.9 +/- 10.7 vs controls: 9.5 +/- 4.1%, p less than 0.001). These results indicate that diabetes influences myocardial contractility and changes cardiac energetics. Post-receptor processes may play a role in myocardial mechanical responses to catecholamines in streptozotocin-diabetic rats.

摘要

15周龄雄性Wistar大鼠(n = 7)通过静脉注射链脲佐菌素(50 mg/kg)诱导糖尿病。年龄匹配的未处理雄性Wistar大鼠(n = 9)作为对照。糖尿病5 - 6周后取出心脏,以0.2 Hz频率测量离体左心室乳头肌的等长收缩张力(T)及其一阶导数(dT/dt)。测试期间,肌肉用台氏液灌注(Ca2+浓度为正常台氏液的一半,pH 7.4,32℃,用95% O2和5% CO2鼓泡)。此外,通过焦磷酸凝胶电泳测定与心肌能量代谢相关的左心室同工酶模式。糖尿病大鼠和对照大鼠之间等长收缩张力无显著差异(糖尿病组:2.90±0.89 vs对照组:2.87±0.85 g/mm2,平均值±标准差),但糖尿病大鼠中,dT/dtmax与对照组相比显著降低(糖尿病组:23.5±4.2 vs对照组:31.9±7.9 g/mm2.s,p < 0.05)。糖尿病大鼠对异丙肾上腺素(10(-7)M)和二丁酰环磷腺苷(10(-5)M)的心肌机械反应也降低。糖尿病大鼠左心室肌球蛋白同工酶模式向VM - 3转变(VM - 3:糖尿病组:74.9±10.7 vs对照组:9.5±4.1%,p < 0.001)。这些结果表明糖尿病影响心肌收缩力并改变心脏能量代谢。受体后过程可能在链脲佐菌素诱导糖尿病大鼠对儿茶酚胺的心肌机械反应中起作用。

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