Selective Accumulation of the First Component of Complement and Leukocytes in Ischemic Canine Heart Muscle: A Possible Initiator of an Extra Myocardial Mechanism of Ischemic Injury

• Published in: Circulation research Vol. 57; no. 1; pp. 119 - 130
• Main Authors: Rossen, Roger D, Swain, Judith L, Michael, Uoyd H, Weakley, Suzanne, Giannini, Edward, Entman, Mark L
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.07.1985; Lippincott
• Subjects: Animals; Biological and medical sciences; Cardiology. Vascular system; Complement Activating Enzymes - metabolism; Complement C1q; Coronary Circulation; Coronary Disease - immunology; Coronary heart disease; Dogs; Heart; Humans; Leukocyte Count; Medical sciences; Myocardium - immunology; Neutrophils - immunology; Regional Blood Flow; Serum Albumin - metabolism; Fissipedia; Immunopathology; Carnivora; Complement C1; Leukocyte; Cardiovascular disease; Coronary heart disease; Vertebrata; Experimental disease; Mammalia; Ischemia; Myocardium; Dog
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.57.1.119

Myocardial concentrations of C1q, a subunit of the first component of complement, were measured 5–120 minutes after ligation of a coronary artery in dogs injected with I-labeled human C1q and I-labeled human albumin. The I-labeled human serum albumin was used as a plasma protein marker. Ischemic regions of myocardium were defined by measuring regional myocardial blood flow by the reference sample method at intervals after coronary artery occlusion. Significant accumulations of I-C1q were demonstrated in the ischemic myocardium after coronary artery occlusions lasting 45 minutes. Some localization of C1q in ischemic myocardium was observed after a 15-minute occlusion, but the accumulations of C1q achieved in this case were not statistically significant. After coronary artery occlusions lasting ±45 minutes, left ventricular concentrations of C1q correlated reciprocally with regional myocardial blood flow. Moreover, high concentrations of C1q persisted in formerly ischemic segments after reperfusion. Radiolabeled neutrophils also accumulated selectively in ischemic segments relatively rich in C1q. It is suggested that complement activation may initiate the neutrophil-dependent portion of ischemic injury, delineated in recent years, that is associated with free radical release by phagocytic cells.