Berger J R, Busto R, Ginsberg M D
Stroke. 1984 Nov-Dec;15(6):1029-32. doi: 10.1161/01.str.15.6.1029.
The potential efficacy of the calcium channel blocker verapamil in modifying ischemic brain injury was evaluated in anesthetized rats subjected to 60 or 90 min of diffuse forebrain ischemia produced by bilateral occlusion of the carotid and vertebral arteries. Treated animals received verapamil, 2 mg/kg intravenously, prior to ischemia. Four hours of postischemic recirculation was permitted by reversing the carotid occlusions. Intermittent high-voltage slow-wave activity was noted on electroencephalograms shortly after verapamil infusion, prior to ischemia. The ischemic insult induced an isoelectric EEG, which tended to persist during recirculation in both treated and untreated animals. Similarly, verapamil pretreatment failed to influence brain water content or cerebral energy metabolites (phosphocreatine, ATP, ADP, AMP) or cerebral energy charge when assayed after four hours of recirculation. Thus, verapamil failed to confer a protective effect on brain electrical activity, water content, or energy metabolites following ischemia in this model.
在通过双侧颈总动脉和椎动脉闭塞产生60或90分钟弥漫性前脑缺血的麻醉大鼠中，评估了钙通道阻滞剂维拉帕米改善缺血性脑损伤的潜在疗效。治疗组动物在缺血前静脉注射2mg/kg维拉帕米。通过解除颈动脉闭塞实现4小时的缺血后再灌注。在缺血前静脉注射维拉帕米后不久，脑电图上记录到间歇性高压慢波活动。缺血性损伤导致脑电图呈等电位，在再灌注期间，治疗组和未治疗组动物的脑电图均倾向于持续保持等电位。同样，在再灌注4小时后检测时，维拉帕米预处理未能影响脑含水量、脑能量代谢物（磷酸肌酸、三磷酸腺苷、二磷酸腺苷、单磷酸腺苷）或脑能荷。因此，在该模型中，维拉帕米未能对缺血后的脑电活动、含水量或能量代谢物产生保护作用。
