Gastric mucous barrier

Visible mucus forms the external layer of Hollander s so-called protective gastric mucous barrier (H28-H30). According to him, the internal layer of this barrier consists of the preformed mucosubstances contained within the juxtaluminal portion of the surface epithelial cells themselves. 

Sober H, Hollander F, Sonneblick BP. Response of gastric mucous barrier in pouch dogs to repeated topical application of eugenol. Am J Physiol 162 120-130, 1950. 

In addition, steroid ulcer has been related recently to mucin deficiency caused by this therapy. Menguy and Masters injected steroids into rats with denen ated antral pouches (M28). They found substantially decreased mucus secretion, as well as compositional change of antral mucus characterized by decrease in its sialic acid concentration (Fig. 14). They concluded that the steroids interfered with the rate of the mucous barrier renewal, caused decreased mucus production, and lowered the threshold of gastric mucosal susceptibility to peptic digestion. Robert and his associates studied the relationship of the mucus secretion to the development of ulcers in fasting rats (R7), as well as in those given large doses of steroids (R8). They determined mucus content by quantitation of hexosamine and found decrease in concentration and output in rats who developed ulcers. The latter appeared only in that portion... 

Bromhexine can cause gastrointestinal intolerance and impair the mucous barrier in the stomach it has been suggested it should not be given to patients with gastric ulceration. Reactivation of ulcers has been reported in a few patients, but hematemesis, melena, or other comph-cations have not been described (2). 

Interaction with local tissues. Sucralfate appears to augment the protective function of the mucous-bicarbonate barrier, partly due to increased bicarbonate and mucous secretion, and partly to an interaction with the unstirred layer overlying gastric epithelium, as well as by making the mucous gel more hydrophobic. It binds bile acids and pepsin and adheres to both ulcerated and nonulcerated mucosa. 

Your stomach is made of protein that is not much different from the protein in a hamburger. The inner walls of your stomach are coated by a basic mucous membrane that protects the stomach from the digestive power of the acid and enzymes. If the stomach contents become too acidic, this basic membrane breaks down by acid-base neutralization reactions. At the point where the barrier is neutralized, the gastric juices can begin to digest the protein that makes up the stomach wall, as shown in Figure 15.14. This causes the discomfort of acid indigestion and may cause more serious problems. 

Naive physiologists had long believed that the mucous layer is a barrier to diffusion of acid and pepsin from the gastric contents to the mucosal surface, and therefore prevents attack on the surface by acid and pepsin. Norman Heatley, a junior colleague of Florey in the penicillin work, showed that a static layer of mucus does not inhibit diffusion of acid or pepsin. Heatley s demonstration was made before the discovery of active secretion of bicarbonate by the surface epithelial cells, and the function of the mucous layer as a dynamic entity had to be reevaluated after 1975. 

Components of the gastric barrier. Illustrated is a mucous coat, which acts as an unstirred layer, inhibiting fast diffusion of secreted HCOs" via an apical anion exchanger. The basal-lateral surface has pH regulatory mechanisms, such as sodium proton exchange or sodium-dependent entry of bicarbonate. The necessary Na gradient is driven by the sodium pump, and bicarbonate is formed by the action of carbonic anhydrase (CA). 

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