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Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation
Author(s) -
Keh,
Gerlach,
Kürer,
Spielmann,
Kerner,
David R. Busch,
Richard A. Hansen,
Falke
Publication year - 1999
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1999.00459.x
Subject(s) - platelet , chemistry , extracorporeal circulation , nitric oxide , platelet activation , biophysics , pharmacology , immunology , medicine , organic chemistry , biology
Background 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. Material and methods 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. Results NO significantly attenuated platelet trapping and reduced intracircuit platelet activation evaluated by the release of β‐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. Conclusions Transmembranous diffusion of gaseous NO revealed protective effects on platelets by reducing thrombocytopenia/pathia and preserving platelet reactivity.