Iwai T, Takeda N, Tuchiya M, Arino T, Tanamura A, Nagano M
Department of Internal Medicine, Aoto Hospital, Jikei University School of Medicine, Tokyo, Japan.
Mol Cell Biochem. 1992 Dec 2;118(1):99-103. doi: 10.1007/BF00249699.
The effects of regression of cardiac hypertrophy on myocardial contractility and ventricular myosin isoenzymes were investigated in rats with renovascular hypertension. Six-week-old male Wistar rats were made hypertensive by constriction of one renal artery with a silver clip. Regression of cardiac hypertrophy was induced following the lowering of blood pressure by nephrectomy on the affected side 5-6 weeks after constriction of the renal artery and was maintained for 5-6 weeks. In contrast, myocardial hypertrophy was induced by 10-11 weeks of the hypertensive state. Isometric developed tension of isolated left ventricular papillary muscles was measured, while they were being perfused with Tyrode solution. Left ventricular myosin isoenzymes were separated by pyrophosphate gel electrophoresis. The ventricular to body weight ratio of the nephrectomized group was significantly lower than that of the hypertensive group, although it was greater than that of age-matched normal control rats. There were no significant differences in the isometric developed tension among three groups, the nephrectomized, hypertensive, and normal control rats. However, dT/dtmax tended to decrease in the hypertensive rats and recovered to normal in the nephrectomized rats. The left ventricular myosin isoenzyme pattern was shifted toward VM-3 in hypertensive rats and was shifted back toward VM-1 again in nephrectomized rats.
在肾血管性高血压大鼠中研究了心肌肥厚消退对心肌收缩力和心室肌球蛋白同工酶的影响。六周龄雄性Wistar大鼠通过用银夹夹闭一侧肾动脉使其患高血压。在肾动脉夹闭后5 - 6周，通过切除患侧肾脏降低血压来诱导心肌肥厚消退，并持续5 - 6周。相比之下，心肌肥厚是由10 - 11周的高血压状态诱导产生的。在使用台氏液灌注离体左心室乳头肌时，测量其等长收缩张力。通过焦磷酸凝胶电泳分离左心室肌球蛋白同工酶。肾切除组的心室与体重比显著低于高血压组，尽管高于年龄匹配的正常对照大鼠。肾切除组、高血压组和正常对照组三组之间的等长收缩张力没有显著差异。然而，高血压大鼠的dT/dtmax趋于降低，而在肾切除大鼠中恢复正常。高血压大鼠左心室肌球蛋白同工酶模式向VM - 3偏移，而在肾切除大鼠中又再次向VM - 1偏移。
