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.

The influence of erythrocyte aggregation on induced platelet aggregation.

Red blood cells (RBCs) affect platelet aggregation in flowing blood (primary hemostasis). We tested the hypothesis that RBC aggregation could influence platelet aggregation. RBC aggregation was altered in vitro by: (i) changing plasma aggregatory properties with 3.7 g% dextran 40 (D40), 3.0 g% dextran 70 (D70) or 1.55 g% dextran 500 (D500); (ii) changing RBC aggregatory properties by incubating RBCs in 50 mU/ml neuraminidase for 60 min (reduction of the surface sialic acid content, thus reducing electrostatic repulsion) and subsequent RBC resuspension in platelet rich plasma (PRP) containing 1 g% dextran 70. RBC aggregation was assessed with the sedimentation rate (ESR). Platelet aggregation was measured: (i) in flowing whole blood with a platelet function analyzer PFA-100(R), which simulates in vivo conditions with RBCs flowing in the center and platelets along the wall, where they adhere to collagen and aggregate; and (ii) in a Chrono-log 700 Aggregometer, which measures changes of impedance by platelet aggregation in whole blood or changes in light transmission in PRP. We found that RBC aggregation increased with increasing molecular weight of dextran (ESR: 4 +/- 3 mm/h, 34 +/- 14 mm/h and 89 +/- 23 mm/hfor D40, D70 and D500, respectively, p < 0.0001) and with neuraminidase-treated RBCs (76 +/- 27 mm/h vs 27 +/- 8 mm/h, respectively, p < 0.0001). Platelet aggregation measured in whole blood under flow conditions (PFA-100) and without flow (Chronolog Aggregometer) was not affected by RBC aggregation. Our data suggest that RBC aggregation does not affect platelet aggregation in vitro and plays no role in primary hemostasis.