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Cigarette smoking increases thromboxane A2 formation without affecting platelet survival in young healthy females.

Artikel i vetenskaplig tidskrift
Författare Annika Dotevall
C Rångemark
E Eriksson
Jack Kutti
Hans Wadenvik
A Wennmalm
Publicerad i Thrombosis and haemostasis
Volym 68
Nummer/häfte 5
Sidor 583-8
ISSN 0340-6245
Publiceringsår 1992
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för internmedicin
Institutionen för invärtesmedicin
Sidor 583-8
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adult, Blood Platelets, cytology, metabolism, Cell Survival, Female, Humans, Middle Aged, Smoking, blood, urine, Thromboxane A2, biosynthesis, Thromboxane B2, analogs & derivatives, urine, beta-Thromboglobulin, urine
Ämneskategorier Klinisk medicin

Sammanfattning

Smoking is a risk factor for the development of atherosclerotic cardiovascular disease, in men as well as in women. An increased urinary excretion of the thromboxane metabolite 2,3-dinorthromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking may facilitate cardiovascular disease via an action on the platelets. The present study addressed the hypothesis that the increased Tx-M excretion in female smokers reflects a true facilitation of platelet reactivity in vivo, rather than an increased destruction of the platelets. In healthy female volunteers (aged 20-46 years, 18 smokers and 17 non-smokers) platelet life-span and indices of platelet activity were determined, together with plasma levels of plasminogen activator inhibitor-1 (PAI-1), fibrinogen, peripheral blood cell counts and hematocrit. The urinary excretion of Tx-M was higher in smokers than in non-smokers (361 vs. 204 pg/mg creatinine, respectively, p < 0.05), while plasma and urinary beta-thromboglobulin, plasma platelet factor 4, platelet mean life-span and platelet production rate did not differ between the groups. PAI-1 activity, white blood cell count and hematocrit were higher in smokers than in non-smokers (p < 0.05). These data indicate that smoking facilitates platelet formation of thromboxane A2 without affecting platelet survival; i.e. it increases the activity of platelets without affecting their viability to a measurable extent. Such an increase in platelet activity, operating in parallel to a reduced fibrinolytic activity and a higher hematocrit and white blood cell count, may play an etiological role in smoking-induced cardiovascular disease in women.

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