Arachidonic acid protection of rat mucosa against stress ulceration.
To evaluate the effect of arachidonic acid (AA), a prostaglandin precursor, on the mucosal level of PGE2 and its possible protective role against stress ulcerations, 40 Holtzman rats were divided into four groups: Group I intragastrically receiving 1 ml of normal saline (NS); Group II, NS pretreatment followed by stress; Group III, intragastric AA pretreatment without stress; and Group IV, intragastric AA followed by stress. AA was administered as a 120 mM solution in a nonionic detergent, adjusted to a pH of 8.0. Stress was provided by the cold-restraint method. After sacrifice, the number of gastric mucosal ulcerations were counted. Specimens of nonulcerated mucosa were assayed for PGE2 by derivatization with panacyl bromide and by using high-performance liquid chromatography. The animals in Groups I, III, and IV developed no gastric ulcerations and their mucosal prostaglandin E2 remained at a normal level, while those in Group II had a significant reduction of mucosal PGE2 (P less than 0.05) and a significantly increased number of gastric ulcerations (P less than 0.002). These data indicate that stress-induced mucosal ulcerations are associated with significant decreases in the gastric mucosal levels of PGE2. Intragastric administration of arachidonic acid prevents the formation of stress mucosal ulcerations and maintains a normal level of mucosal PGE2.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology*; D003080:Cold Temperature; D015232:Dinoprostone; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007103:Immobilization; D011458:Prostaglandins E / Q000378:metabolism*; D051381:Rats; D013276:Stomach Ulcer / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013312:Stress, Physiological / Q000378:metabolism* / Q000473:pathology
D001095:Arachidonic Acids; D011458:Prostaglandins E; D015232:Dinoprostone