Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass

K. Bando, R. Pillai, D. E. Cameron, J. D. Brawn, J. A. Winkelstein, G. M. Hutchins, B. A. Reitz, William A Baumgartner

Research output: Contribution to journalArticle

Abstract

Activated leukocytes and oxygen free radicals have been implicated in the pathogenesis of lung injury associated with cardiopulmonary bypass. To determine whether leukocyte depletion could prevent this injury, we used a dog model simulating routine cardiac operations. Mongrel dogs (11 to 17 kg) were subjected to cardiopulmonary bypass with a bubble oxygenator and cooled to 27°C. After aortic crossclamping and cardioplegic arrest for 90 minutes, control animals (n = 5) were rewarmed and weaned from bypass, and their condition was then stabilized for 90 minutes. Leukocyte-depleted animals (n = 5) had a leukocyte filter incorporated in the bypass circuit. During bypass, circulating leukocyte counts decreased by 60% in control dogs, and by 97% in leukocyte-depleted animals. Free radical generation (estimated by spectrophotometric assays of plasma conjugated dienes) was significantly reduced by leukocyte depletion during and after bypass. Total hemolytic complement activity and the titer of C5 decreased markedly immediately after the onset of bypass in both the control and leukocyte-depleted animals. Pulmonary function after bypass was better preserved in leukocyte-depleted animals. These data suggest that depletion of circulating leukocytes contributes to lung injury during cardiopulmonary bypass and is associated with increased oxygen radical activity, pulmonary edema, and vasoconstriction. Leukocyte depletion substantially reduced the pulmonary injury seen after cardiopulmonary bypass.

Original languageEnglish (US)
Pages (from-to)873-877
Number of pages5
JournalJournal of Thoracic and Cardiovascular Surgery
Volume99
Issue number5
StatePublished - 1990

Fingerprint

Lung Injury
Cardiopulmonary Bypass
Free Radicals
Leukocytes
Dogs
Reactive Oxygen Species
Complement Hemolytic Activity Assay
Oxygenators
Pulmonary Edema
Vasoconstriction
Leukocyte Count
Lung
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Bando, K., Pillai, R., Cameron, D. E., Brawn, J. D., Winkelstein, J. A., Hutchins, G. M., ... Baumgartner, W. A. (1990). Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass. Journal of Thoracic and Cardiovascular Surgery, 99(5), 873-877.

Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass. / Bando, K.; Pillai, R.; Cameron, D. E.; Brawn, J. D.; Winkelstein, J. A.; Hutchins, G. M.; Reitz, B. A.; Baumgartner, William A.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 99, No. 5, 1990, p. 873-877.

Research output: Contribution to journalArticle

Bando, K, Pillai, R, Cameron, DE, Brawn, JD, Winkelstein, JA, Hutchins, GM, Reitz, BA & Baumgartner, WA 1990, 'Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass', Journal of Thoracic and Cardiovascular Surgery, vol. 99, no. 5, pp. 873-877.
Bando K, Pillai R, Cameron DE, Brawn JD, Winkelstein JA, Hutchins GM et al. Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass. Journal of Thoracic and Cardiovascular Surgery. 1990;99(5):873-877.
Bando, K. ; Pillai, R. ; Cameron, D. E. ; Brawn, J. D. ; Winkelstein, J. A. ; Hutchins, G. M. ; Reitz, B. A. ; Baumgartner, William A. / Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass. In: Journal of Thoracic and Cardiovascular Surgery. 1990 ; Vol. 99, No. 5. pp. 873-877.
@article{02420c7e1be84c3fb70bfc7361de0ca9,
title = "Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass",
abstract = "Activated leukocytes and oxygen free radicals have been implicated in the pathogenesis of lung injury associated with cardiopulmonary bypass. To determine whether leukocyte depletion could prevent this injury, we used a dog model simulating routine cardiac operations. Mongrel dogs (11 to 17 kg) were subjected to cardiopulmonary bypass with a bubble oxygenator and cooled to 27°C. After aortic crossclamping and cardioplegic arrest for 90 minutes, control animals (n = 5) were rewarmed and weaned from bypass, and their condition was then stabilized for 90 minutes. Leukocyte-depleted animals (n = 5) had a leukocyte filter incorporated in the bypass circuit. During bypass, circulating leukocyte counts decreased by 60{\%} in control dogs, and by 97{\%} in leukocyte-depleted animals. Free radical generation (estimated by spectrophotometric assays of plasma conjugated dienes) was significantly reduced by leukocyte depletion during and after bypass. Total hemolytic complement activity and the titer of C5 decreased markedly immediately after the onset of bypass in both the control and leukocyte-depleted animals. Pulmonary function after bypass was better preserved in leukocyte-depleted animals. These data suggest that depletion of circulating leukocytes contributes to lung injury during cardiopulmonary bypass and is associated with increased oxygen radical activity, pulmonary edema, and vasoconstriction. Leukocyte depletion substantially reduced the pulmonary injury seen after cardiopulmonary bypass.",
author = "K. Bando and R. Pillai and Cameron, {D. E.} and Brawn, {J. D.} and Winkelstein, {J. A.} and Hutchins, {G. M.} and Reitz, {B. A.} and Baumgartner, {William A}",
year = "1990",
language = "English (US)",
volume = "99",
pages = "873--877",
journal = "Journal of Thoracic and Cardiovascular Surgery",
issn = "0022-5223",
publisher = "Mosby Inc.",
number = "5",

}

TY - JOUR

T1 - Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass

AU - Bando, K.

AU - Pillai, R.

AU - Cameron, D. E.

AU - Brawn, J. D.

AU - Winkelstein, J. A.

AU - Hutchins, G. M.

AU - Reitz, B. A.

AU - Baumgartner, William A

PY - 1990

Y1 - 1990

N2 - Activated leukocytes and oxygen free radicals have been implicated in the pathogenesis of lung injury associated with cardiopulmonary bypass. To determine whether leukocyte depletion could prevent this injury, we used a dog model simulating routine cardiac operations. Mongrel dogs (11 to 17 kg) were subjected to cardiopulmonary bypass with a bubble oxygenator and cooled to 27°C. After aortic crossclamping and cardioplegic arrest for 90 minutes, control animals (n = 5) were rewarmed and weaned from bypass, and their condition was then stabilized for 90 minutes. Leukocyte-depleted animals (n = 5) had a leukocyte filter incorporated in the bypass circuit. During bypass, circulating leukocyte counts decreased by 60% in control dogs, and by 97% in leukocyte-depleted animals. Free radical generation (estimated by spectrophotometric assays of plasma conjugated dienes) was significantly reduced by leukocyte depletion during and after bypass. Total hemolytic complement activity and the titer of C5 decreased markedly immediately after the onset of bypass in both the control and leukocyte-depleted animals. Pulmonary function after bypass was better preserved in leukocyte-depleted animals. These data suggest that depletion of circulating leukocytes contributes to lung injury during cardiopulmonary bypass and is associated with increased oxygen radical activity, pulmonary edema, and vasoconstriction. Leukocyte depletion substantially reduced the pulmonary injury seen after cardiopulmonary bypass.

AB - Activated leukocytes and oxygen free radicals have been implicated in the pathogenesis of lung injury associated with cardiopulmonary bypass. To determine whether leukocyte depletion could prevent this injury, we used a dog model simulating routine cardiac operations. Mongrel dogs (11 to 17 kg) were subjected to cardiopulmonary bypass with a bubble oxygenator and cooled to 27°C. After aortic crossclamping and cardioplegic arrest for 90 minutes, control animals (n = 5) were rewarmed and weaned from bypass, and their condition was then stabilized for 90 minutes. Leukocyte-depleted animals (n = 5) had a leukocyte filter incorporated in the bypass circuit. During bypass, circulating leukocyte counts decreased by 60% in control dogs, and by 97% in leukocyte-depleted animals. Free radical generation (estimated by spectrophotometric assays of plasma conjugated dienes) was significantly reduced by leukocyte depletion during and after bypass. Total hemolytic complement activity and the titer of C5 decreased markedly immediately after the onset of bypass in both the control and leukocyte-depleted animals. Pulmonary function after bypass was better preserved in leukocyte-depleted animals. These data suggest that depletion of circulating leukocytes contributes to lung injury during cardiopulmonary bypass and is associated with increased oxygen radical activity, pulmonary edema, and vasoconstriction. Leukocyte depletion substantially reduced the pulmonary injury seen after cardiopulmonary bypass.

UR - http://www.scopus.com/inward/record.url?scp=0025373760&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025373760&partnerID=8YFLogxK

M3 - Article

VL - 99

SP - 873

EP - 877

JO - Journal of Thoracic and Cardiovascular Surgery

JF - Journal of Thoracic and Cardiovascular Surgery

SN - 0022-5223

IS - 5

ER -