1. The anti-aggregatory effect of adenosine (0.3–10 μmol/l), alone or in combination with the adenosine-uptake inhibitor dipyridamole (2 μmol/l), was studied in vitro in whole blood from 11 healthy subjects by filtragometry.
2. ADP (0.05–0.1 μmol/l) was used to reduce the filter occlusion time (tA, a measure of platelet aggregate formation in blood) from approximately 600 s to 71–101 s in the absence of other agents.
3. Adenosine was infused into the tubing system of the filtragometer, yielding a contact time of >25 s with the blood before the filter. Adenosine did not influence the aggregatory response to ADP significantly at 0.3 μmol/l in plasma, whereas tA was prolonged by 19 ± 6% (P <0.02) at 1 μmol/l adenosine and by 259 ± 78% (P <0.02) at 3 μmol/l adenosine.
4. When the rapid elimination of adenosine from plasma was prevented by 2 μmol/l dipyridamole, adenosine caused marked prolongation of ADP-induced tA, with significant effects at 0.3 μmol/l (± 143 ± 72%, P <0.05). Dipyridamole per se did not affect tA values.
5. The present results suggest that adenosine has a transient anti-aggregatory effect in whole blood at about 0.3 μmol/l, as this is the highest possible calculated concentration of adenosine at the filter of the apparatus when 1 μmol/l adenosine is infused in the absence of dipyridamole or when 0.3 μmol/l adenosine is infused in its presence.
6. It is concluded that adenosine has anti-aggregatory effects at submicromolar (physiological) concentrations in human whole blood. The effect of adenosine seems to be transient, indicating a role for adenosine as a localized platelet-stabilizing factor in the vicinity of, for example, the endothelium.
Molecular Basis forStaphylococcus aureus–Mediated Platelet Aggregate Formation Under Arterial Shear In Vitro
