Abstract

We studied the potential contribution of acetate to the cardiovascular effects of ethanol in 12 healthy male volunteers. Sodium acetate, or sodium chloride in control experiments, was infused i.v. at the rate of 0.033 mEq/kg/min for 60 min. Left ventricular function was examined by M-mode echocardiography and systolic time intervals during infusion and for 60 min thereafter. Blood acetate rose during infusion from 0.19 +/- 0.02 (mean +/- SEM) to a maximum of 0.99 +/- 0.08 mmol/liter. Changes in serum free fatty acids, glycerol, and ketone bodies indicate that acetate inhibited peripheral lipolysis. The volume of urine excreted during the acetate experiment (305 +/- 37 ml) was significantly larger (p less than 0.01) than during the chloride experiment (181 +/- 21 ml). Left ventricular function did not differ between the experiments during the infusions even though at 45 min heart rate was increased by acetate (7%; p less than 0.01, between infusions). After the infusion period, at 75 min the treatment by acetate increased cardiac output from the baseline by 17% (p less than 0.05, between infusions), and decreased peripheral arterial resistance (19%, p less than 0.05), and diastolic blood pressure (10%, p less than 0.01). Circumferential fiber shortening velocity was increased during the acetate experiment maximally by 7% (p less than 0.01) from the baseline at 120 min. These data indicate that acetate is an arterial vasodilator and a mild diuretic and may slightly improve myocardial performance in the concentrations encountered during ethanol metabolism in men.

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