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It is well known that endotoxin (Et) plays an important role in severe surgical infectious diseases such as peritonitis. Recently, it has been reported that increased superoxide (O2-) formation and accelerated lipid-peroxidation cause the progress of Et shock. The present study was designed to estimate the changes in the amount of lipid-peroxides in the liver and the relationship between Et and lipid-peroxidation in bacterial peritonitis. Plasma Et levels, lipid-peroxides in the liver, the number of leukocytes in the blood and the number of bacteria in the blood and peritoneal cavity were determined using an experimental peritonitis model that was induced by intraperitoneal (i.p.) injection of E. coli, E. faecalis and B. fragilis, as well as experimental endotoxemia model induced i.p. injection of Et. The influence of ET on the function of polymorphonuclear leukocytes (PMN), that was considered to be one of the origins O2- production, was studied using PMN from the peritoneal cavity of rats. The plasma Et level was increased in an E. coli group and mixed injection group, and the lipid-peroxide levels in the liver were increased in these two groups as well as in a B. fragilis group. Plasma Et and lipid-peroxide levels in the liver were also increased in Et injected mice. In the study of the influence of Et on PMN function, O2- formation of PMN was increased when PMN was stimulated by Et with a high concentration and hexose monophosphate shunt activity was increased in all PMN stimulated by Et. These results suggest that O2- from PMN stimulated by Et is related to lipid-peroxidation in the liver, which is considered an index of injury in bacterial peritonitis.

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The role of endotoxin in the pathogenesis of bacterial peritonitis with special reference to superoxide in polymorphonuclear leukocytes stimulated by endotoxin.