Nitric oxide thrombus formation

In practice, some anticoagulation agents such as heparin or antiplatelet agents, e.g. nitric oxide (NO) are delivered to sensor sites in order to reduce the risk of thrombus formation. Nitric oxide (NO), which is a potent inhibitor of platelet adhesion and activation as well as a promoter of wound healing in tissue, has been incorporated in various polymer metrics including PVC (poly(vinyl-chloride)), PDMS (poly-dimethyl-siloxane) and PU (poly-urethanes). Those NO release polymers have been tested in animals as outer protection coatings and have shown promising effects for the analytical response characteristics of the sensor devices [137],... 

The aggregation of platelets contributes to the development of atherosclerosis and to the formation of acute thrombus. The activated platelets that adhere to the vascular endothelium generate lipid peroxides and oxygen free radicals, inhibiting the endothelial formation of prostacyclin and nitric oxide. 

Current research and development efforts have focused on the use of more biocompatible coatings to reduce the biological response of both intravascular and subcutaneous devices. These efforts are based on the expectation that such developments wfllbe critical to the ultimate success in developing implanted sensors that yield continuous analytical results that match closely with conventional in vitro test methods. One new approach in this direction employs novel nitric oxide (NO) release polymers to coat the surface of intravascular sensors.The potent antiplatelet activity of NO has been shown to greatly reduce the formation of thrombus on the surface of implantable electrochemical oxygen sensing catheters, and yield much more accurate continuous PO2 values in animal experiments. 

Nitric oxide (NO), a diatomic free radical, naturally produced in the body by endothelial cells, is well known as an antithrombogenic mediator and its continuous release from the surface of endothelial cells effectively prevents the adhesion/activation of platelets on normal blood vessel walls. Hence, materials that release or generate NO locally at the surface to inhibit thrombus formation have been developed with great potential applications in blood-contacting medical devices with improved biocompatibility. 

Argatroban + nitric oxide coating on PU Coating Platelet aggregation and activation Ex vivo Rabbit Reduced thrombus formation, low platelet activation [94]... 

Nitric oxide has been shown to prevent bacterial infection, as well as thrombus formation (Langford et al., 1994 Radomski et al., 1992 Salas et al., 1994). These attributes have the potential to improve the efficacy of catheter devices. Many combinations of polymer chemistries and delivery methods of NO have been investigated (Parker et al., 2009 Tambyah, 2004 van Rooden et al., 2005 Regev-Shoshani et al., 2010 Kishikawa et al., 2013 Ren et al., 2014 Schoenfisch et al., 2000 Hamek et al., 2011). 

Several studies have shown that the extent of coronary artery stenosis due to atherosclerotic plaque formation and expansion into the arterial lumen is not sufficient to explain the incidence of clinical events associated with atherosclerosis [183]. It appears that the generation of clinical events involves plaque mpture, resulting in thrombus formation and arterial occlusion. This mpture is induced by vasomotor disturbances in which oxidized low-density lipoproteins may be involved. Resveratrol is able to regulate vasomotion, which is impaired in atherosclerosis. The key regulators of the vasomotor function are the vasodilator NO and the vasoconstrictor endothelin-1 [167]. A number of in vitro and in vivo studies have shown improved vascular function in response to resveratrol [184, 185]. Resveratrol enhances expression and activity of endothelial nitric oxide synthase [186] and inhibits endothelin-1 secretion and endothelin-1 gene expression in human umbilical vein endothelial cells [187]. Intragastric administration of resveratrol for 12 weeks to hypercholesterolemic rabbits improved the endothelial function, reduced plasma endothelin-1 levels, and induced... 

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