Abstract

Ethanol intoxication, especially binge drinking is a major risk factor for both ischaemic and haemorrhagic stroke. Compared with non–binge drinkers, the risk of stroke doubles within one hour of consuming alcohol even after adjusting for average alcohol consumption, age, and gender. Despite these epidemiological associations the mechanisms have yet to be defined. We tested the hypothesis that binge drinking impairs cerebrovascular reactivity to blood pressure and carbon dioxide.Eight subjects were recruited to undergo a binge drinking protocol wherein ethanol (0.8 g/kg) were consumed within one hour (~6 standard drinks for an 80 kg subject). Heart rate, blood pressure, middle cerebral artery blood velocity, and end‐tidal PCO2 were measured during cerebrovascular reactivity testing at baseline and at peak intoxication. To assess regulation of cerebral blood flow subjects performed a sit to stand maneuver.During the protocol breath alcohol concentration increased to ~0.053±0.010 %Alcohol. Peak breath alcohol concentration was associated with a significant increase in mean arterial pressure (81±9.2 vs. 86±10 mmHg) and attenuated blood pressure decrease when standing (−19±1 vs. −17±1 mmHg). In contract there was a reduction in the Autoregulatory index (4.4±0.4 vs 3.5±0.5, p=0.004) associated with a greater decrease in cerebral blood flow (−11±2 vs. −15±2 %). However, CO2 reactivity remained unchanged.These pilot data suggest that binge drinking impairs the regulation of cerebral blood flow against transient reductions in blood pressure but does not alter vascular reactivity to CO2. Future work is needed to determine how long this impairment persists.

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