Acute effects of short-term exposure to second-hand smoke on induced platelet aggregation.
Passive smoking may increase cardiovascular events by yet insufficiently understood mechanisms. We, therefore, tested the hypothesis that passive smoking could affect platelet aggregation. Fourteen healthy non-smoking males were exposed to second-hand smoke during 60 min in a room with smokers, who maintained the CO-concentration between 4.5-7.0 ppm throughout that period. Citrated blood was drawn before and immediately after smoke exposure (which took place between 6 and 7 p.m.). The last 7 individuals had blood taken also at 9.00 a.m. before and the day after smoke exposure. Platelet aggregation was measured (a) in flowing whole blood using the platelet function analyser PFA-100, which determines the closure time (CT) of a collagen coated membrane pore by shear-induced platelet aggregation, and (b) with a Chrono-log 700 Aggregometer, assessing platelet aggregation either by the change of impedance in diluted whole blood or light transmission in platelet-rich plasma. After short term second-hand smoke exposure we did not observe an increase in platelet aggregation with any of the instruments. We conclude that acute exposure to second-hand smoke is unlikely to increase platelet aggregability. Other mechanisms must be involved in the increased risk of cardiovascular events associated with passive smoking.
Lardi
E
E
Department of Internal Medicine, Kantonsspital Graubünden, Chur, Switzerland.
Ott
C
C
Schulzki
T
T
Kuhn
M
M
Bonetti
P O
PO
Reinhart
W H
WH
D002248:Carbon Monoxide; D006801:Humans; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D010979:Platelet Function Tests; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D014028:Tobacco Smoke Pollution; D002248:Carbon Monoxide