Fibrin in peritonitis. I. Beneficial and adverse effects of fibrin in experimental E. coli peritonitis.
Fibrin has classically been considered a defense mechanism of the peritoneal cavity. We have studied the role of purified fibrin in the pathogenesis of intraperitoneal infection. Implantation of 0.5% bovine fibrin clots containing 2 X 10(8) E. coli into the rat peritoneal cavity reduces the 24-hour mortality rate from 100% to 0% compared to bacteria in a similar volume of saline solution. However, the 10-day mortality rate with fibrin is 90%; 100% develop intraperitoneal abscesses. Animals receiving sterile clots lyse than over 1 to 2 weeks without abscess formation. As few as 10(2) E. coli per fibrin clot produce abscesses, but 10(7) or more are required to produce death; without fibrin less than 10(7) E. coli neither kill nor produce intraperitoneal infections. Both late death and abscess size with 2 X 10(8) E. coli are directly proportional to the fibrin clot size but not the concentration of fibrin in the clot. Operative debridement of the fibrin at 4 or 24 hours completely eliminates abscess formation in surviving animals. In vitro growth of E. coli is neither stimulated nor inhibited by fibrin or fibrinogen. Fibrin delays systemic sepsis, but the entrapped bacteria cannot be easily eliminated by normal intraperitoneal bactericidal mechanisms and abscess formation occurs. Thus radical peritoneal debridement or anticoagulation may reduce the septic complications of peritonitis.
D000038:Abscess / Q000503:physiopathology; D000818:Animals; D004926:Escherichia coli / Q000254:growth & development; D004927:Escherichia coli Infections / Q000401:mortality / Q000503:physiopathology*; D005337:Fibrin / Q000494:pharmacology*; D005340:Fibrinogen / Q000494:pharmacology; D005342:Fibrinolysis; D008297:Male; D010529:Peritoneal Cavity / Q000601:surgery; D010538:Peritonitis / Q000401:mortality / Q000503:physiopathology* / Q000601:surgery; D051381:Rats; D013997:Time Factors
D005337:Fibrin; D005340:Fibrinogen