Key result
Animal models demonstrate that gastric mucosal injury from ethanol and aspirin involves rapid vascular damage and hypoxia, whereas duodenal injury is preceded by excess acid and dysmotility.
Population
Animal models and human studies of gastroduodenal mucosal injury
Design
Review
Authors
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Vascular damage may initiate ethanol- and aspirin-induced gastric injury in animals; leaves open translation to human pathogenesis or therapy.
This review reconstructs the pathogenesis of gastroduodenal mucosal injury from animal models to serve as a basis for designing protective drugs.
Sándor Szabó (1987) conducted a review in Gastroduodenal mucosal injury. Ulcerogenic agents (ethanol, aspirin, cysteamine, mepirizole, MPTP) was evaluated on Mechanisms of mucosal injury. Animal models demonstrate that gastric mucosal injury from ethanol and aspirin involves rapid vascular damage and hypoxia, whereas duodenal injury is preceded by excess acid and dysmotility.
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