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Research Article Free access | 10.1172/JCI109933

Complement Localization and Mediation of Ischemic Injury in Baboon Myocardium

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

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by Pinckard, R. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by O'Rourke, R. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by Crawford, M. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by Grover, F. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by McManus, L. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by Ghidoni, J. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by Storrs, S. in: PubMed | Google Scholar

Department of Pathology, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78284

Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas 78284

Find articles by Olson, M. in: PubMed | Google Scholar

Published November 1, 1980 - More info

Published in Volume 66, Issue 5 on November 1, 1980
J Clin Invest. 1980;66(5):1050–1056. https://doi.org/10.1172/JCI109933.
© 1980 The American Society for Clinical Investigation
Published November 1, 1980 - Version history
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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.

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