Ketamine reduces intestinal injury and inflammatory cell infiltration after ischemia/reperfusion in rats
- Francisco Javier Guzmán-De La Garza,
- Carlos Rodrigo Cámara-Lemarroy,
- Raquel Guadalupe Ballesteros-Elizondo,
- ,
- Paula Cordero-Pérez,
- Nancy Esthela Fernández-Garza
- Departamento de Fisiología
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Abstract
PURPOSE: Intestinal ischemia reperfusion (I/R) induces severe injury and significant mortality. New therapeutic interventions are needed; ketamine is an anesthetic with anti-inflammatory properties, which has shown protective effects on I/R in various organs. This study investigated effects of ketamine on intestinal I/R injury.
METHODS: Male Wistar rats underwent either sham surgery or 30 min of intestinal ischemia followed by 60 min reperfusion. Ketamine pretreatment was administered by intraperitoneal injections at doses of 100, 50, 12.5, or 6.25 mg/kg. The intestinal morphology, mucosal damage, leukocyte infiltration, serum P-selectin, serum intracellular adhesion molecule-1 (ICAM-1), serum antithrombin-III (ATIII), and myenteric ganglion cell structure were evaluated.
RESULTS: Intestinal I/R led to severe mucosal damage, leukocyte (especially neutrophil) infiltration, P-selectin and ICAM-1 elevations, ATIII depletion, and myenteric ganglion cell morphological alterations. The ketamine dose dependently diminished these alterations (except for ICAM-1 serum levels), reaching statistical significance at 100, 50, and 12.5 mg/kg.
CONCLUSIONS: Ketamine protects the intestine against I/R injury. Ketamine anesthesia has been recommended for clinical situations of sepsis and hemodynamic instability, both frequent during intestinal I/R. The clinical application of ketamine in situations of intestinal I/R warrants consideration.
Publication Information
Output type
Original language
EnglishPages from-to (Number of pages)
Pages 1055-1062 (8 pages)Journal (Volume, Issue Number)
Surgery Today (Volume 40, Issue 11)Publication milestones
- Published - 11/2010
Publication status
ISSN
0941-1291Publication IDs
- PubMed: 21046505
- Scopus: 78349273957
- WOS: 000283702200010
