(Stroke. 2000;31:1269.)
© 2000 American Heart Association, Inc.
Original Contributions |
From the Department of Neurology, Oulu University Hospital (H.N., M.H.), Oulu, Finland; and the Department of Clinical Chemistry, Helsinki University Hospital (M.S.), Department of Clinical Physiology, Karolinska Institutet at Huddinge University Hospital (G.B.). and Department of Neurology, Helsinki University Hospital (M.K.), Helsinki, Finland.
Correspondence to Prof Matti Hillbom, MD, Department of Neurology, Oulu University Hospital, FIN-90220, Oulu, Finland. E-mail matti.hillbom{at}oulu.fi
Background and PurposeHeavy binge drinking may trigger the onset of embolic stroke and acute myocardial infarction, but the underlying mechanisms are unclear. The effects of binge drinking on the hemostatic system and its circadian variation have not been investigated. We investigated the effects of an acute intake of a large dose of alcohol (1.5 g/kg).
MethodsTwelve healthy, nonsmoking men participated in sessions where they were served ethanol in fruit juice or served fruit juice alone and, lying in a supine position, were followed up for 12 to 24 hours. The treatments were randomized and separated from each other by a 1-week washout period. Blood and urine were collected for hemostatic measurements.
ResultsThe urinary excretion of the platelet
thromboxane A2 metabolite
2,3-dinor-thromboxane B2 was significantly
(P<0.05) greater during the night after an evening
intake of alcohol than during the control night. A smaller increase was
observed during the daytime after an intake of alcohol in the morning.
The effects on the endothelial prostacyclin metabolite
2,3-dinor-6-ketoprostaglandin F1
excretion
were negligible. A 7-fold increase in plasminogen
activator inhibitor 1 activity was observed
after both morning (P<0.05) and evening
(P<0.01) intakes of alcohol.
ConclusionsThis is the first study to suggest that acute ingestion of a relatively large but tolerable dose of alcohol transiently enhances thromboxane-mediated platelet activation. The observations also demonstrate alcohol-induced changes in the normal circadian periodicity of the hemostatic system in subjects not accustomed to consumption of alcohol.
Key Words: alcohol circadian rhythm hemostasis prostaglandins thrombolysis
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