Bernard M, Menasché P, Fontanarava E, Canioni P, Grousset C, Piwnica A, Cozzone P
Clin Chim Acta. 1985 Oct 31;152(1-2):43-53. doi: 10.1016/0009-8981(85)90174-3.
The ability of nifedipine to enhance myocardial protection was assessed on isolated perfused rat hearts subjected to 180 min of hypothermic (20 degrees C), global ischemia, followed by 45 min of normothermic reperfusion. Intracellular pH, ATP, Pi and phosphocreatine content were serially measured at 4 min intervals by phosphorus-31 nuclear magnetic resonance spectroscopy and correlated with simultaneously recorded hemodynamic parameters. Addition of nifedipine (0.075 mumol/l and 0.5 mumol/l) to Saint Thomas' cardioplegic solution reduced Pi accumulation during ischemic arrest and increased phosphocreatine levels during reperfusion. Post-ischemic functional recovery was not improved at a drug concentration of 0.075 mumol/l and was depressed at 0.5 mumol/l. These results clearly show that the presence of nifedipine in Saint Thomas' cardioplegic solution does not provide significant additional myocardial protection under hypothermic conditions.
在经历180分钟低温（20摄氏度）全心缺血、随后45分钟常温再灌注的离体灌注大鼠心脏上，评估硝苯地平增强心肌保护的能力。通过磷-31核磁共振波谱法每隔4分钟连续测量细胞内pH值、三磷酸腺苷（ATP）、无机磷（Pi）和磷酸肌酸含量，并与同时记录的血流动力学参数相关联。向圣托马斯心脏停搏液中添加硝苯地平（0.075微摩尔/升和0.5微摩尔/升）可减少缺血停搏期间Pi的积累，并增加再灌注期间磷酸肌酸水平。药物浓度为0.075微摩尔/升时，缺血后功能恢复未得到改善，而在0.5微摩尔/升时则受到抑制。这些结果清楚地表明，在低温条件下，圣托马斯心脏停搏液中存在硝苯地平并不能提供显著的额外心肌保护。
