Platelet aggregability in smoking and non‐smoking subjects

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Abstract
The hypothesis was investigated that the arachidonic acid (AA) system has a different impact on platelet function in smoking compared to non-smoking subjects. Arterial blood was sampled from smokers and non-smokers, and platelet-rich plasma (PRP) was prepared. There were no differences in sex and age distribution between the groups. One portion of the PRP was used to determine the lowest amount of AA required to induce platelet aggregation. In other portions the endogenous anti-aggregatory (prostacyclin/PGI2/-like) activity in the blood was determined, after reinforcing it with theophylline. There was no difference between smokers and non-smokers regarding the amount of AA required to induce platelet aggregation. In fresh PRP prepared from blood from non-smoking subjects theophylline (10(-4) M) induced a 12-17% inhibition of the ADP-induced aggregation of platelets, indicating the presence of endogenous subthreshold concentrations of PGI2-like activity in their blood. The corresponding inhibition in fresh PRP prepared from blood from smokers was significantly lower (4-7%), suggesting lower endogenous concentrations of PGI2-like activity in their blood, or alternatively, decreased platelet sensitivity to the action of such activity. From these data we conclude that smokers differ from non-smokers with regard to their platelet function: platelet aggregability in response to AA is unaffected, while the endogenous anti-aggregatory power in the plasma is decreased. These observations may be of significance for the cardiovascular hazards connected with smoking.