Gastroduodenal mucus is present as a water insoluble gel adherent to the mucosal surface and as a viscous mobile solution in the lumen. The protective properties of the mucus against acid (with bicarbonate), pepsin (diffusion barrier) and mechanical damage depend on the quality (structure) and quantity (thickness) of the adherent mucus gel layer. Adherent mucus is a viscoelastic gel which is 95 (v/v) water. It is permeable to ions and smaller molecules (Mrc. 1000), but is impermeable to large proteins (Mr,c. 17,000) including pepsins. However, mucus is solubilized rapidly by pepsin, more slowly (>-1 h) by thiol agents, and is unchanged following exposure to bile, acid and ethanol (<40). Glycoprotein macromolecules (Mr≥2×106) are the structural components of the mucus gel and have a polymeric, structure of glycoprotein subunits (Mrc. 5×105, for gastric mucus) joined by disulphide bridges between their protein cores. This glycoprotein polymerization, which is essential for gel formation and hence function, is the site of action of proteolytic enzymes and thiol agents. The glycoprotein polymeric structure is deficient in antral mucus from patients with peptic ulcer disease.In vivo, adherent mucus forms a thin but continuous cover of variable thickness (50–450 μm in man, about two-fold less in rat) over the gastroduodenal mucosa. Pepsin in gastric juice will rapidly dissolve this mucus cover and can be active up to luminal pH values of 5. Mucus erosion by pepsin or by abrasion must be balanced by its secretion. Prostaglandins and carbachol stimulate a rapid increase (within minutes) in mucus thickness of up to two-fold. Soluble luminal mucus can be increased by mucus secretagogues, mucosal damaging agents, or peptic degradation of adherent mucus. Increases in luminal mucus can occur independently of increased gel thi
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