Ferrari R, Alfieri O, Curello S, Ceconi C, Cargnoni A, Marzollo P, Pardini A, Caradonna E, Visioli O
Cattedra di Cardiologia, University of Brescia, Italy.
Circulation. 1990 Jan;81(1):201-11. doi: 10.1161/01.cir.81.1.201.
We have investigated the relation between occurrence of myocardial oxidative stress and functional recovery during postischemic reperfusion in 20 selected patients subjected to aortocoronary bypass grafting. Patients were selected for having normal percent ejection fraction and left ventricular end-diastolic pressure before the operation. Occurrence of oxidative stress was assessed by measuring the formation and release of oxidized glutathione (GSSG) in the coronary sinus immediately before aortic cross-clamp, 1, 5, 10, and 20 minutes after removal of aortic cross-clamp, and 10 and 20 minutes after the end of cardiopulmonary bypass. Reduced glutathione (GSH), lactate, and creatine phosphokinase release were also monitored with the same timing. Standard hemodynamic measurements were recorded by means of a triple-lumen thermodilution pulmonary artery catheter before sternotomy, 15 minutes after the end of cardiopulmonary bypass, and during the 24 hours after termination of cardiopulmonary bypass. Reperfusion in patients after a short period of ischemia (less than 30 minutes; group 1) resulted in a small and transient release in the coronary sinus of GSSG and GSH and in a progressive improvement of hemodynamic parameters reaching a stable state 4 hours after the operation. In patients with a period of ischemia longer than 30 minutes (group 2), reperfusion induced a marked and sustained release of lactate, GSH, and GSSG; the arteriocoronary sinus difference for GSSG was still negative after the end of cardiopulmonary bypass. The arteriocoronary sinus difference for creatine phosphokinase also remained negative for as long as 20 minutes after cardiopulmonary bypass, and the rate of functional recovery was significantly delayed, reaching the values of group 1 only 12 hours after the operation. In these patients there was a positive correlation (r = 0.88, p less than 0.01) between the duration of ischemia and the myocardial arteriovenous difference for GSSG. In addition, there was a negative correlation between the arteriocoronary sinus difference for GSSG and cardiac index measured 2, 4, and 6 hours after the operation. These data suggest for the first time that, depending on the severity of the ischemic period, oxidative stress occurs during reperfusion of patients with coronary artery disease who are subjected to heart surgery and that it may be linked with a delay in postoperative recovery of cardiac function.
我们研究了20例接受主动脉冠状动脉搭桥术患者缺血后再灌注期间心肌氧化应激的发生与功能恢复之间的关系。入选患者术前射血分数百分比和左心室舒张末期压力均正常。通过在主动脉阻断前、主动脉阻断解除后1、5、10和20分钟以及体外循环结束后10和20分钟测量冠状窦中氧化型谷胱甘肽（GSSG）的形成和释放来评估氧化应激的发生。同时还在相同时间监测还原型谷胱甘肽（GSH）、乳酸和肌酸磷酸激酶的释放。在胸骨切开术前、体外循环结束后15分钟以及体外循环终止后的24小时内，通过三腔热稀释肺动脉导管记录标准血流动力学测量值。短时间缺血（少于30分钟；第1组）患者的再灌注导致冠状窦中GSSG和GSH少量短暂释放，血流动力学参数逐渐改善，术后4小时达到稳定状态。对于缺血时间超过30分钟的患者（第2组），再灌注导致乳酸、GSH和GSSG显著持续释放；体外循环结束后，GSSG的动静脉差值仍为负值。体外循环后长达20分钟，肌酸磷酸激酶的动静脉差值也保持为负值，功能恢复速率明显延迟，术后12小时才达到第1组的值。在这些患者中，缺血持续时间与心肌GSSG动静脉差值之间存在正相关（r = 0.88，p < 0.01）。此外，术后2、4和6小时测量的GSSG动静脉差值与心脏指数之间存在负相关。这些数据首次表明，取决于缺血期的严重程度，接受心脏手术的冠心病患者再灌注期间会发生氧化应激，并且这可能与术后心脏功能恢复延迟有关。
