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The Annals of Thoracic Surgery, Vol 55, 619-624, Copyright © 1993 by The Society of Thoracic Surgeons
AM Gillinov, PA DeValeria, JA Winkelstein, I Wilson, WE Curtis, D Shaw, CG Yeh, AR Rudolph, WA Baumgartner and A Herskowitz
Although complement activation during cardiopulmonary bypass (CPB) is well
documented, its pathogenic role in postperfusion organ injury is unproven.
In this study, soluble human complement receptor type 1 (sCR1), a potent
inhibitor of complement activation, was used to determine the contribution
of complement activation to pulmonary injury in a porcine model of CPB. In
vitro experiments demonstrated that sCR1 inhibits both classic and
alternative complement pathways in the pig. Seven control piglets and 6
piglets treated with sCR1 (12 mg/kg intravenously) underwent 2 hours of
hypothermic (28 degrees C) CPB followed by 2 hours of observation. In
control piglets, total hemolytic complement activity and functional
activities of C3 and C5 declined to 61.3%, 67.8%, and 61.4% of prebypass
values, respectively, after 2 hours of CPB. Plasma from animals treated
with sCR1 had virtually no hemolytic activity (total hemolytic complement
activity < 5% of baseline), demonstrating effective complement
inhibition. Similar degrees of neutropenia developed in the two groups
during CPB, and there was no difference in post-CPB lung tissue
myeloperoxidase level. Two hours after CPB, pulmonary vascular resistance
increased 338% in control piglets but only 147% in piglets pretreated with
sCR1 (p < 0.05); the alveolar-arterial gradient was not significantly
different between controls (331 +/- 52 mm Hg) and piglets receiving sCR1
(290 +/- 85 mm Hg). Histologic examination revealed similar degrees of
pulmonary edema in both groups. These data constitute direct evidence that
complement activation plays a pathogenic role in lung injury after
CPB.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass
Department of Cardiac Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.
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