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Citations to this article

Complement Localization and Mediation of Ischemic Injury in Baboon Myocardium
R. Neal Pinckard, … , S. Brandley Storrs, Merle S. Olson
R. Neal Pinckard, … , S. Brandley Storrs, Merle S. Olson
Published November 1, 1980
Citation Information: J Clin Invest. 1980;66(5):1050-1056. https://doi.org/10.1172/JCI109933.
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Research Article

Complement Localization and Mediation of Ischemic Injury in Baboon Myocardium

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Abstract

We sought to determine whether the third component of complement (C3) is localized in ischemic baboon myocardium after coronary artery ligation. Furthermore, we assessed the effects of prior C3 depletion on myocardial necrosis. We studied seven control baboons (group I) and seven C3-depleted (group II) baboons that were killed 24 h after ligation of the anterior descending coronary artery. Multiple tissue samples were obtained from infarct, intermediate, and normal myocardial sites as defined by serial unipolar epicardial ECG mapping. In group I baboons, myocardial creatine kinase content from infarct sites was reduced as compared with normal sites (12.6±0.92 [SE] vs. 24.4±0.75 IU/mg protein, P < 0.001). The intermediate sites from group I contained more creatine kinase (19.0±1.25 IU/mg protein) than infarct sites (P < 0.001), but less (P < 0.025) than normal sites. In group II, intermediate sites showed no significant reduction in creatine kinase from normal sites and there was significantly less creatine kinase depletion in infarct sites when compared with group I animals (33.7±4.6 and 51.4±1.8% depletion, respectively, P < 0.001). In all seven group I baboons, uniform C3 localization was observed in infarct sites by direct immunofluorescence but appeared in mosaic patterns in intermediate sites. C3 was not demonstrated in any normal sites, nor in any site from group II baboons. Additional studies on baboons killed at earlier times after ligation indicated that C3 was localized focally on swollen myocytes in infarct sites as early as 4 h after coronary ligation. These results strongly implicate the active participation of the complement system of inflammatory proteins in the pathogenesis of myocardial tissue injury following coronary occlusion.

Authors

R. Neal Pinckard, Robert A. O'Rourke, Michael H. Crawford, Frederick S. Grover, Linda M. McManus, John J. Ghidoni, S. Brandley Storrs, Merle S. Olson

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SW Werns, MJ Shea, EM Driscoll, C Cohen, GD Abrams, B Pitt, BR Lucchesi
Circulation research 1985
Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase
SR Jolly, WJ Kane, MB Bailie, GD Abrams, BR Lucchesi
Circulation research 1984
Ibuprofen inhibits granulocyte responses to inflammatory mediators: A proposed mechanism for reduction of experimental myocardial infarct size
PJ Flynn, WK Becker, GM Vercellotti, DJ Weisdorf, PR Craddock, DE Hammerschmidt, RC Lillehei, HS Jacob
Inflammation 1984
Reduction of the extent of ischemic myocardial injury by neutrophil depletion in the dog
JL Romson, BG Hook, SL Kunkel, GD Abrams, MA Schork, BR Lucchesi
Circulation 1983
THERAPEUTIC RAMIFICATIONS OF THE INTERACTION OF COMPLEMENT, GRANULOCYTES, AND PLATELETS IN THE PRODUCTION OF ACUTE LUNG INJURY
HS Jacob, CF Moldow, PJ Flynn, DJ Weisdorf, GM Vercellotti, DE Hammerschmidt
Annals of the New York Academy of Sciences 1982
Complement activation in muscle fiber necrosis: Demonstration of the membrane attack complex of complement in necrotic fibers
AG Engel, G Biesecker
Annals of Neurology 1982
Renal localization of the membrane attack complex in systemic lupus erythematosus nephritis
G Biesecker, S Katz, D Koffler
Journal of Experimental Medicine 1981
Characterization of the binding of purified human C1q to heart mitochondrial membranes
SB Storrs, WP Kolb, RN Pinckard, MS Olson
The Journal of biological chemistry 1981

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