Abstract

Acrolein, a component of tobacco smoke, potentiated platelet aggregation and increased thromboxane A 2 (TXA 2) formation caused by thrombin and arachidonic acid (AA). Acrolein produced these effects at concentrations in the range 50–5000 μM. Acrolein had no effect on platelet responses to ADP, epinephrine, collagen or the ionophore A23187. Acrolein increased the mobilization of [ 3H]arachidonic acid from prelabelled platelets in response to thrombin and arachidonic acid. The increased availability of substrate could partly explain the enhanced production of TXA 2 and increased aggregation observed in the presence of acrolein. These findings could provide an explanation for the increased incidence of vascular disease in cigarette smokers.

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