Ranitidine increases the bioavailability of imbibed alcohol by accelerating gastric emptying.

To investigate the mechanism of the increase in alcohol bioavailability by ranitidine, we determined by nuclear scan the changes in gastric emptying of a 10% ethanol solution (containing 0.3 g ethanol/kg body weight and 300 microCi of technetium-labeled diethylene triamine pentacetic acid) in 8 normal men, before and after treatment with 300 mg ranitidine orally each evening for 1 week. We compared these changes with those of ethanol bioavailability, calculated by integration of the Michaelis-Menten function over the entire alcohol curves after random i.v. and, on a separate day, oral administration of the same ethanol dose, pre- and post-ranitidine. With ranitidine, we found an acceleration of gastric emptying in 7 of 8 subjects, with 20% shortening of the time to 50% emptying (51.8 +/- 4.1 min vs 64.3 +/- 3.4, without ranitidine; P < .001 by paired t test). Despite the disappearance (from the stomach) of most of the dose by the end of the blood alcohol curves, only 83 +/- 4% reached the systemic blood vs 64 +/- 4% without ranitidine (P < .02), most likely because of a shortened exposure of alcohol dehydrogenase to optimal ethanol concentrations. As a result, after oral but not intravenous alcohol administration, ranitidine increased blood alcohol concentrations (29 +/- 4 mg/dl vs 22 +/- 3, without ranitidine; P < .02), with a corresponding decrease in first pass metabolism of ethanol from 107 +/- 16 mg/kg to 47 +/- 16 (P < .01).