DeCampos K N, Keshavjee S, Liu M, Slutsky A S
The Toronto Hospital, Department of Surgery, University of Toronto, Ontario, Canada.
J Heart Lung Transplant. 1998 Nov;17(11):1121-8.
We have found that the instantaneous restoration of blood flow causes acute dysfunction and massive edema in rat lungs after 4 hours of room temperature ischemia. This is associated with an early increase in pulmonary artery pressure (Ppa) and can be prevented by a stepwise increase in flow rate during the first 10 minutes of reperfusion. The objectives of this study were to determine whether rapid reperfusion causes lung injury after hypothermic preservation, and whether this injury can be attenuated by a short-course of prostaglandin E1 (PGE1). Rat lungs were flushed preserved with low-potassium dextran solution for 12 hours at 4 degrees C and randomly divided into three groups: (1) control (no PGE1); (2) PGE1 only in the flush solution; and (3) PGE1 in both flush solution and blood perfusate during the first 10 minutes of reperfusion. Postpreservation pulmonary function was assessed in an isolated rat lung reperfusion model developed previously. We found that rapid initiation of reperfusion led to significant pulmonary dysfunction, which was attenuated by a short-course of PGE1 in the blood perfusate. The addition of PGE1 to the flush solution alone did not have such an effect. Administration of PGE1 to the blood perfusate during the first 10 minutes resulted in significant lower Ppa and airway pressure and better gas exchange. There was a positive correlation between the peak Ppa during the first 10 minutes of reperfusion and the final shunt fraction. The physical forces generated by the rapid initiation of blood reperfusion appear to induce severe injury. The first 10 minutes of reperfusion seem to be a transition phase in which mechanical factors play an important role relating to ultimate post reperfusion lung function. A short course of PGE1 may be a useful maneuver to prevent rapid reperfusion-induced lung injury.
我们发现，室温缺血4小时后，血流的瞬间恢复会导致大鼠肺脏出现急性功能障碍和大量水肿。这与肺动脉压（Ppa）早期升高有关，并且可通过再灌注开始的前10分钟内逐步增加流速来预防。本研究的目的是确定低温保存后快速再灌注是否会导致肺损伤，以及这种损伤是否可通过短期使用前列腺素E1（PGE1）来减轻。将大鼠肺脏用低钾右旋糖酐溶液冲洗并在4℃下保存12小时，然后随机分为三组：（1）对照组（不使用PGE1）；（2）仅在冲洗液中加入PGE1；（3）在再灌注的前10分钟内，冲洗液和血液灌注液中均加入PGE1。在先前建立的离体大鼠肺再灌注模型中评估保存后的肺功能。我们发现，快速开始再灌注会导致明显的肺功能障碍，而血液灌注液中短期使用PGE1可减轻这种障碍。仅在冲洗液中加入PGE1没有这种效果。在再灌注的前10分钟内将PGE1加入血液灌注液中可使Ppa和气道压显著降低，并改善气体交换。再灌注开始的前10分钟内的Ppa峰值与最终分流分数之间存在正相关。快速开始血液再灌注所产生的物理力似乎会诱发严重损伤。再灌注的前10分钟似乎是一个过渡阶段，在此阶段机械因素对最终的再灌注后肺功能起着重要作用。短期使用PGE1可能是预防快速再灌注所致肺损伤的一种有效方法。
