Complement system in sodium taurocholate pancreatitis in the rat.
The role of the complement system was studied in Na-taurocholate pancreatitis in rats. Complement activity (CH 50) was determined at various times in the course of pancreatitis. Immediately after induction of acute pancreatitis, serum complement activity declined and massive C 3 deposits could be detected in the vicinity of acinar necroses and necrobioses. After a phase of recovery three to six hours postoperatively a second complement consumption occurred. Lethality rate increased as serum complement activity fell below 50% of preoperative values. The degree of C 3 deposition increased up to six hours. Decline of serum complement activity and deposition within the pancreas seemed to be correlated with histologically demonstrable tissue lesion. The first decline of complement activity in serum is thought to be caused by liberation of complement activating substances within the pancreas due to the detergent action of Na-taurocholate itself. The second decline, however, may be due to the liberation of complement activating and/or destroying enzymes into the blood stream.
D000818:Animals; D003176:Complement C3 / Q000032:analysis; D003165:Complement System Proteins; D006461:Hemolysis; D010179:Pancreas / Q000276:immunology; D010195:Pancreatitis / Q000139:chemically induced / Q000276:immunology*; D051381:Rats; D013656:Taurocholic Acid
D003176:Complement C3; D013656:Taurocholic Acid; D003165:Complement System Proteins