HUMAN GASTRIC ALCOHOL-DEHYDROGENASE - ITS INHIBITION BY H2-RECEPTOR ANTAGONISTS, AND ITS EFFECT ON THE BIOAVAILABILITY OF ETHANOL

被引：131

作者：

HERNANDEZMUNOZ, R

CABALLERIA, J

BARAONA, E

UPPAL, R

GREENSTEIN, R

LIEBER, CS

机构：

[1] BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151G,130 W KINGSBRIDGE RD,BRONX,NY 10468

[2] CUNY MT SINAI SCH MED,CTR ALCOHOL RES & TREATMENT,NEW YORK,NY 10029

来源：

ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH | 1990年 / 14卷 / 06期

关键词：

alcohol dehydrogenase; Ethanol pharmacokinetics; First pass metabolism; H[!sub]2[!/sub]‐receptor antagonists; Stomach;

D O I：

10.1111/j.1530-0277.1990.tb01843.x

中图分类号：

R194 [卫生标准、卫生检查、医药管理];

学科分类号：

摘要：

Two types of alcohol dehydrogenase isoenzymes (differing in their affinity for ethanol, sensitivity to 4‐methylpyrazole, and electrophoretic migration) have been identified in the human stomach. At the high ethanol concentrations prevailing in the gastric lumen during alcohol consumption, the sum of their activities could account for significant oxidation of ethanol. In vitro, these activities were inhibited by cimetidine and ranitidine, but not by famotidine. In vivo, therapeutic doses of cimetidine (but not of famotidine) increased blood ethanol levels when ethanol was given orally, but not when it was given intravenously, indicating a significant contribution of the gastric ADH to the bioavailability and thereby the potential toxicity of ethanol. Copyright © 1990, Wiley Blackwell. All rights reserved

引用

页码：946 / 950

页数：5

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