Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation

James W. Suliburk, Ernest A. Gonzalez, Stacey D. Moore-Olufemi, Norman Weisbrodt, Frederick A. Moore, David W. Mercer

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Introduction. 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. Materials and 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 < 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. Conclusion. 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.

Original languageEnglish (US)
Pages (from-to)203-207
Number of pages5
JournalJournal of Surgical Research
Volume127
Issue number2
DOIs
StatePublished - Aug 1 2005

Fingerprint

Ketamine
Gastric Emptying
Gastrointestinal Transit
Stomach
Ileus
Nitric Oxide Synthase Type II
Anti-Inflammatory Agents
Injections
Endotoxemia
Gastric Mucosa
Ileum
Anesthetics
Analysis of Variance
Western Blotting

Keywords

  • Anesthetics
  • Gastric
  • Ileum
  • Ileus
  • Ketamine
  • LPS
  • Lipopolysacharide
  • Nitric oxide
  • Transit
  • iNOS

ASJC Scopus subject areas

  • Surgery

Cite this

Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation. / Suliburk, James W.; Gonzalez, Ernest A.; Moore-Olufemi, Stacey D.; Weisbrodt, Norman; Moore, Frederick A.; Mercer, David W.

In: Journal of Surgical Research, Vol. 127, No. 2, 01.08.2005, p. 203-207.

Research output: Contribution to journalArticle

Suliburk, JW, Gonzalez, EA, Moore-Olufemi, SD, Weisbrodt, N, Moore, FA & Mercer, DW 2005, 'Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation', Journal of Surgical Research, vol. 127, no. 2, pp. 203-207. https://doi.org/10.1016/j.jss.2005.03.021
Suliburk, James W. ; Gonzalez, Ernest A. ; Moore-Olufemi, Stacey D. ; Weisbrodt, Norman ; Moore, Frederick A. ; Mercer, David W. / Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation. In: Journal of Surgical Research. 2005 ; Vol. 127, No. 2. pp. 203-207.
@article{e4573e2129694ba8962f7677a9920504,
title = "Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation",
abstract = "Introduction. 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. Materials and 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 < 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. Conclusion. 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.",
keywords = "Anesthetics, Gastric, Ileum, Ileus, Ketamine, LPS, Lipopolysacharide, Nitric oxide, Transit, iNOS",
author = "Suliburk, {James W.} and Gonzalez, {Ernest A.} and Moore-Olufemi, {Stacey D.} and Norman Weisbrodt and Moore, {Frederick A.} and Mercer, {David W.}",
year = "2005",
month = "8",
day = "1",
doi = "10.1016/j.jss.2005.03.021",
language = "English (US)",
volume = "127",
pages = "203--207",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation

AU - Suliburk, James W.

AU - Gonzalez, Ernest A.

AU - Moore-Olufemi, Stacey D.

AU - Weisbrodt, Norman

AU - Moore, Frederick A.

AU - Mercer, David W.

PY - 2005/8/1

Y1 - 2005/8/1

N2 - Introduction. 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. Materials and 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 < 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. Conclusion. 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.

AB - Introduction. 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. Materials and 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 < 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. Conclusion. 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.

KW - Anesthetics

KW - Gastric

KW - Ileum

KW - Ileus

KW - Ketamine

KW - LPS

KW - Lipopolysacharide

KW - Nitric oxide

KW - Transit

KW - iNOS

UR - http://www.scopus.com/inward/record.url?scp=23144443140&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=23144443140&partnerID=8YFLogxK

U2 - 10.1016/j.jss.2005.03.021

DO - 10.1016/j.jss.2005.03.021

M3 - Article

C2 - 15916771

AN - SCOPUS:23144443140

VL - 127

SP - 203

EP - 207

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 2

ER -