Horgan M J, Lum H, Malik A B
Department of Physiology, Albany Medical College of Union University, New York.
Am Rev Respir Dis. 1989 Nov;140(5):1421-8. doi: 10.1164/ajrccm/140.5.1421.
We examined the basis of reperfusion-induced pulmonary edema produced by pulmonary artery occlusion and subsequent reperfusion. After a 24-h period of occlusion of a rabbit pulmonary artery followed by a 2-h period of reperfusion, the lungs were removed from the animal and perfused with a 0.5 g% Ringer's-albumin solution. An increase in lung weight was observed within 60 min compared with control lungs (i.e., lungs subjected to pulmonary arterial occlusion but not reperfusion) (p less than 0.05). Shorter periods of occlusion (6 or 12 h) did not result in edema, which suggests that a period of ischemia was required for the reperfusion-induced pulmonary edema. The extravascular lung water content also increased in the contralateral lung (i.e., the lung not subjected to pulmonary arterial occlusion and reperfusion). The capillary filtration coefficient increased in reperfused lungs compared with controls (p less than 0.05), indicating an increase in lung vascular permeability following reperfusion. Infusion of allopurinol (a xanthine oxidase inhibitor) and superoxide dismutase during the reperfusion period prevented the increases in lung weight and vascular permeability; infusion of catalase was ineffective. We conclude that pulmonary reperfusion following pulmonary artery occlusion increases pulmonary vascular permeability, which is mediated by the generation of oxidants.
我们研究了肺动脉阻塞及随后再灌注所导致的再灌注性肺水肿的发生机制。对兔肺动脉进行24小时阻塞，随后再灌注2小时后，取出动物的肺脏，并用0.5g%的林格氏白蛋白溶液进行灌注。与对照肺（即仅接受肺动脉阻塞但未再灌注的肺）相比，在60分钟内观察到肺重量增加（p<0.05）。较短时间的阻塞（6或12小时）未导致肺水肿，这表明再灌注性肺水肿需要一段缺血时间。对侧肺（即未接受肺动脉阻塞和再灌注的肺）的血管外肺水含量也增加。与对照组相比，再灌注肺的毛细血管滤过系数增加（p<0.05），表明再灌注后肺血管通透性增加。在再灌注期间输注别嘌呤醇（一种黄嘌呤氧化酶抑制剂）和超氧化物歧化酶可防止肺重量和血管通透性增加；输注过氧化氢酶无效。我们得出结论，肺动脉阻塞后的肺再灌注会增加肺血管通透性，这是由氧化剂的产生介导的。
