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.