Gastric mucosal barrier damage

The discovery, in 1979, by Robert [123] of the remarkable ability of prostaglandins (PG) to increase the resistance of the gastric mucosa to damage started research on the role of defensive factors, such as the mucus-bicarbonate barrier, mucosal blood flow, neutralization of free radicals, stabilization of lisosomal membranes or nitric oxide on the gastric mucosal integrity. 

Aspirin and alcohol can damage the mucosal lining of the stomach, one measure of the injury being a fall in the gastric potential difference. Once the protective mucosal barrier is breached, desquamation of the cells occurs and damage to the capillaries follows. Aspirin causes a marked prolongation in bleeding times, and this can be increased by alcohol.The total picture is complex. 

In recent years, infection of the stomach with Helicobacter pylori which disrupts the normal inhibitory control for acid secretion resulting in excess acid destroying the mucosal barrier has been understood to be the main cause of gastric ulcers [147]. Excessive acid secretion in the stomach and reduction in gastric mucosal blood flow are considered responsible for ulcer formatimi. The colonization of H. pylori in the stomach is associated with a phospholipase likely to damage the protective layer of stomach. H. pylori thrives in the stomach by producing the enzyme urease. 

Electron microscopic studies of gastric mucosa damaged by barrier-breaking compounds provided anatomical evidence of increased mucosal permeability, for they all showed initial damage to surface epithelial cells and eventual erosion of gastric pits. " ... 

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