No abstract

Platelet inhibition after aspirin therapy reduces the risk for the development of acute coronary syndromes. However, the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear. We sought to determine the in vitro effects of aspirin on the surface expression of nine platelet receptors using whole blood flow cytometry. Blood from 24 healthy volunteers was incubated for 30 min with 1.8 and 7.2 mg/l phosphate-buffered saline-diluted acetylsalicylic acid in the presence or absence of apyrase. Platelet serotonin release, and the surface expression of platelet receptors with or without apyrase were determined using the following monoclonal antibodies: anit-CD41 [glycoprotein (GP)IIb/IIIa], CD42b (GPIb), CD62p (P-selectin), CD51/CD61 (vitronectin receptor), CD31 [platelet/endothelial cellular adhesion molecule-1 (PECAM-1)], CD107a [lysosomal associated membrane protein (LAMP)-1], CD107b (LAMP-2), CD63 (LIMP or LAMP-3), and CD151 (PETA-3). Samples were then immediately fixed with 2% paraformaldehyde, and run on the flow cytometer within 48 h. Aspirin does not affect serotonin release from human platelets. Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples. Apyrase potentiates the effects of aspirin, and independently inhibits PECAM-1. In addition to the known effect of irreversibly inhibiting platelet cyclooxygenase-1, thereby blocking thromboxane A(2) synthesis, it appears that aspirin exhibits direct effects on selective major platelet receptors.

No abstract

Platelet inhibition after moderate alcohol consumption in patients with ischaemic heart disease may contribute to reducing the risk for developing acute coronary syndromes. However, the mechanism by which ethanol affects platelets is not clarified. We sought to determine the in vitro effects of alcohol on the surface expression of human platelet receptors using whole blood flow cytometry. Blood samples from 10 healthy volunteers were incubated for 30 min with 25 and 50 mmol l(-1) of phosphate buffered saline diluted grain ethanol, concentrations often used in in vitro studies. The surface expression of platelet receptors was determined by flow cytometry after fixation with 2% paraformaldehyde using the following monoclonal antibodies: CD 41 (GP IIb/IIIa), CD 42b (GP Ib), CD 62p (P-selectin), CD 51/CD 61 (vitronectin receptor), CD 31 (PECAM-1), CD 107a (LAMP-1), CD 107b (LAMP-2), CD 63 (LIMP, LAMP-3) and CD 151 (PETA-3). Dose-dependent inhibition of GP IIb/IIIa, P-selectin, CD 63 and CD 107a receptor expression was observed in the ethanol-treated whole blood samples. This study for the first time establishes a direct effect of ethanol on selective major platelet receptors. Beneficial cardiovascular properties of moderate alcohol consumption may be explained by ethanol's antiplatelet action.