PB0863 - The influence of hemolysis on platelet reactivity in patients undergoing aortic valve replacement surgery.

Background: Cardiopulmonary bypass (CPB) with extracorporeal circulation is the procedure that is performed in patients undergoing aortic valve replacement surgery. CPB is a relatively safe technique although may have some complications such as tissue damage via decreased organ perfusion. In this setting hemolysis seems to be an important contributor to these complications since the increase of free haemoglobin in plasma decreases Nitric Oxide (NO)-bioavailability and may lead to platelet aggregation/activation and vasoconstriction, resulting in thrombosis and reduced organ perfusion.

Aims: To investigate the influence of hemolysis on thrombin-receptor activating peptide (TRAP)-induced platelet reactivity in patients undergoing aortic valve replacement.

Methods: Platelet aggregation (by platelet counting) and activation (by P-selectin expression) were measured in seventeen patients by flow cytometry in whole blood in response to thrombin-receptor activating peptide (TRAP), in the absence or presence of a range of different concentrations of NONOate (nitric oxide donor). Vasodilator-stimulated phosphoprotein (VASP) phosphorylation was determined using a cytometric bead (VASPFix) assay as a measure of cAMP/cGMP. All the determinations were measured in three different moments: Before(M1), During(M2) and After(M3) the CPB procedure.

Results: NONOate (nitric oxide donor) inhibited TRAP-induced platelet aggregation and activation in a dose-dependent manner in the three experimental groups (M1, M2 and M3) with no significance difference among them (Table 1). The effects of NONOate were directly related to changes in cAMP/cGMP, assessed by VASP phosphorylation (Table 2).

Conclusion(s): The overall effects of NONOate (nitric oxide donor) on platelet reactivity and VASP phosphorylation are the consequence of an adequate bioavailability of nitric oxide in these patients under our experimental conditions. These results indicate that the level of hemolysis brought about by CPB in these patients might not be sufficient to interfere with the physiological regulation of nitric oxide on platelet function in vivo.