Platelets of habitual smokers have reduced susceptibility to aggregating agent

Thromb Haemost. 1991 Mar 4;65(3):317-9.

Abstract

Platelet aggregation to collagen, and productions of 6-keto-prostaglandin-F1-alpha and thromboxane B2 during aggregation were measured after an overnight fast, involving both food and cigarettes, in 19 clinically healthy habitual smokers (10 or more cigarettes/day) and 23 non-smokers receiving the same diet. The subjects (all males; ages = 21-30 years) were residents of a school hostel. Mean platelet aggregation was significantly lower in smokers than non-smokers (23.2 ohms vs 31.5 ohms, p less than 0.005). Non-smokers had significantly higher mean concentration of 6-keto-prostaglandin-F1-alpha than smokers (109.8 pmol/l vs 92.3 pmol/l, p less than 0.05). The level of thromboxane B2 did not differ significantly between the two groups. These observations suggest that the role of smoking as a risk factor for ischaemic heart disease is unlikely to be related to a direct enhancement of aggregation. On the contrary, the observations seem to suggest that habitual smoking may directly reduce platelet aggregability.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / biosynthesis
  • Adenosine Triphosphate / blood
  • Adult
  • Blood Platelets / metabolism
  • Diet
  • Epoprostenol / biosynthesis*
  • Humans
  • Lipids / blood
  • Male
  • Platelet Aggregation / drug effects*
  • Smoking / blood*
  • Thromboxane A2 / biosynthesis*
  • Thromboxane B2 / blood
  • Vitamin E / blood

Substances

  • Lipids
  • Vitamin E
  • Thromboxane B2
  • Thromboxane A2
  • 6-Ketoprostaglandin F1 alpha
  • Adenosine Triphosphate
  • Epoprostenol