Capasso J M, Li P, Zhang X, Meggs L G, Anversa P
Department of Medicine, New York Medical College, Valhalla, New York 10595.
Am J Physiol. 1993 Jun;264(6 Pt 2):H2056-67. doi: 10.1152/ajpheart.1993.264.6.H2056.
To determine the effects of coronary arterial occlusion on the contractile response of the heart to angiotensin II (ANG II) administration, large infarcts were surgically induced in Sprague-Dawley rats at 2 mo of age. Forty-eight hours later, hearts from experimental animals presented a hemodynamic profile indicative of left ventricular failure and right ventricular dysfunction and revealed a loss of mass of 49.3 +/- 10.8% of the left ventricle inclusive of the interventricular septum. Plasma renin activity was found to be decreased by 48% in animals with occlusion of the left main coronary artery. Left and right posterior papillary muscles removed from these same hearts were evaluated mechanically in the presence and absence of ANG II. Contractile performance was impaired in left ventricular myocardium from infarcted rats as evidenced by the inability to attain developed tension similar to that seen in control rats. In addition, peak rates of tension rise and decay were significantly depressed. A reduction in contraction duration was also found in experimental animals, limiting the active state of the myocardium. ANG II resulted in a depression in the force-generating ability of left and right papillary muscles of control and experimental animals. Importantly, the negative inotropic effect of ANG II affected the left and right myocardium from infarcted rats by nearly twofold and threefold more than the corresponding muscles from controls. Morphometric evaluation revealed the absence of damage in both papillary muscles from control hearts and in the right muscles from experimental animals. However, necrotic tissue comprised 28.3 +/- 9.8% of left papillary muscles obtained from infarcted ventricles. It is concluded that ANG II administration resulted in reduced mechanical performance of rat myocardium. Coronary arterial ligation potentiated this phenomenon, and such a negative effect may have implication in infarction induced heart failure in vivo.
为了确定冠状动脉闭塞对心脏对血管紧张素II（ANG II）给药的收缩反应的影响，在2月龄的Sprague-Dawley大鼠中通过手术诱导大面积梗死。48小时后，实验动物的心脏呈现出左心室衰竭和右心室功能障碍的血流动力学特征，并且显示左心室（包括室间隔）质量损失49.3±10.8%。发现左主冠状动脉闭塞的动物血浆肾素活性降低了48%。从这些相同心脏中取出的左、右后乳头肌在有和没有ANG II的情况下进行机械评估。梗死大鼠左心室心肌的收缩性能受损，这表现为无法达到与对照大鼠相似的舒张期张力。此外，张力上升和下降的峰值速率显著降低。在实验动物中还发现收缩持续时间缩短，限制了心肌的活动状态。ANG II导致对照动物和实验动物的左、右乳头肌产生力的能力降低。重要的是，ANG II的负性肌力作用对梗死大鼠的左、右心肌的影响比对对照相应肌肉的影响分别高出近两倍和三倍。形态计量学评估显示对照心脏的两个乳头肌以及实验动物的右肌肉均未受损。然而，从梗死心室获得的左乳头肌中坏死组织占28.3±9.8%。得出的结论是，给予ANG II会导致大鼠心肌机械性能降低。冠状动脉结扎会增强这种现象，并且这种负面影响可能对体内梗死诱导的心力衰竭有影响。
