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The Journal of Thoracic and Cardiovascular Surgery, Vol 99, 873-877, Copyright © 1990 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
K Bando, R Pillai, DE Cameron, JD Brawn, JA Winkelstein, GM Hutchins, BA Reitz and WA Baumgartner
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 degrees 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 assay 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.
ARTICLES
Leukocyte depletion ameliorates free radical-mediated lung injury after cardiopulmonary bypass
Division of Cardiac Surgery, Johns Hopkins Medical Institutions, Baltimore, Md.
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