PT  - JOURNAL ARTICLE
AU  - Takada, Kohei
AU  - Yamashita, Kimihiro
AU  - Sakurai-Yamashita, Yasuko
AU  - Shigematsu, Kazuto
AU  - Hamada, Yoshinori
AU  - Hioki, Kohshiro
AU  - Taniyama, Kohtaro
TI  - Participation of Nitric Oxide in the Mucosal Injury of Rat Intestine Induced by Ischemia-Reperfusion
DP  - 1998 Oct 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 403--407
VI  - 287
IP  - 1
4099  - http://jpet.aspetjournals.org/content/287/1/403.short
4100  - http://jpet.aspetjournals.org/content/287/1/403.full
SO  - J Pharmacol Exp Ther1998 Oct 01; 287
AB  - The dual role of nitric oxide as a cytoprotective or a cytotoxic free radical gas has been noted in various types of pathophysiological conditions, including the digestive system. The aim of this study was to examine the role of nitric oxide in the mucosal injury induced by ischemia-reperfusion in the rat small intestine. A transient intestinal ischemia was produced in the catheterized ileal segments of rats by occluding the anterior mesenteric artery for 60 min. Nitric oxide metabolites (NO2− and NO3−) and lactate dehydrogenase activity in perfusates of the intestinal lumen were measured over 5 hr periods. The time-course of histological changes in small intestine was also observed. After ischemia-reperfusion, nitric oxide release in the intestinal lumen increased significantly and the dynamics of nitric oxide release correlated with that of lactate dehydrogenase leakage. The administration of NG-nitro-l-arginine methyl ester (1.0–2.5 mg/kg) inhibited this increased nitric oxide release and the lactate dehydrogenase leakage and afforded protection against the mucosal injury induced by ischemia-reperfusion. In conclusion, the nitric oxide production that was accelerated by ischemia-reperfusion of small intestine may possibly participate in the breakdown of intestinal mucosa after ischemia-reperfusion insult. The American Society for Pharmacology and Experimental Therapeutics