Circulation, Vol 78, 1449-1458, Copyright © 1988 by American Heart Association
MH Crawford, FL Grover, WP Kolb, CA McMahan, RA O'Rourke, LM McManus and RN Pinckard
Complement depletion with cobra venom factor (CVF) before coronary artery
ligation has been previously shown to reduce subsequent ischemic myocardial
tissue injury in the baboon; however, whether complement depletion after
the initiation of acute myocardial ischemia affords similar myocardial
preservation is not known. Both complement depletion with CVF or the
administration of certain nonsteroidal anti- inflammatory drugs, including
ibuprofen, are thought to decrease myocardial infarct size by reducing
polymorphonuclear leukocytic (PMN) infiltration; nevertheless, complement
activation also could alter tissue injury by PMN-independent actions. Thus,
the relative effects of CVF administered after coronary artery ligation on
the subsequent development of myocardial tissue injury were assessed in a
baboon myocardial infarction model. The animals were randomized into three
treatment groups (n = 6): either CVF (125 units/kg) or saline was given 30
minutes after coronary artery ligation, and ibuprofen (12.5 mg/kg) was
administered 30 minutes and 4 hours after ligation. The extent of ischemic
myocardial injury was assessed 24 hours later. Relative to saline-treated
baboons, both CVF and ibuprofen reduced PMN infiltration (36 +/- 4 vs. 24
+/- 4 and 24 +/- 4 PMN/mm2, respectively; mean +/- SEM) and histological
evidence of transmural myocardial infarction (100% vs. 47% and 53%,
respectively) in electrocardiographically designated, expected infarct
sites. In both saline- and ibuprofen- treated animals, there was extensive
localization of C4, C3, and C5 in all infarct sites; in contrast, there was
only C4 localization in the CVF-treated baboons. When expected infarct
sites were assessed for creatine kinase content as an indicator of tissue
injury, there was significantly less epicardial and endocardial creatine
kinase depletion in the CVF-treated animals (31.7 +/- 5.6% and 39.3 +/-
4.8%) than in the saline-treated animals (54.1 +/- 5.4% and 59.0 +/- 4.7%;
p = 0.012 and 0.011, respectively). The percent creatine kinase depletion
in the ibuprofen-treated animals was intermediate between the two other
groups. These results suggest that depletion of complement after coronary
ligation has beneficial effects in reducing tissue injury that cannot be
explained solely on the basis of reducing PMN infiltration into the
ischemic myocardium.
ARTICLES
Complement and neutrophil activation in the pathogenesis of ischemic myocardial injury
Department of Medicine, University of Texas Health Science Center, San Antonio 78284-7872.
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