Evidence of complement catabolism in experimental acute pancreatitis.
Serum specimens from guinea pigs with experimentally induced acute pancreatitis were examined for evidence of protease-antiprotease imbalance and complement catabolism. Pancreatitis was induced in 22 male Hartley guinea pigs by the injection of sodium taurocholate into the pancreatic parenchyma. Only a laparotomy was performed in 6 control animals. In 10 experimental animals that survived for less than 24 hours, there was a significant, early reduction of serum trypsin inhibitory capacity (a measure of antiprotease activity). Levels of total hemolytic complement as well as titers of hemolytic C3 and C4 fell significantly in all experimental animals during the first 24 hours. Factor B activity, however, did not change. Only serum from experimental animals contained chemotactic activity for human polymorphonuclear leukocytes. These findngs indicate that circulating complement components are cleaved during the course of experimental acute pancreatitis. As a consequence, complement-derived peptides are generated that may mediate local and systemic tissue injury.
D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D002630:Chemotactic Factors / Q000032:analysis; D003176:Complement C3 / Q000378:metabolism; D003181:Complement C4 / Q000378:metabolism; D003165:Complement System Proteins / Q000378:metabolism*; D006168:Guinea Pigs; D008297:Male; D009504:Neutrophils / Q000276:immunology; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism*; D013656:Taurocholic Acid; D014361:Trypsin Inhibitors / Q000032:analysis
D002630:Chemotactic Factors; D003176:Complement C3; D003181:Complement C4; D014361:Trypsin Inhibitors; D013656:Taurocholic Acid; D003165:Complement System Proteins; D000681:Amylases