title: Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation.
abstract: BACKGROUND
  Lipopolysacharide (LPS) causes gastrointestinal ileus and gastric luminal fluid accumulation. Ketamine, an anti-inflammatory anesthetic agent attenuates accumulation of luminal fluid. However, its effects on gastrointestinal transit induced by endotoxemia are unknown. The purpose of this study was to determine if the anti-inflammatory properties of ketamine improve impaired gastric emptying and gastrointestinal transit because of LPS.
  
  
  METHODS
  Rats were given ketamine (70 mg/kg i.p.) or saline 1 h before LPS (20 mg/kg, i.p.) or saline injection. Five hours after LPS injection, rats were gavaged with 1 cc consisting of 0.1 ml of 5 mm FITC Dextran added to 0.9 ml of saline. After 30 min, rats were sacrificed, and gastric emptying, gastrointestinal transit, and gastric fluid accumulation determined. Gastric and ileal mucosa were harvested for analysis of inducible nitric oxide synthase (iNOS) (Western immunoblot). Results are reported as mean +/- SE (n > or = 5 per group; ANOVA).
  
  
  RESULTS
  Ketamine did not prevent LPS induced gastrointestinal ileus, nor did it improve gastric emptying. More importantly, it did not worsen gastrointestinal function or gastric emptying when compared to saline controls. However, it did decrease LPS induced gastric luminal fluid accumulation and blunted iNOS expression in both the stomach and ileum.
  
  
  CONCLUSIONS
  These data indicate that the ability of ketamine to attenuate gastric fluid accumulation is not because of improved gastric emptying or improved gastrointestinal transit. Moreover, while iNOS may play a role in LPS induced gastric luminal fluid accumulation, it does not appear to be a major mediator of the gastrointestinal ileus caused by LPS.
authors.affiliation: Department of General Surgery, The University of Texas Medical School at Houston, Houston, Texas 77026, USA.
authors.forename: James W
authors.initials: JW
authors.lastname: Suliburk
authors.forename: Ernest A
authors.initials: EA
authors.lastname: Gonzalez
authors.forename: Stacey D
authors.initials: SD
authors.lastname: Moore-Olufemi
authors.forename: Norman
authors.initials: N
authors.lastname: Weisbrodt
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Moore
authors.forename: David W
authors.initials: DW
authors.lastname: Mercer
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D015153:Blotting, Western; D001826:Body Fluids / Q000187:drug effects* / Q000378:metabolism*; D005746:Gastric Emptying / Q000187:drug effects; D005753:Gastric Mucosa / Q000378:metabolism*; D005767:Gastrointestinal Diseases / Q000139:chemically induced; D005772:Gastrointestinal Transit / Q000187:drug effects; D007082:Ileum / Q000201:enzymology; D045823:Ileus / Q000139:chemically induced / Q000503:physiopathology; D007649:Ketamine / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D051381:Rats; D017207:Rats, Sprague-Dawley; D013270:Stomach / Q000201:enzymology
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D007649:Ketamine; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat