Brezinski M E, Darius H, Lefer A M
Arzneimittelforschung. 1986 Mar;36(3):464-6.
The ability of anipamil, a calcium channel blocker, to protect ischemic myocardial tissue was investigated in pentobarbital anesthetized cats. Two bolus injections of anipamil (1.0 mg/kg i.v.) or their vehicle (i.e., 95% ethanol) were given 30 and 150 min post-ligation of the left anterior descending coronary artery. Anipamil significantly reduced the elevated S-T segment elevation and T wave amplitude suggesting a moderating influence on cellular ischemia. The drug also significantly blunted the loss in myocardial creatine kinase activity and amino-nitrogen concentrations from ischemic myocardial tissue, compared to cats receiving only the vehicle. These changes are suggestive of a cardioprotective effect of this calcium channel blocker. Since no significant change in the pressure rate index was seen with anipamil, a decrease in myocardial oxygen demand does not appear to be the major mechanism of the cardioprotective action of the agent. Therefore, anipamil protected the heart from ischemic damage, possibly by a direct cytoprotective action.
在戊巴比妥麻醉的猫身上研究了钙通道阻滞剂阿尼帕米保护缺血心肌组织的能力。在结扎左冠状动脉前降支后30分钟和150分钟，分别静脉注射两次大剂量阿尼帕米（1.0毫克/千克）或其溶媒（即95%乙醇）。阿尼帕米显著降低了升高的S-T段抬高和T波振幅，提示对细胞缺血有缓解作用。与仅接受溶媒的猫相比，该药物还显著减轻了缺血心肌组织中肌酸激酶活性和氨基氮浓度的损失。这些变化提示该钙通道阻滞剂具有心脏保护作用。由于阿尼帕米对压力心率指数没有显著影响，心肌需氧量的降低似乎不是该药物心脏保护作用的主要机制。因此，阿尼帕米可能通过直接的细胞保护作用保护心脏免受缺血损伤。
