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Title: Ketamine and the myenteric plexus in intestinal ischemia/reperfusion injury. Author: Guzmán-de la Garza FJ, Cámara-Lemarroy CR, Ballesteros-Elizondo RG, Alarcón-Galván G, Cordero-Pérez P, Fernández-Garza NE. Journal: Dig Dis Sci; 2010 Jul; 55(7):1878-85. PubMed ID: 19760156. Abstract: BACKGROUND AND AIMS: Intestinal ischemia/reperfusion (I/R) is a common clinical entity with severe consequences. We studied the effects of ketamine and the participation of the myenteric plexus in I/R injury. METHODS: Rats were divided into six groups: sham, IR (30 min ischemia/60 min reperfusion), KET+IR (50 mg/kg i.p. ketamine injection before I/R), DEN (myenteric plexus ablated with benzalkonium chloride (BAC) and sham operation performed), DEN+IR (BAC treated and I/R induced), and DEN+KET+IR (BAC treated, ketamine administered, and I/R induced). Serum concentrations of p-selectin, intracellular adhesion molecule-1 (ICAM-1), and antithrombin III (ATIII) were measured, and tissue samples were obtained for histological analysis. RESULTS: IR group had higher intestinal mucosa injury and elevated serum concentrations of ICAM-1 and p-selectin, as well as ATIII depletion, compared with sham group (P < 0.05). In KET+IR group these alterations were significantly reduced (P < 0.05). DEN group showed ICAM-1 elevations when compared with sham group (P < 0.05), and DEN+IR group showed no difference in any parameter compared with IR group. However, ketamine administration in group DEN+KET+IR had no effect on any parameter when compared with DEN+IR group. CONCLUSIONS: Ketamine was able to diminish alterations induced by I/R. Myenteric plexus ablation with BAC treatment alone had no effects on intestinal I/R injury. However, this procedure abolished ketamine's protective effects. Ketamine seems to require an intact enteric nervous system to exert its protective action.[Abstract] [Full Text] [Related] [New Search]