Gastric Microcirculatory Changes Associated with Physicochemical and Ionic Mediators
The mechanism of stress-induced acute gastric mucosal lesions (AGML) has been investigated for some time. We have reported that in hemorrhagic shock, the decrease of gastric mucosal blood flow, volume, and its oxygenation precedes the gastric ulceration which appears usually after infusion of blood or at the recovery stage in rats and humans. It is believed that the microcirculatory disturbance resulting in hypoxia in the gastric mucosa produced an incipient mucosal state for ulcerogenesis and that in this hydrochloric acid and histamine played an aggressive role. The precise mechanism leading to cell death after ischemia is, however, obscure. In this symposium, we presented a movie film which showed the process of gastric mucosal microcirculatory disturbance and bleeding caused by indomethacin, leukotriene C4 (LTC4), platelet-activating factor (PAF) and HCI and also reported the role of chemical and ionic factors in the repefusion state in the etiology of gastric ulceration.
KeywordsGastric Mucosa Calcium Antagonist Hemorrhagic Shock Lipid Peroxide Level Mucosal Blood Flow
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