The Relationship Of Heme Oxygenase-1 And Gastric Mucosal Lesions In Portal Hypertensive Rats

Portal hypertensive gastropathy(PHG) is now recognized as a clinical entity that is found frequently in patients with portal hypertension. The pathogenesis of portal hypertensive gastropathy is not clearly defined. Morphologic studies have demonstrated that the gastric lesions are characterized by pronounced dilatation of mucosal and submucosal blood vessels. In experimental models of chronic portal hypertension, both dilatation of mucosal vessels and increased gastric mucosal blood flow have been observed. The mechanisms underlying gastric hyperemia in portal hypertension are not clearly understood but are thought to be either part of the overall splanchnic vasodilatation or a consequence of local gastric vascular alteration. Most of the scientist thought that there had been many explainations for the pathogenesis of PHG. Over-production of glucagons, prostaglandin, and nitric oxide (NO) in the gastric mucosa may contribute to hyperdynamic circulation, especially NO. Increased NO production has also been implicated in the pathogenesis of PHG as it is a potent vasodilator, and increased levels have been described in cirrhosis. Specifically, increased serum NO levels have been described in patients with PHG. Furthermore, those with PHG...