Effects of a Small Dose of Ethanol and Calcium Carbimide-Induced Acetaldehyde Intoxication on Human Platelet Aggregation, Associated Thromboxane Formation and Urinary Excretion of 2,3-dinor-6-Keto Prostaglandin F_1α

Abstract

We studied ADP-induced platelet aggregation, associated thromboxane B₂ (TXB₂) formation, urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto prostaglandin F_1α (2,3-dinor-6-keto PGF_1α) and formation of malondialdehyde in 10 healthy volunteers after ingestion of a small dose of ethanol (0.25 g per kg of body weight) and calcium carbimide (50 mg). Platelet aggregation in platelet-rich plasma (PRP) was suppressed (p≥0.05) by ethanol, but no change occurred in platelet TXB₂ formation. Ingestion of calcium carbimide caused significant elevations in blood acetaldehyde (p≥0.001) and ethanol (p≥0.05) levels, but acetaldehyde did not influence platelet aggregability or the aggregation-associated TXB₂ formation. However, calcium carbimide per se significantly (p≥0.05) elevated TXB₂ formation. No effects were found on plasma malondialdehyde levels and urinary excretion of 2,3-dinor-6-keto PGF_1α. These observations indicate that a small dose of ethanol attenuates platelet aggregation without any significant effect on aggregation-associated TXB₂ formation. By contrast, ingestion of calcium carbimide per se may enhance TXB₂ formation.