Experimental studies on the pathophysiology of peptic ulcer disease.
The pathophysiology of clinical peptic ulcer, which is diverse for duodenal, chronic gastric or stress ulcer in humans, has been only partially elucidated by experimental animal studies. A central role of vascular disturbance and acid back diffusion for human stress and animal stress ulcers is evident, whereas a complex and variable set of functional disorders may relate to duodenal ulcer, though the role of acid is paramount. Mucosal resistance factors are of major importance in all types of ulcer and are of particular interest in chronic gastric ulcer. The importance of selecting, for anti-ulcer drug testing, appropriate ulcer models is emphasized, and more extensive use of chronic experimental ulcer healing rate changes, mucus glycoprotein analysis, and cytoprotective changes is recommended. Novel compounds such as pirenzepine, which act on some muscarinic receptors, will help elucidate ulcer pathophysiology as well as provide medical therapy, particularly since all postganglionic vagal transmitter substances in gastric or duodenal mucosae have not yet been identified.
D000818:Animals; D004195:Disease Models, Animal; D005744:Gastric Acid / Q000502:physiology; D005753:Gastric Mucosa / Q000098:blood supply; D006801:Humans; D009093:Mucus / Q000502:physiology; D010437:Peptic Ulcer / Q000503:physiopathology*; D013276:Stomach Ulcer / Q000209:etiology