Abstract
The absence of a protective endothelial surface on membrane oxygenators during extracorporeal circulation (ECC) promotes platelet trapping and damage, leading to increased bleeding complications. We investigated the effects of transmembranous diffusion of gaseous nitric oxide (NO) on platelets during simulated ECC. Two paired circuits were run in parallel with fresh, heparinized (1 U mL-1) blood from healthy human donors for 240 min. To one of the paired circuits, 20 ppm NO was added transmembranously. NO significantly attenuated platelet trapping and reduced intracircuit platelet activation evaluated by the release of beta-thromboglobulin, platelet factor 4 and soluble P-selectin. Furthermore, NO significantly preserved platelet reactivity to stimulating agents (ADP and adrenaline), evaluated as the ability to expose P-selectins and activate glycoprotein (GP)-IIb-IIIa. Nevertheless, circulating activated platelets expressing P-selectin or activated GPIIb-IIIa were not different and were not significantly increased. The mean fluorescence intensity of GPIb and GPIIb-IIIa decreased in both circuits equally. Transmembranous diffusion of gaseous NO revealed protective effects on platelets by reducing thrombocytopenia/pathia and preserving platelet reactivity.
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