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1997 Abstract: 134 Role of gastric mucosal energy metabolism and lipid peroxidation in the pathogenesis of acute gastric mucosal lesions induced by water immersion and restraint stress in obstructive jaundice in rats.

Abstracts
1997 Digestive Disease Week

Role of gastric mucosal energy metabolism and lipid peroxidation in the pathogenesis of acute gastric mucosal lesions induced by water immersion and restraint stress in obstructive jaundice in rats.

I Sasaki, H Naito, Y Funayama, K Fukushima, W-M Shian, T Masuko, S Matsuno. The First Department of Surgery, Tohoku University School of Medicine, Sendai, Japan.


Backgrounds: It is well known that in patients with obstructive jaundice acute gastric ulceration tend to develop under some kind of stress such as surgical operations. However, little has been known about the mechanism. Although we previously reported that gastric mucosal ulceration were easily induced and gastric mucosal potential difference decreased by stress in rats with jaundice by stress (Tohoku J. Exp. Med., 1987; Scand. J. Gastroenterol., 1989), the precxise mechanism of the pathogenesis has been obscure. Aim: In this study we investigated that role of gastric mucosal energy metabolism and lipid peroxidation in the generation of acute gastric mucosal lesions in rats with obstructive jaundice. Materials and Methods: 240 SD rats were randomly divided into two groups as follows; control group (simple laparotomy) and jaundiced group (cut and ligation of common bile duct). Two weeks after the operation, water-immersion and restraint stress procedure (WIRS) was performed in these groups. The gravity of acute gastric ulceration was calculated by ulcer index. Gastric mucosal blood flow was measured using hydrogen clearance technique. Gastric mucosa was obtained by stop freeze method (Menguy 1974) and energy charge was detected. Gastric mucosal phosphatidylcholine hydroperoxide (PCOOH) was measured by sensitive and selective assay for phospholipid hydroperoxides using high performance liquid chromatography combined with chemiluminescence detection (Miyazawa, 1993,1994). Glutathion levels of both the liver and gastric mucosa were measured by Akerboom's method. Reduced glutathion (600mg/Kg) was intraperitoneally administrated 15 min. before WISR. Results: The jaundiced group showed significantly higher ulcer index and early significant decrease of gastric mucosal blood flow after the stress. Energy charge of gastric mucosa was significantly reduced in jaundiced group after the stress. Glutathion levels in both gastric mucosa and the liver were significantly lower in jaundiced group than that in control group both before and after the stress. The values of PCOOH in gastric mucosa were significantly higher in jaundiced group than that in control group both before and after stress. Pretreatment of reduced glutathion increased glutathion level of gastric mucosa and decreased both ulcer index and PCOOH levels of gastric mucosa after the stress. Conclusion: Reduction of gastric mucosal blood flow induced by WIRS may easily cause both impairment of energy metabolism and lipid peroxidation in gastric mucosa in rats with obstructive jaundice, which may play an important role in the pathogenesis of acute gastric ulceration.




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