Irit Kürer

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Nitric oxide (NO) is known to modulate platelet adhesion and aggregation, which are both mediated by fibrinogen receptor glycoprotein (GP)IIb/IIIa. To investigate effects of NO on GPIIb/IIIa activation and inactivation, platelets were exposed to NO donor 3-morpholino-sydnonimine (SIN-1) before and after stimulation with different agonists: thromboxane(More)
Bleeding during extracorporeal circulation (ECC) is often induced and/or aggravated by thrombocytopenia due to platelet-trapping in hollow fiber membrane oxygenators (HFMO). Nitric oxide (NO) has platelet anti-aggregating and dis-aggregating properties. In a paired system we tested whether gaseous NO, added to the gas compartment of one of two parallel(More)
Nitric oxide (NO) is known as a regulator of platelet function by its anti-adhesive, anti-aggregating, and disaggregating properties. We investigated the modulating effects of the NO-releasing compound SIN-1 (3-morpholino-sydnonimine) on platelet surface glycoprotein (GP) expression during stimulation with human alpha-thrombin. Analysis was performed with(More)
OBJECTIVE Nitric oxide (NO) has antithrombotic properties by regulating platelet function, whereas direct effects on plasmatic coagulation are rarely described. In sepsis and inflammation, when synthesis of NO, oxygen radicals and toxic metabolites is crucial, the expression of tissue factor (TF) on monocytes stimulated by lipopolysaccharides (LPS) induces(More)
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(More)