Mechanisms of XXXX in the stomach and duodenum: time-sequence analysis of morphologic, functional, biochemical and histochemical studies.

@entity5212 @entity1 @entity548 @entity1819 @entity167 @entity6672 @entity117 @entity1066 @entity39 @entity8488 @entity3157 @entity1504 @entity519 @entity4423 @entity1068 @entity3137 @entity9317
This review is based on results from our laboratory and those published by others, and is focused on the early stages of pathogenesis that can be studied mostly in animals. @entity1819 is analysed on the examples of @entity1068 - and @entity117 -induced lesions. @entity1068 (50-100%) rapidly penetrates the mucosa, causes directly and/or indirectly (e.g., release of vasoactive products) endothelial damage in superficial and deep capillaries and venules. The @entity1504 results in increased vascular permeability and decrease in blood flow leading to complete circulatory standstill in superficial capillaries 1-2 min after intragastric administration of concentrated @entity1068 . The direct chemical damage to surface mucosal epithelium is then followed by @entity519 and @entity548 in 1-5 min (erosion or @entity1066 ). Unionized @entity117 initiates a similar and complex yet slower progressing and less extensive erosion than @entity167 . @entity9317 and @entity1066 produced by @entity8488 , @entity6672 or @entity5212 are preceded by excess acid in the proximal duodenum. This could be due to increased gastric acid output (1-4 hr), decreased @entity3157 secretion or duodenal @entity4423 (0.5-8 hr) preventing the proper mix of acid and base in duodenal bulb. @entity39 and desquamation of absorptive cells in duodenal villi are evident 2-4 hr, followed by villus amputation (4-8 hr), erosion and @entity1066 (8-24 hr). The pathogenesis of @entity3137 can thus be reconstructed from results obtained with animal models and from @entity1 studies. The results should serve as a basis to design protective drugs that are active on the basis of pathogenetic events.
