Inhaled @entity842 inhibits platelet-leukocyte interactions in @entity1 with acute XXXX .

@entity1 @entity649 @entity1989 @entity8729 @entity842 @entity1453
INTRODUCTION: In addition to its effects on platelet function, recent studies suggest that inhaled @entity842 (NO) also influences the function of circulating leukocytes. Therefore, the aim of this work was to investigate the formation of platelet-leukocyte aggregates (PLAs) and platelet and leukocyte cell surface receptor expression during NO therapy in @entity1 with acute @entity649 . METHODS: In 16 @entity1 responding to NO therapy with an improvement in oxygenation (NO group) and in four nonresponders (control), platelet @entity8729 expression, platelet fibrinogen binding, the expression @entity1453 on leukocytes, and the formation of PLAs were investigated at 0, 60, 120, and 180 mins of therapy or at corresponding time points by means of flow cytometry. In addition, @entity1989 was investigated in 30 healthy volunteers during NO inhalation, in five mechanically ventilated @entity1 without acute @entity649 and without NO inhalation, and during NO incubation in platelet-rich plasma of ten healthy volunteers in vitro. RESULTS: NO therapy inhibited @entity1989 formation at 60 (13% +/- 4% in the NO group vs. 19% +/- 7% in the control group, p <.01) and 120 mins (14% +/- 4% vs. 18% +/- 7%, p <.05) and slightly decreased @entity1453 expression at 60 mins (152 +/- 22 arbitrary units vs. 187 +/- 36 arbitrary units, p <.05). Furthermore, besides inhibiting platelet fibrinogen binding, NO also led to a significant inhibition of @entity8729 expression at 120 (38% +/- 4% vs. 43% +/- 5%, p <.05) and 180 mins (34% +/- 5% vs. 43% +/- 6%, p <.01), demonstrating a significant correlation between changes in @entity8729 expression and @entity1989 formation. In contrast, @entity1989 formation was not influenced by mechanical ventilation in @entity1 without acute @entity649 . These results were further supported by additional studies showing inhibition of @entity1989 formation in healthy volunteers as well. CONCLUSIONS: NO-dependent inhibition of @entity1989 formation in @entity1 with acute @entity649 can be explained by the inhibition in platelet @entity8729 expression. Thus, this study provides rational evidence of systemic antileukocytic and antiplatelet properties of NO therapy in the clinical setting.
