Korean J Physiol Pharmacol.
1998 Aug;2(4):511-519.
Protective mechanism of nitric oxide and mucus against
ischemia/reperfusion-induced gastric mucosal injury
- Affiliations
-
- 1Department of Pharmacology and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul 120 752, South Korea.
Abstract
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This study investigated the role of nitric oxide on the oxidative
damage in gastric mucosa of rats which received ischemia/reperfusion
and its relation to mucus. Nitric oxide synthesis modulators such as
L-arginine and NG-nitro-L-arginine methyl ester, and sodium
nitroprusside, a nitric oxide donor, were injected intraperitoneally to
the rats 30 min prior to ischemia/reperfusion which was induced by
clamping the celiac artery and the superior mesenteric artery for 30
min and reperfusion for 1 h. Lipid peroxide production, the contents of
glutathione and mucus, and glutathione peroxidase activities of gastric
mucosa were determined. Histological observation of gastric mucosa was
performed by using hematoxylin-eosin staining and scanning electron
microscopy. The result showed that ischemia/reperfusion increased lipid
peroxide production and decreased the contents of glutathione and mucus
as well as glutathione peroxidase activities of gastric mucosa.
Ischemia/reperfusion induced gastric erosion and gross epithelial
disruption of gastric mucosa. Pretreatment of L-arginine, a substrate
for nitric oxide synthase, and sodium nitroprusside prevented
ischemia/reperfusion-induced alterations of gastric mucosa. However,
NG-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor,
deteriorated oxidative damage induced by ischemia/reperfusion. In
conclusion
, nitric oxide has an antioxidant defensive role on gastric
mucosa by maintaining mucus, glutathione, and glutathione peroxidase of
gastric mucosa.