Bora P S, Srivastava L M, Bhatt S D
Indian J Exp Biol. 1989 Jul;27(7):615-20.
The effects of a beta-blocker, propranolol, on the enzyme and isoenzyme activities in the heart muscle in vitro and concomitant histopathology of the component cells of the islets of Langerhans were studied in the Wistar rats after treatment with streptozotocin and isoproterenol. The biochemical data indicated that the isoproterenol induced myocardial infarction (MI) precipitates an acute diabetic response in the rat heart. The superimposition of MI in diabetes mellitus caused significant inhibition of phosphofructokinase and hexokinase in the heart muscle. The lactate dehydrogenase depicted shifting of H-type to M-type in diabetes with or without MI. The drugs, when administered in combination, brought distinctive histopathological changes in beta-cells of the pancreatic islets including degranulation, hyalinosis and a near-total destruction; however A and D cells remained more or less unaffected. The effect of propranolol in diabetes mellitus was uncertain but in MI with or without prior diabetes, the drug inversely altered the activities of all the cardiac enzymes, besides stimulating a mild recuperation of the cells of the endocrine parenchyma.
在用链脲佐菌素和异丙肾上腺素处理后的Wistar大鼠中，研究了β受体阻滞剂普萘洛尔对体外心肌中酶和同工酶活性以及胰岛组成细胞伴随的组织病理学的影响。生化数据表明，异丙肾上腺素诱导的心肌梗死（MI）在大鼠心脏中引发急性糖尿病反应。糖尿病合并心肌梗死导致心肌中磷酸果糖激酶和己糖激酶受到显著抑制。乳酸脱氢酶显示，无论有无心肌梗死，糖尿病患者的H型向M型转变。联合使用这些药物时，胰岛β细胞出现了包括脱颗粒、玻璃样变性和几乎完全破坏在内的明显组织病理学变化；然而，A细胞和D细胞或多或少未受影响。普萘洛尔在糖尿病中的作用尚不确定，但在有或无糖尿病史的心肌梗死中，该药物除了刺激内分泌实质细胞有轻度恢复外，还反向改变了所有心脏酶的活性。
