VASCULAR INJURY IN ISOLATED SHEEP LUNGS - ROLE OF ISCHEMIA, EXTRACORPOREAL PERFUSION, AND OXYGEN

Extracorporeal perfusion of isolated sheep lungs with blood after 30 m in of ischemia caused injury manifested by polymorphonuclear (PMN) leu kocyte sequestration, pulmonary hypertension, thromboxane release, and increased pulmonary vascular permeability. To determine the roles of ischemia, extracorporeal perfusion, and oxygen in this injury, lungs v entilated with 28% O-2-5% CO2 and subjected to 30 min of ischemia foll owed 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 is chemia and perfusion during ventilation with 95% N-2 (anoxic ischemic- perfused, n = 15). Compared with ischemic-perfused lungs, ischemic lun gs had an increased reflection coefficient for albumin (sigma(alb), 0. 82 +/- 0.03 versus 0.54 +/- 0.05) and decreased filtration coefficient (K-f, 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 le ukocytes, and sigma(alb) (0.74 +/- 0.05); K-f was not different. Anoxi c ischemic-perfused lungs had decreased pulmonary hypertension and thr omboxane release, but sigma(alb) and K-f were not altered. These resul ts suggest that extracorporeal perfusion caused PMN leukocyte sequestr ation, thromboxane release, and pulmonary hypertension, whereas ischem ia caused derecruitment of vascular surface area. Injury required both ischemia and perfusion, but it was not decreased by anoxia, suggestin g that oxygen radicals were not involved.