SHORT-TERM STIMULATION BY PROPRANOLOL AND VERAPAMIL OF CARDIAC CELLULAR AUTOPHAGY
SHORT-TERM STIMULATION BY PROPRANOLOL AND VERAPAMIL OF CARDIAC CELLULAR AUTOPHAGY
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DOI：
10.1016/s0022-2828(87)80527-8
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发表时间：
1987-12-01
影响因子：
5
通讯作者：
PFEIFER, U
中科院分区：
文献类型：
--
作者：
BAHRO, M;PFEIFER, U
本文研究了普萘洛尔和维拉帕米这两种药理作用不同的强心药对大鼠左心室心肌细胞自噬的影响。在第一个实验系列中，对10只动物皮下给予普萘洛尔（3 mg/kg体重）。10个对照组接受生理盐水。在第二个系列中，8只动物皮下注射维拉帕米（9 mg/kg体重），8只对照动物注射生理盐水。第一组注射后2 ~ 4 h，第二组注射后1 3/4 ~ 3 h，经腹主动脉用多聚甲醛-戊二醛混合物进行逆行灌注固定。从左前壁心肌组织进行电子显微镜处理，并进行形态计量学评价的体积分数和自噬空泡（AV）的早期阶段的数密度。普萘洛尔和维拉帕米分别使AV容积分数增加4.3倍和2.7倍。两种药物增加了数密度，尽管程度较小（分别为2.3倍和1.7倍）。由于维拉帕米既不影响β-肾上腺素受体，也不影响第二信使cAMP的细胞内水平，刺激细胞自噬的唯一共同点似乎是两种药物的心脏抑制作用。这些数据表明，细胞自噬的增加是心肌质量适应降低工作负荷的早期调节步骤。
The influence of propranolol and verapamil, i.e. two cardiodepressant drugs differing in their pharmacological actions, on cellular autophagy in the left ventricular myocardium of the rat was investigated. In the first experimental series 10 animals were given propranolol subcutaneously (3 mg/kg weight). Ten controls received physiological saline. In the second series 8 animals were treated with verapamil subcutaneously (9 mg/kg body weight) and 8 controls with physiological saline. Two to 4 h after the injections in the first series and 1 3/4 to 3 h in the second series retrograde perfusion fixation was carried out via the abdominal aorta with a paraformaldehyde-glutaraldehyde mixture. Myocardial tissue from the left anterior wall was processed for electron microscopy and was morphometrically evaluated for volume fraction and numerical density of early stages of autophagic vacuoles (AVs). Propranolol and verapamil significantly increased the AV volume fraction 4.3- and 2.7-fold, respectively. The numerical density was increased by the two drugs, although to a lesser degree (2.3-fold, and 1.7-fold, respectively). As verapamil afflects neither the beta-adrenoreceptors nor the intracellular levels of the second messenger cAMP, the only common denominator for the stimulation of cellular autophagy seems to be the cardiodepressive effect of the two drugs. The data suggest that the rise in cellular autophagy is an early regulatory step in the adaptation of heart muscle mass to reduced work load.