The phlogistic role of C3 leukotactic fragments in myocardial infarcts of rats.
An improved method is described for extraction from rat myocardium of an enzyme that cleaves the third component of complement (C3) into leukotactic fragments. Direct cleavage of C3 has been shown by the use of a radiolabeled preparation of human C3. The enzyme elutes slightly beyond (retarded to) an albumin marker in gel filtration. After surgical ligation of a coronary artery, leukotactic activity can be extracted from infarcted rat myocardium. Described in terms of its time of appearance in infarcted tissue, the leukotactic activity has been identified as cleavage products of rat C3. The C3 fragments are of low molecular weight and heterogenous in size. Rats, if treated with the C3 inactivator (isolated from cobra venom) so as to ablate serum C3, fail to develop leukotactic activity in the infarcted myocardium. In turn, few if any of the usual intense accumulations of neutrophils in response to infected myocardium are seen during the first 48 hr after coronary artery ligation. These studies suggest a nonimmunologic role for C3 in the mediation of the acute inflammatory response in nonspecific tissue injury.
D000818:Animals; D002499:Centrifugation, Density Gradient; D002633:Chemotaxis; D002850:Chromatography, Gel; D003165:Complement System Proteins / Q000502:physiology*; D005260:Female; D005779:Immunodiffusion; D007249:Inflammation / Q000276:immunology*; D009203:Myocardial Infarction / Q000276:immunology* / Q000473:pathology; D009504:Neutrophils / Q000276:immunology*; D051381:Rats; D014020:Tissue Extracts / Q000032:analysis
D014020:Tissue Extracts; D003165:Complement System Proteins