TY - JOUR
T1 - Vascular injury in isolated sheep lungs
T2 - Role of ischemia, extracorporeal perfusion, and oxygen
AU - Pearse, David B.
AU - Sylvester, J. T.
PY - 1996
Y1 - 1996
N2 - 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 (σ(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 leukocytes, and σ(alb) (0.74 ± 0.05); K(f) was not different. Anoxic ischemic-perfused lungs had decreased pulmonary hypertension and thromboxane release, but σ(alb) and K(f) 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.
AB - 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 (σ(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 leukocytes, and σ(alb) (0.74 ± 0.05); K(f) was not different. Anoxic ischemic-perfused lungs had decreased pulmonary hypertension and thromboxane release, but σ(alb) and K(f) 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.
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U2 - 10.1164/ajrccm.153.1.8542116
DO - 10.1164/ajrccm.153.1.8542116
M3 - Article
C2 - 8542116
AN - SCOPUS:0030022870
SN - 1073-449X
VL - 153
SP - 196
EP - 202
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 1
ER -