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Psychosomatic Medicine 28:564-569 (1966)
© 1966 American Psychosomatic Society
1 Biochemical Research Section, Department of Psychiatry and the State University Alcoholism Clinic, State University of New York, Downstate Medical Center, Brooklyn, New York.; Present address: Psychiatry and Aging Research Laboratories, Veterans Administration Hospital, Albany, N.Y.
2 Biochemical Research Section, Department of Psychiatry and the State University Alcoholism Clinic, State University of New York, Downstate Medical Center, Brooklyn, New York
3 Biochemical Research Section, Department of Psychiatry and the State University Alcoholism Clinic, State University of New York, Downstate Medical Center, Brooklyn, New York.; Present address: Department of Entomology, College of Agriculture, University of Arizona, Tucson, Ariz.
Previous studies in alcoholic patients and normal control subjects demonstrated a characteristic increase in urinary tryptamine after acute ingestion of ethanol. This response could be attributable only in part to monoamine oxidase (MAO) inhibition, verified by in vitro experiments. Evidence for an amine-releasing action of ethanol (suggestive but not conclusive in man) indicated a possible mechanism to account for this discrepancy. Other studies, conducted separately on a similar population, indicated activation of adrenocortical function by acute ingestion of ethanol. Similarly, activation of the sympathoadrenal system was suggested by increased excretion of epinephrine after ethanol. Present experiments were done to explore the possibility of adrenal activation being related to increased amine excretion seen with tryptamine after ethanol. Patients injected with 100-mg. hydrocortisone failed to show any demonstrable changes in urinary amines. Injection of epinephrine was followed by changes in urinary amines similar to those found with ethanol. These preliminary findings suggest further approach to question of amine-releasing action of ethanol.
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