Complement localization in ischemic baboon myocardium.

Complement localization was examined by direct immunoperoxidase procedures on frozen sections of baboon myocardium obtained 24 hours after ligation of the left anterior descending coronary artery. There was extensive localization of C3, C4, and C5 in most infarcted myocardial fibers; however, in these infarcted areas of myocardium, complement components were not found in myocytes immediately adjacent to either the endocardium or epicardium. Although C3, C4, and C5 were all present within the same myocardial fibers as assessed in adjacent serial sections, the light microscopic distribution of these components was dissimilar, i.e., C3 and C5 were present in both a granular and a diffuse pattern within myocytes, whereas C4 was always localized in a diffuse pattern. Complement components C3 and C5, but not C4, were also localized in the walls of small muscular arteries in infarcted myocardium. No complement was observed in myocardial fibers or blood vessels in normal baboon myocardium. Electron microscopic evaluation of C3 localization within infarcted myocardium indicated that C3 was associated with contractile elements of myocytes, as well as with membranes of myocyte nuclei, mitochondria, and sarcoplasmic reticulum. Within vascular smooth muscular cells, C3 was associated with myofilaments and mitochondrial membranes. Thus, the results of this study provide new information regarding the cellular and subcellular distribution of complement components in infarcted baboon myocardium. If this localization of C3, C4, and C5 is a result of their in situ activation within the ischemic myocardium, a variety of complement-derived phlogistic products would be expected to have been produced and to have effected, in part, the subsequent inflammatory response.