Ouriel K, Ginsburg M E, Patti C S, Pearce F J, Hicks G L
J Surg Res. 1987 Aug;43(2):164-71. doi: 10.1016/0022-4804(87)90160-0.
Calcium channel blockers have been advocated as agents which enhance myocardial protection during ischemia and reperfusion. Unfortunately, while cellular integrity is preserved, myocardial function is depressed as a result of the negative inotropic effects of these agents. In order to assess the efficacy of verapamil cardioplegia, 25 isolated perfused rabbit hearts were studied. A model of normothermic ischemic arrest was utilized, employing either verapamil-free crystalloid cardioplegia or cardioplegia containing verapamil in concentrations of 0.5, 1.0, or 5.0 mg/liter. All three verapamil-treated groups demonstrated increased postischemic left ventricular developed pressure and improved postischemic compliance when compared with the untreated group (P less than 0.05). However, myocardial function was significantly depressed at 15 min of reperfusion in the 1.0 and 5.0 mg/liter verapamil-treated groups when compared with the 0.5 ml/liter group (P less than 0.05). These data suggest that the addition of verapamil to crystalloid cardioplegia results in enhanced myocardial function while minimizing the early reperfusion depression associated with higher dose therapy.
钙通道阻滞剂已被推荐作为在缺血和再灌注期间增强心肌保护的药物。不幸的是,虽然细胞完整性得以保留,但由于这些药物的负性肌力作用,心肌功能受到抑制。为了评估维拉帕米心脏停搏液的疗效,对25个离体灌注兔心脏进行了研究。采用常温缺血性停搏模型,使用不含维拉帕米的晶体心脏停搏液或含有浓度为0.5、1.0或5.0毫克/升维拉帕米的心脏停搏液。与未治疗组相比,所有三个维拉帕米治疗组在缺血后左心室舒张末压均升高,缺血后顺应性改善(P小于0.05)。然而,与0.5毫克/升组相比,1.0和5.0毫克/升维拉帕米治疗组在再灌注15分钟时心肌功能明显受抑制(P小于0.05)。这些数据表明,在晶体心脏停搏液中添加维拉帕米可增强心肌功能,同时将与高剂量治疗相关的早期再灌注抑制降至最低。