Jackson C V, Mitsos S E, Simpson P J, Driscoll E M, Lucchesi B R
Pharmacology. 1985;30(6):320-32. doi: 10.1159/000138086.
The effectiveness of the calcium entry blocker bepridil in protecting the myocardium from ischemic injury, was assessed in a canine model of regional ischemia and in a feline model of global ischemia. Bepridil administration (5 mg/kg or 15 mg/kg/24 h intravenously) did not reduce ultimate infarct size as assessed in anesthetized, open-chest dogs subjected to 90 min of occlusion of the left circumflex coronary artery and 24 h of reperfusion. Bepridil (5 mg/kg administered intravenously to a blood donor cat) did not provide any protection of the isolated blood-perfused cat heart from 90 min of normothermic global ischemia and 60 min of reperfusion. Treatment of the perfused cat heart with bepridil did not prevent tissue accumulation of calcium or loss of tissue potassium and ATP. Bepridil, however, significantly reduced reperfusion tachyarrhythmias in the dog model for assessing ultimate infarct size and prevented reperfusion-induced ventricular fibrillation of the cat isolated heart. These results indicate that the calcium entry blocker, bepridil, as assessed in the models employed, does not protect the myocardium from ischemic reperfusion injury. However, it does prevent reperfusion-induced tachyarrhythmias and ventricular fibrillation.
在犬局部缺血模型和猫全心缺血模型中评估了钙通道阻滞剂苄普地尔对心肌缺血性损伤的保护作用。在接受左旋冠状动脉闭塞90分钟和再灌注24小时的麻醉开胸犬中，静脉注射苄普地尔（5毫克/千克或15毫克/千克/24小时）并未减少最终梗死面积。苄普地尔（5毫克/千克静脉注射给供血猫）对离体血液灌注的猫心脏在90分钟常温全心缺血和60分钟再灌注过程中未提供任何保护。用苄普地尔处理灌注的猫心脏并不能防止钙在组织中的蓄积或组织钾和ATP的丢失。然而，在评估最终梗死面积的犬模型中，苄普地尔显著减少了再灌注性心律失常，并防止了猫离体心脏的再灌注诱导的心室颤动。这些结果表明，在所采用的模型中评估的钙通道阻滞剂苄普地尔并不能保护心肌免受缺血再灌注损伤。然而，它确实能预防再灌注诱导的心律失常和心室颤动。
