Cold restraint stress-induced gastric mucosal dysfunction : Role of Nitric oxide

• Published in: Digestive diseases and sciences 1996-05, Vol.41 (5), p.956-963
• Main Authors: COSKUN, T, YEGEN, B. C, ALICAN, I, PEKER, Ö, KURTEL, H
• Format: Article
• Language: English
• Subjects: Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Cell Membrane Permeability - drug effects; Cold Temperature - adverse effects; Edetic Acid - pharmacokinetics; Enzyme Inhibitors - pharmacology; Female; Gastric Mucosa - drug effects; Gastric Mucosa - physiopathology; Gastroenterology. Liver. Pancreas. Abdomen; Male; Medical sciences; NG-Nitroarginine Methyl Ester; Nitric Oxide - physiology; Other diseases. Semiology; Peroxidase - drug effects; Peroxidase - metabolism; Rats; Rats, Sprague-Dawley; Restraint, Physical; Stereoisomerism; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Stress, Physiological - etiology; Stress, Physiological - physiopathology
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1007/BF02091537

The objectives of this study were to determine the cold restraint stress-induced changes in gastric mucosal permeability and to assess whether nitric oxide synthesis inhibition affects gastric mucosal integrity after cold-restraint administration. Cold-restraint stress caused multiple gastric lesions in 90% of animals. The lesion index was found to be 3.87 +/- 0.97 mm. Gastric mucosal permeability to the [51CR]EDTA molecule was significantly elevated in the cold-restraint group compared to control. In order to evaluate the role of nitric oxide in cold restraint stress-induced gastropathy, L-arginine analog NG-nitro-L-arginine methyl ester (L-NAME) was given as a bolus (10 mg/kg, intravenously) and infused at a rate of 2 mg/ml/hr for 2 hr after cold-restraint administration. L-NAME greatly exacerbated gastric mucosal dysfunction associated with cold-restraint stress. D-NAME, the biologically inactive enantiomer, did not enhance mucosal dysfunction, whereas L-arginine, the substrate for nitric oxide, reversed the effect of L-NAME. In an additional group of experiments, effects of cold-restraint stress and L-NAME on net transmucosal fluid flux as well as tissue myeloperoxidase activity (MPO) were assessed. Cold-restraint stress administration significantly reduced the absorptive capacity of stomach, whereas L-NAME treatment did not affect the stress-induced alterations on net fluid absorption. Furthermore, L-NAME treatment did not affect the cold restraint stress-induced changes in tissue MPO activity. Our results suggest that gastric barrier function is altered after cold-restraint stress and nitric oxide production is important in minimizing mucosal barrier dysfunction associated with cold-restraint stress administration. Our results also indicate that L-NAME-induced alterations on mucosal permeability are not related to net transmucosal fluid flux and tissue neutrophils.