Nakanishi K, Zhao Z Q, Vinten-Johansen J, Lewis J C, McGee D S, Hammon J W
Department of Cardiothoracic Surgery, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157-1096.
Ann Thorac Surg. 1994 Jul;58(1):191-9. doi: 10.1016/0003-4975(94)91099-5.
This study tests the hypothesis that blood cardioplegia (BCP) attenuates endothelial dysfunction related to nitric oxide after global normothermic ischemia, cardioplegic arrest, and reperfusion in anesthetized open-chest dogs placed on cardiopulmonary bypass. The dogs were divided into five groups to identify the time when endothelial injury occurred: group 1 = control without ischemia; group 2 = 45 minutes of normothermic ischemia only; group 3 = 45 minutes of normothermic ischemia plus unmodified reperfusion; group 4 = 45 minutes of ischemia plus intermittent BCP without reperfusion; and group 5 = ischemia plus BCP and reperfusion. In vitro coronary vascular relaxation responses to the nitric oxide stimulator acetylcholine (endothelium-dependent, receptor-dependent), the calcium ionophore A23187 (endothelium-dependent, receptor-independent), and acidified NaNO2 (endothelium-independent) were measured at the end of the protocol. Maximum in vitro coronary vascular responses to acetylcholine were similar among groups 1, 2, and 4, indicating an absence of endothelial injury. In contrast, significantly impaired relaxations to acetylcholine were demonstrated in the two reperfused groups (groups 3 and 5). Relaxation responses to A23187 and NaNO2 were not altered markedly in any group. Electron microscopy showed intact endothelium in groups 1, 2, and 4. However, moderately severe endothelium damage was seen in groups 3 and 5. We conclude that morphologic and functional endothelial damage occurs after blood reperfusion with or without BCP, and 1-hour hypothermic BCP arrest after normothermic ischemia is not associated with extension of endothelial damage.
在接受体外循环的麻醉开胸犬中，血液停搏液（BCP）可减轻与一氧化氮相关的内皮功能障碍，该内皮功能障碍发生于全身常温缺血、心脏停搏及再灌注之后。将犬分为五组以确定内皮损伤发生的时间：第1组 = 无缺血的对照组；第2组 = 仅45分钟常温缺血组；第3组 = 45分钟常温缺血加未改良的再灌注组；第4组 = 45分钟缺血加间歇性BCP但无再灌注组；第5组 = 缺血加BCP及再灌注组。在实验结束时，测量体外冠状动脉对一氧化氮刺激剂乙酰胆碱（内皮依赖性、受体依赖性）、钙离子载体A23187（内皮依赖性、受体非依赖性）及酸化亚硝酸钠（非内皮依赖性）的血管舒张反应。第1、2和4组对乙酰胆碱的体外冠状动脉最大血管反应相似，表明无内皮损伤。相比之下，两个再灌注组（第3组和第5组）对乙酰胆碱的舒张反应明显受损。任何组对A23187和亚硝酸钠的舒张反应均未明显改变。电子显微镜检查显示第1、2和4组内皮完整。然而，第3组和第5组可见中度严重的内皮损伤。我们得出结论，无论有无BCP，血液再灌注后均会发生形态学和功能性内皮损伤，常温缺血后1小时低温BCP停搏与内皮损伤的扩展无关。
