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Effects of Ethanol on Human Platelets Stimulated with Platelet‐Activating Factor, a Biologically Active Ether Phospholipid
Author(s) -
Baker Rodney C.,
Fish H. T.,
Fitzpatrick Frank A.
Publication year - 1989
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1989.tb00430.x
Subject(s) - chemistry , platelet activating factor , platelet , arachidonic acid , ethanol , phospholipid , epinephrine , biochemistry , platelet activation , adenosine diphosphate , thromboxane a2 , biological activity , endocrinology , medicine , platelet aggregation , receptor , in vitro , enzyme , biology , membrane
The interaction between ethanol and 1–0‐alkyl‐2‐acetyl‐sn‐glycerol‐3‐phosphocholine (platelet activating factor, PAF) was addressed using platelets obtained from normal nonalcoholic volunteers. Ethanol at concentrations of 20 to 100 mM inhibited PAF activation of human platelets. Ethanol inhibited prominently the second or arachidonic acid metabolite dependent wave of platelet aggregation, which occurs with human platelets in citrated plasma. It also inhibited serotonin release and thromboxane A P formation associated with this secondary phase of aggregation. Ethanol did not readily inhibit the primary wave of PAF‐induced aggregation. The incorporation of PAF into platelets or metabolism of PAF was not influenced by up to 100 mM ethanol. Since ethanol inhibited only the secondary response, a direct interaction between PAF, ethanol, and a platelet PAF receptor is unlikely. The effect of ethanol on PAF‐induced platelet aggregation shows a selectivity similar to that demonstrated by other investigators for epinephrine and adenosine diphosphate.