Platelet function during acetaldehyde intoxication in healthy male volunteers.
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.
Dept. of Clinical and Experimental Alcohol, Addiction Research, Karolinska Institutet, Stockholm, Sweden.
J
J
Neiman
M
M
Hillbom
A W
AW
Jones
G
G
Benthin
C
C
Löwbeer
D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000652:urine; D000079:Acetaldehyde / Q000494:pharmacology*; D000328:Adult; D000435:Alcoholic Intoxication; D001792:Blood Platelets / Q000187:drug effects*; D000431:Ethanol / Q000494:pharmacology; D006801:Humans; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects; D013929:Thromboxane B2 / Q000096:biosynthesis
D000431:Ethanol; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; D000079:Acetaldehyde