乙醇引起的胃黏膜损伤与胃黏膜对乙醇的氧化作用无关。
Gastric mucosal oxidation of ethanol is not involved in ethanol-induced mucosal damage.
作者信息
Puurunen J, Laitinen L A
出版信息
Toxicol Lett. 1982 Dec;14(3-4):195-200. doi: 10.1016/0378-4274(82)90051-0.
The involvement of gastric mucosal metabolism of ethanol in ethanol-induced mucosal damage was studied in urethane anaesthetised rats. Pyrazole, an inhibitor of alcohol dehydrogenase (ADH), slightly aggravated the mucosal lesions produced by intragastric instillation of 30% (v/v) ethanol, but had no effect on increased mucosal permeability to ions, pepsinogen and fluid output or on gastric mucosal blood flow associated with mucosal injury. Induction of ADH by ethanol pre-treatment had no effect on the above-mentioned parameters. Intragastric instillation of acetaldehyde, the product of ethanol oxidation, did not cause lesions in the gastric mucosa. The results suggest that the gastric mucosal toxicity of ethanol may not be related to its metabolism in the gastric mucosa.
在氨基甲酸乙酯麻醉的大鼠中研究了乙醇的胃黏膜代谢在乙醇诱导的黏膜损伤中的作用。吡唑，一种酒精脱氢酶（ADH）抑制剂，略微加重了通过胃内灌注30%（v/v）乙醇产生的黏膜损伤，但对黏膜对离子、胃蛋白酶原的通透性增加以及液体输出或与黏膜损伤相关的胃黏膜血流量没有影响。乙醇预处理诱导ADH对上述参数没有影响。胃内灌注乙醛，乙醇氧化的产物，不会引起胃黏膜损伤。结果表明，乙醇的胃黏膜毒性可能与其在胃黏膜中的代谢无关。
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