Lipopolysaccharide transport from the peritoneal cavity to the blood: is it controlled by the vagus nerve?

Vagotomy suppresses fever and hyperalgesia caused by intraperitoneal lipopo lysaccharide (LPS) but has little effect on the febrile response to intrave nous or intramuscular LPS. This suggests that some vagus-mediated mechanism s are recruited only when LPS is administered via the intraperitoneal route . We hypothesized that such mechanisms are associated with LPS transport fr om the peritoneal cavity to the circulation. Adult Wistar rats underwent to tal subdiaphragmatic, bilateral selective celiac, or sham vagotomy. On day 28-32 after surgery, they were injected IP with Escherichia coli LPS (5, 20 , or 100 mug/kg) or saline and decapitated 90 min thereafter. Their plasma levels of LPS and their plasma interleukin-6, adrenocorticotropin, and cort icosterone responses to LPS were measured. Success of intraperitoneal admin istration of LPS was verified by increased interleukin-1 beta and interleuk in-6 concentrations in the peritoneal lavage fluid. Effectiveness of vagoto mies was confirmed by increased stomach mass (food retention) and pancreas mass (hypertrophy). In the shams, LPS caused a dose-dependent endotoxemia a nd increased plasma levels of interleukin-6, adrenocorticotropin, and corti costerone. Neither celiac nor total vagotomy affected any of these response s. LPS escapes from the peritoneal cavity by two primary routes, viz., the hematogenous (via the portal vein) and lymphogenous (via the lymphatic syst em). The design of the present study did not allow for evaluating the rapid , hematogenous transport. The results obtained suggest that the abdominal v agus does not control the slow, lymphogenous escape of LPS from the periton eal cavity. (C) 2000 Elsevier Science B.V. All rights reserved.