Bhan R D, Giacomelli F, Wiener J
Am J Pathol. 1982 Jul;108(1):60-71.
Adrenoreceptor blockade has been used to separate the actions of elevated blood pressure, angiotensin II, and catecholamines on the coronary vasculature and myocardium of rats. Twenty-two male Wistar-Kyoto rats received phentolamine (an alpha-receptor blocker, 10 mg/kg body weight) and/or propranolol (a beta-receptor blocker, 1 mg/kg body weight) followed by an infusion for 2 hours of angiotensin amide (1.7 micrograms/min/kg) or saline. Sections of left ventricle were examined by light and electron microscopy. Blood pressure was elevated only in animals receiving angiotensin II with or without propranolol. Epicardial arteries were devoid of lesions in all animals. Small intramural arteries and arterioles in the hypertensive animals exhibited vasoconstriction, endothelial cell vacuolization with bleb formation, and medial smooth muscle cell fragmentation and necrosis. Foci of irreversible ischemic or anoxic myocardial injury consisting of contraction zones and bands and translocated mitochondria with granular matrix densities were seen in angiotensin-infused animals. Similar but less severe myocardial changes were found in the animals pretreated with propranolol. Vascular lesions were also seen in animals receiving phentolamine, propranolol, and angiotensin II; but myocardial alterations consisted solely of areas with contraction zones. Vascular but not myocardial lesions were observed in animals that received angiotensin II and phentolamine. It is concluded that angiotensin II can produce vascular injury in the absence of elevated systemic blood pressure or catecholamine effects. In contrast, irreversible myocardial injury seems to depend upon the increased pressure and/or coronary artery vasoconstriction associated with angiotensin administration.
肾上腺素能受体阻断已被用于区分血压升高、血管紧张素 II 和儿茶酚胺对大鼠冠状动脉血管系统和心肌的作用。22 只雄性 Wistar-Kyoto 大鼠接受酚妥拉明（一种 α 受体阻滞剂，10 毫克/千克体重）和/或普萘洛尔（一种 β 受体阻滞剂，1 毫克/千克体重），随后输注血管紧张素酰胺（1.7 微克/分钟/千克）或生理盐水 2 小时。通过光学显微镜和电子显微镜检查左心室切片。仅在接受血管紧张素 II 且有或无普萘洛尔的动物中血压升高。所有动物的心外膜动脉均无病变。高血压动物的小壁内动脉和小动脉表现出血管收缩、内皮细胞空泡化并形成泡状突起，以及中层平滑肌细胞破碎和坏死。在输注血管紧张素的动物中可见不可逆缺血或缺氧心肌损伤灶，由收缩带和条带以及线粒体移位伴颗粒状基质密度组成。在预先用普萘洛尔处理的动物中发现了类似但较轻的心肌变化。接受酚妥拉明、普萘洛尔和血管紧张素 II 的动物也出现血管病变；但心肌改变仅由有收缩带的区域组成。在接受血管紧张素 II 和酚妥拉明的动物中观察到血管而非心肌病变。结论是，血管紧张素 II 在无全身血压升高或儿茶酚胺作用的情况下可产生血管损伤。相比之下，不可逆心肌损伤似乎取决于与血管紧张素给药相关的压力升高和/或冠状动脉血管收缩。
