[Microcirculation of gastric mucosa in pathogenesis of stomach ulcer]

During the last decade, evidence increased that microcirculatory disorders play a pivotal role in the development of mucosal injury, and, hence, formation of gastric ulcer. Mucosal microcirculation is altered at least by two distinct mechanisms: Stimulation of acid secretion leads to a rise of blood flow in the acid-secreting areas, and, concomitantly, due to a steal-phenomenon to a decrease of mucosal capillary perfusion of the antrum, which results in temporary ischemia. In addition, surface noxae-induced release of potent mediators, such as histamine, leukotrienes, thromboxane, platelet-activating factor and reactive oxygen metabolites cause vasoconstriction, capillary stasis and increase of microvascular permeability (loss of endothelial integrity), which aggravate mucosal injury. Therefore, therapeutic strategies should consider leukotriene-synthesis inhibitors, histamine-, thromboxane- and platelet-activating factor receptor antagonists, oxygen radical scavengers, as well as counteracting mediators and hormones, such as prostaglandins and somatostatin, inasmuch as these compounds have been shown to additionally prevent mucosal microvascular injury, in particular capillary perfusion failure and loss of endothelial integrity, during gastric ulcer formation.