Abstract
Introduction. LPS causes a gastrointestinal ileus and gastric luminal fluid accumulation. Ketamine, an antiinflammatory agent, attenuates accumulation of luminal fluid. However its effects on gastrointestinal transit during endotoxemia are unknown. The purpose of this study was to determine if the antiinflammatory properties of ketamine improve impaired gastrointestinal transit due to LPS. We hypothesized that ketamine would improve impaired GI transit caused by LPS. Methods. Rats were given ketamine (70 mg/kg ip) or saline 1 h prior to LPS (20 mg/kg, ip) or saline injection. Five hours following LPS injection, rats were gavaged with 0.1 ml of 5 mM FITC Dextran followed by 0.9 ml of saline. After 30 min rats were sacrificed; transit was determined as the mean geometric center of the FITC Dextran tracer signal; gastric fluid accumulation was determined, and gastric and ileal mucosa were harvested for analysis of iNOS as an inflammatory marker (Western immunoblot). Results are reported as mean ± SE ( n ≥ 5 per group; ANOVA). Results. As shown in the table TABLE—ABSTRACT P84 GI transit Gastric fluid Gastric iNOS Ileal iNOS Sal/Sal 6.35 ± .16 .21 ± .02 .03 ± .001 .02 ± .001 Sal/LPS 2.71 ± .34 ∗ 2.71 ± .46 ∗ .31 ± .13 ∗ .4 ± .08 ∗ Ket/Sal 6.33 ± .38 .24 ± .08 .02 ± .01 .01 ± .002 Ket/LPS 2.86 ± .28 ∗ 1.23 ± .4 ∗∗ .13 ± .02 ∗∗ .24 ± .02 ∗∗ ∗ P < .05 versus saline counterpart; ∗∗ P < .05 versus saline/LPS above, ketamine did not reverse LPS-induced gastrointestinal ileus. However it did decrease LPS-induced gastric luminal fluid accumulation and blunted iNOS expression in both the stomach and the ileum. Conclusion. These data indicate that ketamine’s ability to attenuate gastric fluid accumulation is not due to improved gastric emptying. Moreover, while iNOS may play a role in LPS-induced gastric luminal fluid accumulation, it does not appear to play a significant role in the gastrointestinal ileus caused by LPS.
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