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1 Tulane University School of Medicine, New Orleans, La.; Southeast Louisiana Hospital, Mandeville, La.
The results of this study indicate that hepatic production of 4-hydroxypropranolol, the active metabolite of propranolol, is not significantly altered in alcoholic patients who have been chronically exposed to alcohol, if the baseline laboratory evaluations are within normal limits. Coltart and Shand3 have demonstrated that the intravenous dose of propranolol required to block a given degree of exercise induced-tachycardia is about three times greater than the oral dose. This finding suggested that an active metabolite of propranolol, 4-hydroxypropranolol, is formed in the liver after oral administration. It should be specifically noted that 4-hydroxypropranolol, a beta-adrenergic blocker, can be detected only after oral administration, and not after intravenous administration.3
The statistical analysis of data from the three measures used to evaluate clinical effectiveness of propranolol yielded conflicting results. The fact that there was statistically significant improvement in the global ratings of the propranolol group at the 0.05 level, as determined by an experienced psychiatrist who was "blind" as to which groups the subject belonged, is provocative enough to warrant further study of the potential anti-anxiety activity of propranolol. It must also be noted that in different circumstances where other therapies are not as effective as they were in the setting of the present study, propranolol may significantly reduce anxiety.
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