Morphological and functional gastric cytoprotection by prostaglandin in rats receiving absolute ethanol orally.

Abstract

Pretreatment with prostaglandins at non-antisecretory doses protects the gastric mucosa, including the parietal cells, from deep necrosis produced by intragastric administration of necrotising agents such as absolute ethanol. Whether the parietal cells also retained their ability to secrete acid when rats were pretreated with a prostaglandin, in spite of exposure to ethanol, was investigated. Gastric acid secretion was abolished 4 hours after ethanol, and secretion returned to control values only after 5-6 days. Pretreatment The aims of the present studies were to determine whether (a) the secretory impairment is due to the extensive damage to the parietal cells produced by ethanol, and (b) dmPGE2 maintains the acid secretory function of the parietal cells by preserving their morphological integrity. The time course of secretory and morphological (histological) changes induced by ethanol in control and prostaglandin-pretreated animals was also determined to establish a correlation between the structure and function of parietal cells. To this end, gastric acid secretion and histological injury were measured at various times after oral administration of absolute ethanol in rats, with and without pretreatment with dmPGE2 given at cytoprotective doses (that is non-antisecretory doses). The changes in secretion were correlated with the extent of gastric damage assessed by quantitative histology. These experiments were conducted in rats whose stomach was stimulated to secrete by either carbachol, pentagastrin, histamine, or vagal electrical stimulation. MethodsMale and female Sprague-Dawley rats of 220-320 g were fasted for 24 hours. During the last 18 hours, they were placed in individual cages to prevent coprophagy, and drinking water was removed. In the gastric secretory studies, gastric juice was collected from conscious and anaesthetised rats. In conscious animals, gastric secretion was collected after pylorus ligation and carbachol stimulation, a procedure that yields large amounts of acid. Anaesthetised rats with gastric fistulas were also used because the basal values being very low, individual secretagogues acting by different mechanisms (histamine, pentagastrin, vagal, electrical stimulation) can be studied separately. These studies were approved by the Animal Welfare Committee.

Association of Helicobacter pylori infection with lifestyle, chronic disease, body-indices, and age at menarche in Danish adults

“…Regular intake of alcoholic beverages was associated with lower rates of H. pylori infection; a finding which is in agreement with previous studies on H. pylori infection (7,52,53), peptic ulcer occurrence (45,54,55), and ulcer healing (54,56). Long-term alcohol consumption may lead to atrophic gastritis, which is known to impair the adhesion of H. pylori to the gastric epithelium (57,58).…”

Mechanisms of gastroprotection by lansoprazole pretreatment against experimentally induced injury in rats: role of mucosal oxidative damage and sulfhydryl compounds

“…Moreover, lansoprazole blocked the oxygen-derived free radical output from neutrophils activated by Helicobacter pylori (Suzuki et al, 1995) and reverted the increase in plasma levels of peroxidated lipids in patients with duodenal ulcer (Manjari and Das, 1998). However, polymorphonuclear infiltration does not seem to occur early after ethanol administration (Robert et al, 1992), and in the present study, the examination of gastric mucosa, 90 min after intraluminal ethanol-HCl injection, did not reveal a significant number of infiltrating polymorphonuclear cells. Overall, in our experimental model, the antioxidant action of lansoprazole against oxygen radicals generated during inflammatory processes (Suzuki et al, 1995) does not appear to be the major mechanism accounting for gastroprotection.…”

Influence of gender difference and gastritis on gastric ulcer formation in rats

“…In addition, PGE 2 , a substance closely related to mucus production 34 and mucosal gel thickness, 35 and plays an important role in gastric cytoprotection, 14,36 was also found to be indifferent between the treatment groups just before ulcer induction (Table 4). However, the higher PGE 2 level found in the female gastritis rats could lead to a lesser ulcer formation in that treatment group, when compared to the corresponding male treatment groups (Fig.…”