Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Background The absence of a protective endothelial surface on membrane oxyg enators during extracorporeal circulation (ECC) promotes platelet trapping and damage, leading to increased bleeding complications. We investigated th e effects of transmembranous diffusion of gaseous nitric oxide (NO) on plat elets during simulated ECC. Material and methods Two paired circuits were run in parallel with fresh, h eparinized (1 U mL(-1)) blood from healthy human donors for 240 min. To one of the paired circuits, 20 ppm NO was added transmembranously. Results NO significantly attenuated platelet trapping and reduced intracirc uit platelet activation evaluated by the release of beta-thromboglobulin, p latelet factor 4 and soluble P-selectin. Furthermore, NO significantly pres erved platelet reactivity to stimulating agents (ADP and adrenaline), evalu ated as the ability to expose P-selectins and activate glycoprotein (GP)-II b-IIIa. Nevertheless, circulating activated platelets expressing P-selectin or activated GPIIb-IIIa were not different and were not significantly incr eased. The mean fluorescence intensity of GPIb and GPIIb-IIIa decreased in both circuits equally. Conclusions Transmembranous diffusion of gaseous NO revealed protective eff ects on platelets by reducing thrombocytopenia/pathia and preserving platel et reactivity.