The participation of complement in the pathogenesis of DIC was studied using experimental model of DIC in rats.
Experimental DIC was induced by sustained infusion of bacterial endotoxin (ET) (100mg/kg; lipopolysaccharide B, E. coli 055, B5, Difco) into the femoral vein for 4h in female rats of the Wistar strain with weights ranging from 200 to 230g. The severity of DIC was determined with reference to several coagulation parameters, such as fibrinogen (Fbg), fibrin-fibrinogen degradation products (FDP), prothrombin time (PT), partial thromboplastin time (PTT), platelet count (PLT), and number of the renal glomeruli having fibrin thrombi (% glomerular fibrin deposits; % GFD).
At 4h after the sustained infusion of ET, C3 and CH50 levels were markedly decreased compared with those of the control rats treated with saline. C3 and CH50 levels showed rapid decrease by 1h followed by gradual loss by 4h. The rats which showed marked decrease in CH50 levels revealed a tendency of marked increase in % GFD as well as FDP.
These data suggested that there was a close relationship between complement system and ET-induced DIC in rats. The further examination for the role of complement in the pathogenesis of DIC is now under investigation.