Changes in platelet glycoprotein receptors after smoking - a flow cytometric study

Citation
S. Nair et al., Changes in platelet glycoprotein receptors after smoking - a flow cytometric study, PLATELETS, 12(1), 2001, pp. 20-26
Citations number
24
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
PLATELETS
ISSN journal
0953-7104 → ACNP
Volume
12
Issue
1
Year of publication
2001
Pages
20 - 26
Database
ISI
SICI code
0953-7104(200102)12:1<20:CIPGRA>2.0.ZU;2-F
Abstract
Cigarette smoking is accepted to be one of the major factors which increase the risk of coronary artery disease, peripheral vascular disease and strok e. A number of studies have been carried out on the acute and chronic effec ts of tobacco smoking on platelet activation. An enhancing effect of high n icotine cigarette smoking on platelet aggregation has been reported. Since platelet receptors are involved in the final stage of platelet aggreg ation, the intention of this study was to investigate platelet receptors in acute and chronic smokers before and after smoking, Nineteen chronic smoke rs, 18 acute smokers and 18 healthy non-smoking controls were included in t he present study. Platelet aggregation was carried out using ristocetin, ad enosine diphosphate (ADP) and collagen both before and after smoking in acu te and chronic smokers. Flow cytometric studies of platelets were carried o ut utilizing fluorescein isothiocyanate (FITC)-labelled anti-human fibrinog en antibody in unstimulated and ADP-stimulated platelets, FITC-labelled ant i-GP IIb/IIIa antibody, FITC-labelled anti-GP Ib/IX antibody and FITC-label led P-selectin antibody. The intensity of fluorescence was graded into three groups and expressed in arbitrary units. The interesting data generated in the present work is tha t in vivo platelet activation occurs immediately after smoking a cigarette which is detected by using FITC-labelled anti-human fibrinogen antibody bin ding to platelet and by P-selectin expression. It is also quite evident fro m the present study that a significant number of circulating platelets are in the activated state in chronic smokers. Therefore this study suggests that smoking-induced platelet activation may be an important contributory mechanism for acute coronary events in smokers .