Studies on the mechanism of ethanol-induced gastric damage in rats
| Autor: | Peter J. Oates, John P. Hakkinen |
|---|---|
| Rok vydání: | 1988 |
| Předmět: |
Male
Pathology medicine.medical_specialty Methysergide Hyperemia Constriction Pathogenesis chemistry.chemical_compound Phentolamine medicine Animals Mast Cells Cimetidine Leukotriene Ethanol Hepatology business.industry Stomach Gastroenterology Videotape Recording Rats Vasodilation Nordihydroguaiaretic acid medicine.anatomical_structure chemistry Gastric Mucosa Vasoconstriction cardiovascular system business circulatory and respiratory physiology medicine.drug |
| Zdroj: | Gastroenterology. 94:10-21 |
| ISSN: | 0016-5085 |
| DOI: | 10.1016/0016-5085(88)90604-x |
| Popis: | Concentrated ethanol causes gastric lesions by a mechanism that is poorly understood. We have investigated this mechanism in the rat stomach via gross morphologic, videomicroscopic, histochemical, and pharmacologic approaches. Within 1 min of contact, ethanol caused diffuse mucosal hyperemia. By 5 min, hyperemia greatly intensified at some mucosal sites. Beneath sites where mucosal hyperemia developed, intramural venules strongly constricted at 3-13 s postethanol, whereas submucosal arterioles dilated more than two times in diameter by 25 s. Submucosal venular constriction began sooner than arteriolar dilation (9 vs. 16 s, p less than 0.05). One-third of the gastric mucosal mast cells degranulated by 15 s postethanol; 50% discharged by 30 s. Ethanol-induced hyperemia was markedly reduced by lipoxygenase-selective inhibitors BW755C or nordihydroguaiaretic acid, or by the H1-antihistamine pyrilamine, but not by indomethacin, cimetidine, phentolamine, or methysergide. Based on these results, a model for the pathogenesis of ethanol-induced gastric lesions is proposed. |
| Databáze: | OpenAIRE |
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