Gastric mucosal defence mechanisms.
Gastric mucosa has a particular ability to resist acid/peptic digestion. The nature of the presumed barrier to acid and pepsin has been elusive but recent work suggests that a combination of mechanisms is likely to be involved. Amongst these the mucus gel layer combined with secretion of alkali by the surface epithelium is likely to form a first line defence. The demonstration of a pH gradient within the mucus gel layer supports such a hypothesis. Agents which damage the mucosa such as aspirin and bile salts inhibit the maintenance of the pH gradient allowing the luminal surface of the epithelium to become more acid. Prostaglandins enhance this pH gradient, an observation which may be relevant to the protective properties of prostaglandins. This alkaline zone can be compromised by high levels of luminal acidity and it thus has a limited capacity to prevent acid reaching the mucosa. The local microcirculation is of importance in maintaining surface epithelial metabolic integrity and interstitial fluid bicarbonate may be important in neutralising any acid which may reach the subepithelial layers. This may in part explain the ability of an actively secreting gastric epithelium to resist damage to a greater extent than a resting mucosa. Recent exciting work has focussed on the ability of gastric epithelium to reform by a process which has been termed restitution, after acute mucosal damage. This process appears to be rapid and occurs within an hour or so. Repeated rapid repair may be a common occurrence in the maintenance of mucosal integrity. Finally, it has been proposed that a hydrophobic property of surface epithelium in the stomach may be relevant to mucosal protection.
D000222:Adaptation, Physiological; D001639:Bicarbonates / Q000378:metabolism; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000502:physiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D009093:Mucus / Q000502:physiology
D001639:Bicarbonates