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维拉帕米对猫缺血心肌组织细胞完整性和电解质浓度的影响。

Influence of verapamil on cellular integrity and electrolyte concentrations of ischemic myocardial tissue in the cat.

作者信息

Lefer A M, Polansky E W, Bianchi C P, Narayan S

出版信息

Basic Res Cardiol. 1979 Sep-Oct;74(5):555-67. doi: 10.1007/BF01907648.

Abstract

Verapamil, at a dose of 1 mg/kg, was given intravenously to anesthetized cats one hour after coronary artery occlusion. Verapamil significantly reduced mean arterial blood pressure, but produced an increase in heart rate, partially offsetting the reduction in myocardial oxygen demand resulting from the reduction in pressure. Verapamil failed to prevent the elevations in the S-T segment of the electrocardiogram observed in cats subjected to myocardial ischemia (MI) and given only the vehicle for verapamil (i.e., 0.9% NaCl). Moreover, verapamil also did not prevent the accumulation of creatine phosphokinase (CPK) activity in the circulating blood after MI. Nevertheless, verapamil significantly prevented the loss in CPK and in amino-nitrogen observed in the ischemic region of the myocardium, indicating some protective effect on myocardial integrity. The major effects of verapamil on electrolyte content of ischemic myocardial tissue were a decrease in sodium and an increase in potassium. However, calcium gain by the heart was not prevented by verapamil. Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.

摘要

冠状动脉闭塞一小时后,给麻醉的猫静脉注射剂量为1mg/kg的维拉帕米。维拉帕米显著降低平均动脉血压,但使心率增加,部分抵消了因血压降低导致的心肌需氧量减少。维拉帕米未能阻止在遭受心肌缺血(MI)且仅给予维拉帕米溶媒(即0.9%氯化钠)的猫中观察到的心电图ST段抬高。此外,维拉帕米也未阻止MI后循环血液中肌酸磷酸激酶(CPK)活性的积累。然而,维拉帕米显著阻止了在心肌缺血区域观察到的CPK和氨基氮的损失,表明对心肌完整性有一定保护作用。维拉帕米对缺血心肌组织电解质含量的主要影响是钠减少和钾增加。然而,维拉帕米并未阻止心脏钙的增加。因此,维拉帕米对缺血心肌有一定程度的保护作用,但也产生了一些其他作用,这些作用无助于防止心肌缺血损伤的扩散。

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