Alcohol-Induced Changes of Extra- and Intracranial Volume Flow

Clinical and animal trials have shown alcohol-induced peripheral vasodilation with a corresponding decrease in systemic arterial blood pressure. Scintigraphic studies have demonstrated conflicting data about the effects of ethanol on autoregulated cerebrovascular hemodynamics. We tested the extra- and intracranial hemodynamic changes induced by alcohol uptake (appr. 1g/kg) in 22 healthy volunteers (14 male, 8 female; mean age 23 years) non-invasively by ultrasonic techniques. We determined almost simultaneously the extracranial blood flow volume in the common (CCA) (n=22) and internal (ICA) (n=11) carotid arteries bilaterally (duplex system) as well as the intracranial blood flow velocities (transcranial Doppler) in the middle cerebral arteries (MCA) (n=22) before and one hour after alcohol consumption. Mean alcohol concentration one hour after intake was 1.04% (spirometric exhaled air analysis). Flow volume in the CCA increased from 903ml/min to 1124ml/min (+24%, p<0.0001), volume flow in the ICA increased only from 481ml/min to 518ml/min (+8%, p<0.05). The average MCA peak systolic flow velocity rose by 7.5% from 122cm/s to 131cm/s (p<0.0002). Subtracting ICA volume flow rates from the CCA volume flow rates, we calculated a mean volume flow increase in the external carotid arteries of 46%. These data indicate only a moderate alcohol-induced vasodilation of the intracranial resistance vessels causing a mild hyperperfusion state compared to a massive dilation in the extracranial vascular territory. MCA flow velocity changes correspond closely to the ICA flow volume changes indicating no dilatory or constrictory effect of alcohol on the major basal cerebral arteries.