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The Annals of Thoracic Surgery, Vol 57, 345-352, Copyright © 1994 by The Society of Thoracic Surgeons
AM Gillinov, JM Redmond, JA Winkelstein, KJ Zehr, A Herskowitz, WA Baumgartner and DE Cameron
Cardiopulmonary bypass (CPB) is known to cause complement and neutrophil
activation, but the relative importance and interaction of these components
in CPB-induced inflammation is unknown. In this study, a strain of dogs
genetically deficient in the third component of complement (C3) was used to
determine the contribution of C3 to neutrophil activation and pulmonary
injury after CPB. Eleven dogs (5 C3- deficient and 6 controls) underwent
150 minutes of hypothermic CPB (28 degrees C) followed by 2 hours of
observation. Before CPB, C3 levels were normal in controls and less than 1%
of normal in C3-deficient dogs. In control dogs, functional activity of C3
decreased to 53.2% of baseline after 1 hour of CPB and there was
immunohistochemical evidence of C3 deposition in lung after CPB;
C3-deficient dogs had no C3 deposition in lung. Although similar degrees of
neutropenia occurred during CPB in the two groups, expression of neutrophil
adhesion molecule subunit CD18 was significantly lower in C3-deficient dogs
than controls after 1 hour of CPB (45.9 +/- 3.7 versus 82.9 +/- 10.0 mean
fluorescence units; p < 0.02). Postbypass lung tissue myeloperoxidase
content was also less in C3-deficient dogs (43.8 +/- 4.6 versus 71.1 +/-
8.6 mumol x 10 mg-1 x min-1; p < 0.03). Cardiopulmonary bypass-
associated lung injury (assessed by alveolar-arterial oxygen gradient,
pulmonary vascular resistance, percent lung water, and light and electron
microscopic appearance) was similar between groups. These results
demonstrate that (1) C3 is deposited on pulmonary vascular endothelium
during CPB and (2) C3 mediates increased expression of neutrophil CD18 and
neutrophil sequestration in lung after CPB.(ABSTRACT TRUNCATED AT 250
WORDS)
ARTICLES
Complement and neutrophil activation during cardiopulmonary bypass: a study in the complement-deficient dog
Division of Cardiac Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.
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