Vascular injury in isolated sheep lungs

Role of ischemia, extracorporeal perfusion, and oxygen

David B Pearse, J. T. Sylvester

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)196-202
Number of pages7
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume153
Issue number1
StatePublished - 1996

Fingerprint

Vascular System Injuries
Sheep
Ischemia
Perfusion
Oxygen
Lung
Pulmonary Hypertension
Thromboxanes
Albumins
Neutrophils
Wounds and Injuries
Capillary Permeability
Lung Injury
Blood Vessels
Ventilation
Reactive Oxygen Species

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Vascular injury in isolated sheep lungs : Role of ischemia, extracorporeal perfusion, and oxygen. / Pearse, David B; Sylvester, J. T.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 153, No. 1, 1996, p. 196-202.

Research output: Contribution to journalArticle

@article{823c035e66844b9698a53fac4be39177,
title = "Vascular injury in isolated sheep lungs: Role of ischemia, extracorporeal perfusion, and oxygen",
abstract = "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.",
author = "Pearse, {David B} and Sylvester, {J. T.}",
year = "1996",
language = "English (US)",
volume = "153",
pages = "196--202",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "1",

}

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.

UR - http://www.scopus.com/inward/record.url?scp=0030022870&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030022870&partnerID=8YFLogxK

M3 - Article

VL - 153

SP - 196

EP - 202

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 1

ER -