Bishop M J, Giclas P C, Guidotti S M, Su M L, Chi E Y
Department of Anesthesiology, University of Washington School of Medicine, Seattle.
Am Rev Respir Dis. 1991 Feb;143(2):386-90. doi: 10.1164/ajrccm/143.2.386.
We have previously demonstrated that reperfusion of a rabbit lung in vivo after 24 h of unilateral pulmonary artery occlusion results in edema, transient leukopenia, and intravascular leukocyte aggregation. We hypothesized that complement was activated by reperfusion and that this in turn contributed to lung injury. In the preliminary phase of the study, we found that ischemia followed by reperfusion resulted in a drop in C3 to 15 +/- 10% (mean +/- SEM) of the prereperfusion value as compared with no change in a group of control animals that had undergone an identical thoracotomy but without pulmonary artery occlusion and reperfusion (p less than 0.05). We then studied three groups of animals to determine if complement depletion with cobra venom factor (CVF) prior to ischemia and reperfusion would prevent the injury. Rabbits treated with CVF but without occlusion and reperfusion did not develop significant lung edema, with left and right lung wet/dry ratios of 5.32 +/- 0.11 and 5.26 +/- 0.12, respectively. For rabbits that were not treated with CVF but underwent ischemia and reperfusion, the comparable numbers were 6.15 +/- 0.36 and 5.19 +/- 0.32 (p less than 0.05 for right versus left). For CVF-treated rabbits that underwent ischemia and reperfusion, the right/left difference persisted (6.77 +/- 0.48 versus 5.35 +/- 0.14, p less than 0.01). Immunocytochemistry documented C3 deposition in non-CVF rabbits that underwent ischemia and reperfusion but not in CVF-treated rabbits. We conclude that ischemia/reperfusion of the lung results in complement activation, but it is not a complement-dependent injury.
我们之前已经证明，在单侧肺动脉闭塞24小时后对兔肺进行体内再灌注会导致肺水肿、短暂性白细胞减少和血管内白细胞聚集。我们推测再灌注激活了补体，进而导致肺损伤。在研究的初步阶段，我们发现缺血后再灌注导致C3降至再灌注前值的15±10%（平均值±标准误），而一组接受相同开胸手术但未进行肺动脉闭塞和再灌注的对照动物则无变化（p<0.05）。然后我们研究了三组动物，以确定在缺血和再灌注前用眼镜蛇毒因子（CVF）消耗补体是否能预防损伤。用CVF处理但未进行闭塞和再灌注的兔子未出现明显的肺水肿，左肺和右肺的湿/干比分别为5.32±0.11和5.26±0.12。对于未用CVF处理但经历缺血和再灌注的兔子，相应的数值为6.15±0.36和5.19±0.32（右肺与左肺相比，p<0.05）。对于接受缺血和再灌注的CVF处理的兔子，右/左差异仍然存在（6.77±0.48对5.35±0.14，p<0.01）。免疫细胞化学证明，经历缺血和再灌注的非CVF处理兔子中有C3沉积，而CVF处理的兔子中没有。我们得出结论，肺的缺血/再灌注会导致补体激活，但这不是补体依赖性损伤。
