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Sökning: WFRF:(Wadenvik Hans 1955) > (1990-1994) > Cigarette smoking i...

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

Dotevall, Annika, 1957 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
Rångemark, C (författare)
Eriksson, E (författare)
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Kutti, Jack (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine
Wadenvik, Hans, 1955 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine
Wennmalm, A (författare)
visa färre...
 (creator_code:org_t)
1992
1992
Engelska.
Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 68:5, s. 583-8
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine (hsv//eng)

Nyckelord

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

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