Cigarette smoking and its effects on the platelet-vessel wall interaction.
The effect of smoking and of carbon monoxide on the platelet-vessel wall interaction was investigated. After smoking two high-nicotine content cigarettes (2.6 mg nicotine/cigarette) the mean bleeding time decreased 1.6 min (P less than 0.05) in five habitual smokers whereas the platelet aggregability was only moderately inhibited. After inhibiting the platelet cyclooxygenase by ingesting acetylsalicylic acid (ASA) 2 days prior to the study, smoking caused a markedly and significantly shortened bleeding time (-3.8 min; P less than 0.05). The bleeding time was unaffected by smoking when both the platelet cyclooxygenase and the vessel wall prostaglandin was inhibited by ASA 1 h prior to the study. When smoking two cigarettes with a low content of nicotine (0.25 mg nicotine/cigarette) no changes in the haemostatic mechanism were observed. Inhalation of carbon monoxide in high amounts in five non-smokers had a significant short-lasting effect on the bleeding time (-1.2 min, P less than 0.05). No changes in the bleeding time were observed after carbon monoxide inhalation when the platelet cyclooxygenase or when both the platelet cyclooxygenase and the vessel wall prostaglandin production were blocked. Based on the results it is concluded that the effect of smoking on the haemostasis is mainly mediated through an inhibitory effect on the prostacyclin production in the vessel wall by nicotine and that carbon monoxide only plays a minor role.
D001760:Bleeding Time; D001792:Blood Platelets / Q000187:drug effects*; D001808:Blood Vessels / Q000187:drug effects*; D002248:Carbon Monoxide / Q000494:pharmacology*; D006487:Hemostasis / Q000187:drug effects; D006801:Humans; D009538:Nicotine / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects; D012907:Smoking
D009538:Nicotine; D002248:Carbon Monoxide