Pathophysiology of the gastric microcirculation

Abstract

Mucosal blood flow performs an extremely important role in microcirculation wherein alterations necessarily lead to severe gastric and duodenal mucosal lesions. The removal of back-diffused H+ ions through the adaptation of microcirculatory flow represents a valid defence mechanism. The blood flow's inability to contain H+ back-diffusion lies at the bottom of rapid-onset acute mucosal lesions; moreover, it probably contributes to the onset of chronic ulcer in certain areas already precariously supplied, because of the breakdown of the mucosal barrier or a further reduction in blood supply. Portal hypertension leads to altered blood flow in the gastric microcirculation. This haemo-dynamic condition brings about a series of endoscopically evident changes which are probably a consequence of the conspicuous increase in mucosal and submucosal vascular area. This haemodynamic situation may be an aetiopatho-genetic factor in the cirrhotic subject's marked sensitivity to gastric mucosal damage.