Gastric Ulcer Literature Review

REVIEW OF LITERATURE
2. 1. Gastric acid
A great deal has been learned about the pathogenesis of gastric ulcer over the past two decades, as a result of the painstaking efforts of inspired researchers. In an attempt to protect the gastric mucosa from gastric acid, enhance ulcer healing, and prevent ulcer recurrence, pharmacological control of gastric acid secretion has long represented a desirable goal (Aihara et al., 2003;Tuorkey and bdul-Aziz, 2009;Tuorkey and Karolin, 2009b). Since, gastric acid hypersecretion is one of the major pathogenic factors for the induction of gastric ulcer disease. Furthermore, luminal acid interferes with the process of restitution, resulting in the conversion of superficial injury to deeper mucosal lesion and inactivates the acid-labile growth factors important for maintenance of mucosal integrity and repair of superficial injury (Wallace and Muscara, 2001). Impairment of gastric ulcer healing depends upon the increased

Since, histamine may cause increase in gastric mucosal permeability to electrolytes and renders the stomach more susceptible to acid-induced damage (Gislason et al., 1995). The role of histamine in the secretion of reported (Tairov et al., 1983;Tairov et al., 1984;Norlen et al., 2000). Where, histamine activates histamine-2 receptors on the acid-producing parietal cells to stimulate acid production, the over production of acid inhibits through low antral pH gastrin release from G-cells, thus preventing the stimulatory effect of gastrin on entero chromaffin-like (ECL) cells and further histamine release (El-Omar et al., 1997). This inhibitory control is mediated via the release of somatostatin from D-cells situated acid from acid-producing parietal cells is widely in close proximity to the G-cells. The mechanism of stimulating and inhibiting acid production in the