Cerebral blood flow and dynamic cerebral autoregulation during ethanol intoxication and hypercapnia.
More than one-third of patients diagnosed with head injury are intoxicated with ethanol. Most clinical and animal studies have shown alcohol to have a deleterious impact in the setting of cerebrovascular trauma; however, there are also data showing neuroprotective effects in low ethanol doses. Human studies using imaging modalities suggest that small doses of alcohol produce cerebral vasodilatation and higher doses cerebral vasoconstriction. The aim of this study was to investigate the effect of ethanol intake on dynamic cerebral autoregulation and velocities in the middle cerebral arteries, and compare these changes with the effects of hypercapnia. Dynamic cerebral autoregulation and cerebral blood flow velocities were analysed before and after alcohol intake (1.1 g/kg of body weight) in six adult volunteers. Cerebral blood flow velocities in both middle cerebral arteries were monitored continuously by transcranial Doppler. A value for dynamic cerebral autoregulation was calculated from the rate of increase in middle cerebral artery velocities after a rapid-step decrease in arterial blood pressure. A sudden decrease in blood pressure was achieved by the release of previously inflated large blood pressure cuffs around the subject's thighs. Three volunteers were also tested before alcohol intake with CO(2) challenge (breathing 6% CO(2)) during the autoregulation procedure. Blood alcohol level reached 90 mg/dl approximately 60 min after ethanol ingestion. Cerebral blood velocities increased by 8% from baseline for uncorrected end-tidal (et) CO(2) and by 24% for correction to et CO(2)=40. Dynamic cerebral autoregulation measured as an autoregulation index decreased from 4.3+/-1.3 to 2.9+/-1.1 (p=0.089), which did not reach statistical significance. During hypercapnic conditions, dynamic cerebral autoregulation dropped from 4+/-0.8 to 0.9+/-0.9. In conclusion, mild alcohol intoxication caused cerebral vasodilatation with a subsequent increase in cerebral blood flow of 8-24%. Dynamic cerebral autoregulation was not found to be significantly impaired by ethanol. Hypercapnia almost completely destroys the physiological autoregulatory mechanism. A mild hyper-ventilation to etCO(2)=34-36 may be a compensatory contra-measure for ethanol-induced vasodilatation in the setting of head trauma.
Blaha
Martin
M
Department of Neurological Surgery, School of Medicine, University of Washington, Seattle, WA, USA. drmartinblaha@yahoo.com
Aaslid
Rune
R
Douville
Colleen M
CM
Correra
Reinaldo
R
Newell
David W
DW
D000328:Adult; D000428:Alcohol Drinking; D000437:Alcoholism / Q000097:blood / Q000503:physiopathology*; D001776:Blood Circulation Time / Q000379:methods; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D002492:Central Nervous System Depressants / Q000097:blood / Q000633:toxicity*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D000431:Ethanol / Q000097:blood / Q000633:toxicity*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects*; D006801:Humans; D006935:Hypercapnia / Q000097:blood / Q000503:physiopathology*; D008297:Male; D020768:Middle Cerebral Artery / Q000187:drug effects / Q000503:physiopathology; D013997:Time Factors; D017585:Ultrasonography, Doppler, Transcranial / Q000379:methods
D002492:Central Nervous System Depressants; D002245:Carbon Dioxide; D000431:Ethanol