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Ethanol inhibits platelet thromboxane A2 production but has no effect on lung prostacyclin synthesis in humans.

Abstract：

:Ethanol (88-880 mmol/l) inhibited the formation of proaggregatory, vasoconstricting thromboxane A2 (TxA2) during whole blood clotting and during thrombin-induced aggregation of platelet rich plasma. This inhibition was counteracted by the addition of exogenous arachidonic acid, which suggested that ethanol suppressed the liberation of arachidonic acid, evidently by inhibiting phospholipase A2. Ethanol had no effect on the formation of prostacyclin (PGI2, epoprostenol), the endogenous antagonist of TxA2, by human lung. Thus our results suggest that ethanol may shift the balance between TxA2 and PGI2 to the dominance of antiaggregatory, vasodilating PGI2 by suppressing the release of arachidonic acid in platelets. This finding might partly explain why ethanol protects against atherosclerosis and also the increased risk of subarachnoidal haemorrhage after heavy ethanol intake.

journal_name

Thromb Res

journal_title

Thrombosis research

authors

Toivanen J,Ylikorkala O,Viinikka L

doi

10.1016/0049-3848(84)90149-x

subject

Has Abstract

pub_date

1984-01-01 00:00:00

pages

1-8

issue

1

eissn

0049-3848

issn

1879-2472

pii

0049-3848(84)90149-X

journal_volume

33

pub_type

杂志文章

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