The hypothesis that early verapamil (VP) treatment in acute myocardial ischemia can enhance the effects of subsequent reperfusion was tested in open-chest dogs submitted to 3 h of left anterior descending artery occlusion and 2 h of reperfusion. 2. Arterial pressure and heart rate were monitored continuously. The area at risk (AR) was determined by left atrial injection of 99technetium-labeled microspheres soon after occlusion. The area of necrosis (AN) was identified histologically with triphenyl tetrazolium chloride and calculated as percent of AR. Myocardial preservation is reported as percent of AR spared from necrosis (AR-AN) x 100/AR. 3. Fourteen dogs received 0.2 mg VP, iv, 15 min after occlusion and 9 untreated dogs served as controls. Verapamil significantly reduced heart rate but did not affect blood pressure or the pressure-heart rate product. 4. Myocardial preservation was significantly greater in verapamil-treated dogs than in control animals (51 +/- 20 vs 31 +/- 19%, mean +/- SD). However, area at risk (%) in the left ventricle was not significantly different in treated and control animals (31 +/- 12 vs 32 +/- 4%). 5. These data indicate that verapamil protects the ischemic myocardium in this occlusion/reperfusion model and that the mechanism of protection is probably related to a non-hemodynamic, metabolic activity of verapamil.
摘要
在开胸犬身上进行实验,检验急性心肌缺血早期使用维拉帕米(VP)治疗能否增强后续再灌注效果。实验中使犬的左前降支动脉闭塞3小时,然后再灌注2小时。2. 持续监测动脉血压和心率。闭塞后不久通过经左心房注射99锝标记的微球来确定危险区域(AR)。用氯化三苯基四氮唑进行组织学鉴定坏死区域(AN),并计算为AR的百分比。心肌保存情况报告为未发生坏死的AR部分(AR - AN)×100/AR的百分比。3. 14只犬在闭塞后15分钟静脉注射0.2毫克VP,9只未治疗的犬作为对照。维拉帕米显著降低心率,但不影响血压或压力 - 心率乘积。4. 接受维拉帕米治疗的犬心肌保存情况显著优于对照动物(51±20 vs 31±19%,均值±标准差)。然而,治疗组和对照组动物左心室的危险区域(%)无显著差异(31±12 vs 32±4%)。5. 这些数据表明,在这种闭塞/再灌注模型中维拉帕米可保护缺血心肌,且保护机制可能与维拉帕米的非血流动力学、代谢活性有关。