Objective:We sought to test the hypothesis that ileal mucosal oxygen consumption is impaired in endotoxemic rats.Methods:Male Sprague-Dawley rats were injected intravenously with eitherEscherichia colilipopolysaccharide (5 mg/kg) or a similar volume of vehicle. A segment of ileum was excised 8 hrs later, and the serosal and muscular layers of the bowel were stripped away from the mucosa. A strip of mucosa was mounted in a polarographic chamber containing air-saturated Krebs-Henseleit buffer plus 20 mM glucose, PO2being monitored during a 10-min period. Some rats were injected intraperitoneally with the inducible nitric oxide synthase inhibitor, aminoguanidine (30 mg/kg per dose), or a similar volume of vehicle, at 1, 3 and 6 hrs after injection of lipopolysaccharide.Results:In an initial experiment, the rate of oxygen consumption was significantly lower for mucosal samples from endotoxemic rats as compared with control rats (0.76 ± 0.11 ng-atoms vs. 1.42 ± 0.22 ng-atoms of 0/min per μg dry weight, respectively; n = 8 per group;p< .05). The rate of mucosal oxygen consumption was higher in aminoguanidine-treated as compared with vehicle-treated endotoxemic rats (1.25 ± 0.11 ng-atoms and 0.73 ± 0.07 ng-atoms of 0/min per μg, respectively; n = 7 and n = 6, respectively;p< .05).Conclusion:Endotoxemia is associated with diminished intestinal mucosal oxygen utilization due to an intrinsic acquired derangement in cellular respiration that is caused, at least in part, by an aminoguanidine-inhibitable mechanism.