[Cardiovascular and metabolic changes in the antabuse-alcohol reaction: basis for the diagnosis of degree of severity].

The clinical symptoms and signs, certain metabolic aspects (including ethanol, acetaldehyde and glucose concentrations in plasma) and hemodynamic parameters (cardiac rate, blood pressure and cardiac output) were assessed in 16 ambulatory alcoholics (3 female, 13 male, average age 46 years) following pretreatment with disulfiram (total dose 1.2 to 2.4 g) and oral administration of 0.2 g ethanol 94% per kg body weight. Since the only selection criterion for inclusion was a diagnosis of alcohol dependence (DSM III, 303.9), the group was heterogeneous and exhibited a variety of concomitant diseases such as alcoholic liver disease in 9, chronic bronchitis in 5 and arterial hypertension in 3. Whereas peak plasma alcohol concentrations were comparable (median: 0.33 mg/ml; range: 0.19 to 0.40) in all subjects, peak acetaldehyde levels varied over 40-fold (median 5.1 micrograms/ml; range: 0.2 to 8.8). In consequence, there were marked interindividual differences in cardiovascular reaction, in contrast to the virtually constant finding of flush, palpitations and dyspnoea. Since the decrease in peripheral vascular resistance (to a median of 46% of control) was only in part compensated by increased cardiac output (median: 161%), both systolic and diastolic blood pressures were reduced by 30 and 45 mm Hg respectively. In 4 patients systolic pressure fell to shock levels (less than 70 mm Hg). The presumed toxic effect of acetaldehyde is again supported by close correlations between acetaldehyde plasma concentrations and the changes in blood pressures and peripheral resistances. We were able to demonstrate that disulfiram-induced inhibition of hepatic microsomal function - measured with the aminopyrine breath test - predicts the expected acetaldehyde peak levels following ethanol administration.(ABSTRACT TRUNCATED AT 250 WORDS)