Prevention of stress-induced erosive gastritis by parenteral administration of arachidonic acid

Stress-induced mucosal ulcerations are associated with a decreased synthesis of mucosal prostaglandin (PG) E₂. This phenomenon is poorly understood. To investigate whether it is due to a decreased availability of the necessary substrates to the mucosa, four groups of 10 Holtzman rats were studied: group 1 received normal saline by intraperitoneal (ip) injection; group 2 also received ip normal saline, then were submitted to stress, by the cold restraint method; group 3 received a solution of arachidonic acid (AA) ip; and group 4 also received ip AA, then were submitted to stress. After sacrifice, the number of gastric ulcerations were counted and specimens of nonulcerated mucosa were assayed for PGE₂ by high-performance liquid chromatography; the mean numbers of ulcers were 0, 5.8, 0.8, and 3 and the mean levels of PGE₂ were 55, 41, 125, and 62 pg/mg of wet tissue for groups 1, 2, 3, and 4, respectively. It is concluded that parenteral administration of AA reduces but does not completely eliminate stress-induced gastric ulcerations and that the stressed animals synthesized half as much PGE₂ as the nonstressed ones after ip administration of equal amounts of AA, suggesting that stress reduces the availability of AA to the gastric mucosa, possibly by vascular spasm.