The acute effect of smoking on platelet and endothelial release reaction is suppressed in chronic smokers.
Whilst increased plasma beta-thromboglobulin (beta TG), platelet factor 4 and thrombospondin levels are regarded as reflecting the release reaction of platelets, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) levels represent endothelial release reaction and/or damage. In this study including 12 smokers and 9 nonsmokers, we investigated the acute and chronic effect of smoking on these parameters and antithrombin III, protein S and fibrinogen, as well. Nonsmokers were found to have somewhat higher plasma levels of beta TG, t-PA and PAI-1 than chronic smokers, and 30 minutes after smoking two cigarettes, these levels and protein S levels of nonsmokers showed more prominent increases than of chronic smokers. It is speculated that chronic exposure to cigarette smoke may cause "exhaustion" or "receptor down-regulation" of platelets and endothelial cells, resulting with diminished release reaction of platelets and endothelium in response to acute smoking.
Ozdemir
O
O
Department of Hematology, Hacettepe University Medical School, Ankara, Turkey.
Karaaslan
Y
Y
Ozcebe
O
O
Dündar
S
S
Kirazli
S
S
D000328:Adult; D001792:Blood Platelets / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D015849:Plasminogen Inactivators / Q000097:blood; D012907:Smoking / Q000097:blood*; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D001620:beta-Thromboglobulin / Q000378:metabolism
D015849:Plasminogen Inactivators; D001620:beta-Thromboglobulin; D010959:Tissue Plasminogen Activator