6-ketoprostaglandin-f1-alpha and Alcoholic-Intoxication

Heavy 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).. Twelve 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.. The urinary excretion of the platelet thromboxane A(2) metabolite 2, 3-dinor-thromboxane B(2) 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 F(1alpha) 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.. This 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.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Disease; Adult; Alcoholic Intoxication; Biomarkers; Circadian Rhythm; Creatinine; Cross-Over Studies; Disease Susceptibility; Drug Administration Schedule; Ethanol; Fibrinolysis; Hemorheology; Hemostasis; Humans; Male; Myocardial Infarction; Plasminogen Activator Inhibitor 1; Platelet Activation; Platelet Aggregation; Stroke; Supine Position; Thromboxane B2

ADP-induced platelet aggregation, associated thromboxane B2 (TXB2) formation and urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto prostaglandin F1 alpha (PGI2-M) were studied in healthy male volunteers after ingestion of ethanol (0.25 g per kg of body weight) and calcium carbimide (50 mg). Platelet aggregation was suppressed (p less than 0.05) by ethanol, but no changes were observed in platelet TXB2 formation. Ingestion of calcium carbimide caused a significant elevation in blood acetaldehyde (p less than 0.001) and ethanol (p less than 0.05) levels, but acetaldehyde did not influence platelet aggregation or TXB2 formation. However, calcium carbimide per se elevated TXB2 production (p less than 0.05). Ethanol and acetaldehyde appeared not to have any significant effect on urinary excretion of PGI2-M.

Topics: 6-Ketoprostaglandin F1 alpha; Acetaldehyde; Adult; Alcoholic Intoxication; Blood Platelets; Ethanol; Humans; Male; Platelet Aggregation; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Alcoholic Intoxication; Arachidonic Acid; Arachidonic Acids; Dinoprostone; Humans; Kinetics; Male; Physical Exertion; Prostaglandins; Prostaglandins E; Reference Values; Running; Thromboxane B2