Protective mechanism of nitric oxide and mucus against ischemia/ reperfusion-induced gastric mucosal injury

H. Kim, K. Nam, Hwan Kim Kyung Hwan Kim

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Abstract

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 N(G)-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, N(G)-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.

Original languageEnglish
Pages (from-to)511-519
Number of pages9
JournalKorean Journal of Physiology and Pharmacology
Volume2
Issue number4
Publication statusPublished - 1998 Jan 1

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Mucus
Gastric Mucosa
Reperfusion
Stomach
Nitric Oxide
Ischemia
Wounds and Injuries
Glutathione Peroxidase
Glutathione
Lipid Peroxides
NG-Nitroarginine Methyl Ester
Nitroprusside
Nitric Oxide Synthase
Arginine
Celiac Artery
Superior Mesenteric Artery
Nitric Oxide Donors
Hematoxylin
Eosine Yellowish-(YS)
Constriction

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology

Cite this

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abstract = "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 N(G)-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, N(G)-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.",
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Protective mechanism of nitric oxide and mucus against ischemia/ reperfusion-induced gastric mucosal injury. / Kim, H.; Nam, K.; Kyung Hwan Kim, Hwan Kim.

In: Korean Journal of Physiology and Pharmacology, Vol. 2, No. 4, 01.01.1998, p. 511-519.

Research output: Contribution to journalArticle

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