Tachibana H
First Department of Surgery, Asahikawa Medical College, Japan.
Nihon Kyobu Geka Gakkai Zasshi. 1990 Apr;38(4):630-40.
This study was undertaken to assess the effect of a calcium antagonist, nicardipine (N), added in a cardioplegic solution on the ischemic myocardium. Isolated rat hearts were perfused with oxygenated Krebs Ringer Bicarbonate (KRB) solution by Langendorff's perfusion method and were subjected to 2 hours of ischemic arrest at 30 degrees C with multidose cardioplegia (every 30 min, for 5 min) and a subsequent 60 min of reperfusion. HR, LVP, coronary flow and oxygen tension of coronary effluent were monitored. Oxygen saturation of intracellular myoglobin and redox state of mitochondrial cytochrome aa3 in the myocardial cell were continuously measured throughout studies by a spectrophotometer. Oxygenated crystalloid cardioplegic solution (KRB) containing 25 mM of potassium was used. 40 rats were divided into 4 groups (10 rats each) according to the concentration of N (none, 0.5, 1 and 2 mg/L) in fully oxygenated potassium cardioplegic solution (PO2: 601 +/- 31 mmHg). The percent recovery of pressure-rate product after reperfusion was compared in each group and the optimal concentration of N was found to be 1 mg per liter of cardioplegic solution. No significant difference was found between Group Ia (N = 0 mg/L) and Group Ib (N = 1 mg/L) in metabolic or hemodynamic recovery after reperfusion. In other experiments, 40 rats in Group IIa (N = 0 mg/L, n = 20) and Group IIb (N = 1 mg/L, n = 20) received 10 ml of poorly oxygenated cardioplegic solution (PO2: 215 +/- 10 mmHg) on each reinfusion followed by a 25 min interval of ischemic arrest. The index of oxygen utilization, MVO2/pressure-rate product after reperfusion was significantly lower in Group IIb than in Group IIa (p less than 0.05). The results show that the addition of N (1 mg/L) to the cardioplegic solution preserved a more aerobic state (higher intracellular oxygen level) in the myocardium by further suppressing myocardial oxygen demand during the ischemic period which resulted in better myocardial protection. Therefore, it is concluded that the addition of N to the cardioplegic solution enhances myocardial preservation during myocardial ischemia.
本研究旨在评估添加到心脏停搏液中的钙拮抗剂尼卡地平(N)对缺血心肌的影响。采用Langendorff灌注法,用含氧的 Krebs 林格碳酸氢盐(KRB)溶液灌注离体大鼠心脏,并在30℃下进行2小时的缺血停搏,采用多剂量心脏停搏液(每30分钟,持续5分钟),随后再灌注60分钟。监测心率(HR)、左心室压(LVP)、冠状动脉血流量和冠状动脉流出液的氧张力。在整个研究过程中,用分光光度计连续测量心肌细胞内肌红蛋白的氧饱和度和线粒体细胞色素aa3的氧化还原状态。使用含25 mM钾的含氧晶体心脏停搏液(KRB)。根据完全含氧的钾心脏停搏液中N的浓度(无、0.5、1和2 mg/L),将40只大鼠分为4组(每组10只)(PO2:601±31 mmHg)。比较每组再灌注后压力-心率乘积的恢复百分比,发现心脏停搏液中N的最佳浓度为每升1 mg。在再灌注后的代谢或血流动力学恢复方面,Ia组(N = 0 mg/L)和Ib组(N = 1 mg/L)之间未发现显著差异。在其他实验中,IIa组(N = 0 mg/L,n = 20)和IIb组(N = 1 mg/L,n = 20)的40只大鼠每次再灌注时接受10 ml低氧心脏停搏液(PO2:215±10 mmHg),随后进行25分钟的缺血停搏。IIb组再灌注后的氧利用指数、MVO2/压力-心率乘积显著低于IIa组(p < 0.05)。结果表明,在心脏停搏液中添加N(1 mg/L)可通过在缺血期进一步抑制心肌需氧量,使心肌保持更有氧的状态(更高的细胞内氧水平),从而产生更好的心肌保护作用。因此,得出结论:在心脏停搏液中添加N可增强心肌缺血期间的心肌保护作用。