Vascular injury in isolated sheep lungs. Role of ischemia, extracorporeal perfusion, and oxygen.
Vascular injury in isolated sheep lungs. Role of ischemia, extracorporeal perfusion, and oxygen.
复制标题
离体绵羊肺部的血管损伤。
DOI：
10.1164/ajrccm.153.1.8542116
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发表时间：
1996
影响因子：
24.7
通讯作者：
Sylvester,JT
中科院分区：
文献类型：
--
作者：
Pearse,DB;Sylvester,JT
离体绵羊肺缺血30min后用血液体外灌流可引起中性粒细胞(PMN)白细胞隔离、肺动脉高压、血栓素释放和肺血管通透性增加等损伤。为确定缺血、体外灌流和氧气在肺损伤中的作用，将28%O2-5%CO2通气组和缺血30min+180min灌注组(n=23)与(1)缺血组(n=7)、(2)灌注组(n=20)、(3)缺血组(n=15)和缺氧组(n=15)比较。与缺血肺相比，缺血肺对白蛋白的反射系数增加(sigma alb，0.82+/-0.03vs0.54+/-0.05)，过滤系数降低(Kf0.05+/-0.01vs0.11+/-0.03g.min-1.mm Hg-1.100 g-1)。肺灌流使肺动脉高压、肺中性粒细胞、Sigma-Alb升高(0.74+/-0.05)，KF无差异。缺氧缺血肺可降低肺动脉高压和血栓素释放，但对Sigma-Alb和KF无明显影响。这些结果表明，体外灌流导致PMN白细胞隔离、血栓素释放和肺动脉高压，而缺血则导致血管表面积减少。损伤需要缺血和灌流，但缺氧并不能减轻损伤，这表明氧自由基没有参与。
Extracorporeal perfusion of isolated sheep lungs with blood after 30 min of ischemia caused injury manifested by polymorphonuclear (PMN) leukocyte sequestration, pulmonary hypertension, thromboxane release, and increased pulmonary vascular permeability. To determine the roles of ischemia, extracorporeal perfusion, and oxygen in this injury, lungs ventilated with 28% O2-5% CO2 and subjected to 30 min of ischemia followed by 180 min of perfusion (ischemic-perfused, n = 23) were compared with lungs subjected to (1) ischemia without perfusion (ischemic, n = 7), (2) perfusion without ischemia (perfused, n = 20), or (3) both ischemia and perfusion during ventilation with 95% N2 (anoxic ischemic-perfused, n = 15). Compared with ischemic-perfused lungs, ischemic lungs had an increased reflection coefficient for albumin (sigma alb, 0.82 +/- 0.03 versus 0.54 +/- 0.05) and decreased filtration coefficient (Kf, 0.05 +/- 0.01 versus 0.11 +/- 0.03 g.min-1.mm Hg-1.100 g-1). Perfused lungs had increased pulmonary hypertension, lung PMN leukocytes, and sigma alb (0.74 +/- 0.05); Kf was not different. Anoxic ischemic-perfused lungs had decreased pulmonary hypertension and thromboxane release, but sigma alb and Kf were not altered. These results suggest that extracorporeal perfusion caused PMN leukocyte sequestration, thromboxane release, and pulmonary hypertension, whereas ischemia caused derecruitment of vascular surface area. Injury required both ischemia and perfusion, but it was not decreased by anoxia, suggesting that oxygen radicals were not involved.