| Popis: |
Endogenous prostaglandin E2 (PGE2) and prostacyclin produced by the gastric mucosa are thought to protect the stomach against the necrotizing effects of various damaging agents including gastric acid and pepsin [1]. Although gastric mucosal protection has been demonstrated experimentalls, especially in rats [1], its contribution to gastric and duodenal ulcer healing is still unexplored. Acceleration of the ulcer healing process occurs in response to treatment by drugs inhibiting acid and pepsin secretion. However, a number of ulcer-healing substances are effective by some other yet unknown mechanisms because they do not inhibit gastric secretion; among these are carbenoxolone, sucralfate, and tripotassium-dicitrato bismuthate (Table 1). Potential mediators of acid-independent ulcer-healing effects are locally synthesized prostaglandins. It is, therefore, reasonable to review the current knowledge on the role of endogenous prostaglandins in peptic ulcer therapy (Table 2). |
