Mucus and bicarbonate combine to neutralize gastric acid at the gastric mucosal surface. Both are secreted by the surface mucous cells and by mucous neck cells located in the acid-secreting portion of the stomach and the antrum. The mucus is a viscoelastic gel that contains approximately 85% water and 15% glycoproteins and provides a mechanical barrier to injury by contributing to the unstirred layer of water found at the luminal surface of the gastric mucosa. It provides some impediment to ion movement from the lumen to the apical cell membrane and is relatively impermeable to pepsins. It is also in a constant state of flux because it is secreted continuously by mucosal cells on the one hand and solubilized by luminal pepsin on the other. Vagal stimulation, cholinergic agonists, prostaglandins, and some bacterial toxins stimulate mucus production, whereas anticholinergic drugs and nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit its secretion. H. pylori, however, secretes various proteases and lipases, which break down mucin that impairs the protective function of the mucous layer.
In the acid-secreting portion of the stomach, bicarbonate secretion is an active process, whereas in the antrum, both active and passive secretion of bicarbonate occur. It is noteworthy that the magnitude of bicarbonate secretion is considerably less than that of acid secretion, yet although the luminal pH is 2, the pH observed at the surface epithelial cell layer is usually 7.1 ' The pH gradient found at the epithelial surface is the result of the aforementioned unstirred layer of water contained within the mucous gel and to the continuous secretion of bicarbonate by the surface epithelial cells. Gastric cell surface pH remains greater than 5 until the luminal pH is less than 1.4. However, the luminal pH in duodenal ulcer patients is frequently less than 1.4, so the cell surface is exposed to lower pH in these patients. This reduction in pH may reflect a reduction in gastric bicarbonate secretion as well as decreased duodenal bicarbonate secretion and may explain why some duodenal ulcer patients have a higher relapse rate following treatment. Gastric Barrier Function and Peptic Ulcer Disease
Gastric barrier function depends on a number of physiologic and anatomic factors. These include, but are not limited to, cell membranes, tight junctions, cell renewal
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