Even at low doses, alcohol has been reported to impair left ventricular pump function. To characterize further the effects of alcohol on the normal cardiovascular system, using the Swan-Ganz thermodilution catheter, we studied 6 healthy physicians, aged 27-36 years, while they were lightly intoxicated. Within a period of 30 min the subjects ingested 0.5 g/kg of ethanol diluted to 15% (w/v) in fruit juice. Hemodynamic measurements were obtained before the first ingestion and every half-hour thereafter for 2 hours. A peak blood ethanol concentration (mean +/- SE) of 13.3 +/- 1.6 mmol/l (0.61 mg/dl) was recorded at 60 min. Unexpectedly, pulmonary artery pressure rose during the early part of the increasing blood ethanol phase, probably due to pulmonary vascular constriction. At 30 min, the systolic pulmonary artery pressure had increased by 10% (p less than 0.05) and the diastolic pressure by 14% (p less than 0.001); both returned to baseline levels by the end of the experiment. Calculated pulmonary vascular resistance rose from a baseline value of 0.50 +/- 0.30 to 0.85 +/- 0.34 units (p less than 0.01) at 30 min. Left ventricular preload decreased significantly during the declining blood ethanol phase: mean pulmonary capillary wedge pressure decreased from 12 +/- 3 to 10 +/- 2 mmHg (p less than 0.01), and mean right atrial pressure decreased significantly. This study suggests that alcohol causes changes in cardiac function by altering its loading conditions. The combined diuretic and systemic venodilatory actions of alcohol provide the most probable explanation for the decrease in preload.