Rahusen F D, van Gilst W H, Robillard G T, Dijkstra K, Wildevuur C R
Department of Cardiopulmonary Surgery, The Netherlands.
Basic Res Cardiol. 1988 Sep-Oct;83(5):540-9. doi: 10.1007/BF01906683.
The effect of captopril on energy-rich phosphates and pH during normothermic ischemic arrest, hypothermic cardioplegic arrest and subsequent reperfusion was investigated in the isolated rat heart using 31P-nuclear magnetic resonance. The hearts remained in the probe during all perfusion procedures and captopril (80 ml.l-1) treatment was started directly after cannulation. After normothermic ischemic arrest (15 min), the ATP content of captopril-treated hearts was not significantly different from that of untreated hearts (53 +/- 9% and 52 +/- 8%, respectively). Accumulation of inorganic phosphate at the end of ischemia was significantly less in treated hearts, suggesting a higher end-ischemic nucleotide content in treated hearts. Hypothermic cardioplegic arrest (St. Thomas' Hospital solution, 4 degrees C) lasted for 3 h at 10 degrees C. Adenosine triphosphate in untreated hearts was significantly lower at the end of ischemia; 36 +/- 6% compared to 53 +/- 9% for untreated hearts. Adenosine triphosphate in untreated hearts recovered to 76 +/- 9% after normothermic ischemia and to 72 +/- 7% after hypothermic ischemia at the end of 30 min reperfusion. Captopril significantly improved adenosine triphosphate recovery in both treated groups; 89 +/- 4% after normothermic and 83 +/- 4% hypothermic ischemia. We conclude that captopril has a beneficial effect on recovery of adenosine triphosphate both after normothermic and after hypothermic ischemia.
利用31P-核磁共振技术，在离体大鼠心脏中研究了卡托普利在常温缺血性停搏、低温心脏停搏及随后再灌注过程中对富含能量的磷酸盐和pH值的影响。在所有灌注过程中，心脏均置于探头内，插管后立即开始用卡托普利（80 μmol·L-1）进行处理。常温缺血性停搏（15分钟）后，卡托普利处理组心脏的三磷酸腺苷（ATP）含量与未处理组无显著差异（分别为53±9%和52±8%）。缺血末期，处理组心脏无机磷酸盐的蓄积明显较少，提示处理组心脏缺血末期核苷酸含量较高。低温心脏停搏（圣托马斯医院溶液，4℃）在10℃下持续3小时。未处理组心脏在缺血末期三磷酸腺苷明显较低；与未处理组的53±9%相比为36±6%。未处理组心脏在常温缺血后三磷酸腺苷恢复至76±9%，低温缺血后30分钟再灌注末期恢复至72±7%。卡托普利在两个处理组中均显著改善了三磷酸腺苷的恢复情况；常温缺血后为89±4%，低温缺血后为83±4%。我们得出结论，卡托普利在常温缺血和低温缺血后对三磷酸腺苷的恢复均有有益作用。
