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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1993-4-15
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pubmed:abstractText |
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)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0003-4975
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
55
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pubmed:owner |
NLM
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pubmed:authorsComplete |
N
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pubmed:pagination |
619-24
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8383955-Animals,
pubmed-meshheading:8383955-Cardiopulmonary Bypass,
pubmed-meshheading:8383955-Complement Activation,
pubmed-meshheading:8383955-Complement C3,
pubmed-meshheading:8383955-Complement C5,
pubmed-meshheading:8383955-Complement Hemolytic Activity Assay,
pubmed-meshheading:8383955-Leukocyte Count,
pubmed-meshheading:8383955-Lung,
pubmed-meshheading:8383955-Neutrophils,
pubmed-meshheading:8383955-Peroxidase,
pubmed-meshheading:8383955-Pulmonary Circulation,
pubmed-meshheading:8383955-Receptors, Complement,
pubmed-meshheading:8383955-Reperfusion Injury,
pubmed-meshheading:8383955-Swine,
pubmed-meshheading:8383955-Vascular Resistance
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pubmed:year |
1993
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pubmed:articleTitle |
Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass.
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pubmed:affiliation |
Department of Cardiac Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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