Half-life of nitric oxide in aqueous solutions with and without haemoglobin

Hakim, T. S.; Sugimori, Kunio; Camporesi, Enrico M.; Anderson, George M.

doi:10.1088/0967-3334/17/4/004

Cited by 141 publications

(101 citation statements)

References 27 publications

(46 reference statements)

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“…The initial water uptake of the polymer and leaching of SNAP on the outer surface of the catheters contributes to the higher level of NO release observed during this initial test period. In blood, NO has a short half-life due to its rapid scavenging by hemoglobin 50 ; therefore, initial NO release levels that are somewhat higher than physiological levels, such as what is observed on Day 0, are not be a significant concern. This is because the surface areas of the catheters studied here are very small compared to the entire surface areas of the inner walls of all blood vessels within the body that are producing NO at physiological levels continuously.…”

Section: In Vitro No Release From Catheters and Effects Of Ethylene Omentioning

confidence: 99%

Reduction in thrombosis and bacterial adhesion with 7 day implantation of S-nitroso-N-acetylpenicillamine (SNAP)-doped Elast-eon E2As catheters in sheep

et al. 2015

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Thrombosis and infection are two common problems associated with blood-contacting medical devices such as catheters. Nitric oxide (NO) is known to be a potent antimicrobial agent as well as an inhibitor of platelet activation and adhesion. Healthy endothelial cells that line the inner walls of all blood vessels exhibit a NO flux of 0.5~4×10 −10 mol cm −2 min −1 that helps prevent thrombosis. Materials with a NO flux that is equivalent to this level are expected to exhibit similar anti-thrombotic properties. In this study, NO-releasing catheters were fabricated by incorporating S-nitroso-N-acetylpenicillamine (SNAP) in the Elast-eon E2As polymer. The SNAP/E2As catheters release physiological levels of NO for up to 20 d, as measured by chemiluminescence. Furthermore, SNAP is stable in the E2As polymer, retaining 89% of the initial SNAP after ethylene oxide (EO) sterilization. The SNAP/E2As and E2As control catheters were implanted in sheep veins for 7 d to examine the effect on thrombosis and bacterial adhesion. The SNAP/E2As catheters reduced the thrombus area when compared to the control (1.56 ± 0.76 and 5.06 ± 1.44 cm 2 , respectively). A 90% reduction in bacterial adhesion was also observed for the SNAP/E2As catheters as compared to the controls. The results suggest that the SNAP/E2As polymer has the potential to improve the hemocompatibility and bactericidal activity of intravascular catheters, as well as other blood-contacting medical devices (e.g., vascular grafts, extracorporeal circuits).

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Section: In Vitro No Release From Catheters and Effects Of Ethylene Omentioning

confidence: 99%

Reduction in thrombosis and bacterial adhesion with 7 day implantation of S-nitroso-N-acetylpenicillamine (SNAP)-doped Elast-eon E2As catheters in sheep

et al. 2015

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“…; Hakim et al, 1996). In addition, it has recently been proposed that RBCs possess an intrinsic barrier that limits NO consumption still further (Vaughn et al, 2000).…”

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confidence: 99%

Inhibition of human platelet aggregation by a novel S‐nitrosothiol is abolished by haemoglobin and red blood cells in vitro: implications for anti‐thrombotic therapy

Megson

Sogo

Mazzei

et al. 2000

British J Pharmacology

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1 S-Nitrosothiols are nitric oxide (NO) donor drugs that have been shown to inhibit platelet aggregation in platelet rich plasma (PRP) in vitro and to inhibit platelet activation in vivo. The aim of this study was to compare the platelet eects of a novel S-nitrosated glyco-amino acid, RIG200, with an established S-nitrosothiol, S-nitrosoglutathione (GSNO) in PRP, and to investigate the eects of cell-free haemoglobin and red blood cells on S-nitrosothiol-mediated inhibition of platelet aggregation. 2 The eects of GSNO and RIG200 in collagen (2.5 mg ml 71 )-induced platelet aggregation in PRP and whole blood were investigated in vitro. Both compounds were found to be powerful inhibitors of aggregation in PRP, and RIG200 was signi®cantly more potent (IC 50 =2.0 mM for GSNO and 0.8 mM for RIG200; P=0.04). 3 Neither compound inhibited aggregation in whole blood, even at concentrations of 100 mM. Red blood cell concentrations as low as 1% of the haematocrit, and cell-free haemoglobin (52.5 mM), signi®cantly reduced their inhibitory eects on platelets. 4 Experiments involving measurement of cyclic GMP levels, electrochemical detection of NO and electron paramagnetic resonance of haemoglobin in red blood cells, indicated that scavenging of NO generated from S-nitrosothiols by haemoglobin was responsible for the lack of eect of Snitrosothiols on platelets in whole blood. 5 These studies suggest that scavenging of NO by haemoglobin in blood might limit the therapeutic application of S-nitrosothiols as anti-platelet agents.

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“…37,38 Additionally, normalization using AUC30 better represents the half-life of NO ( Figure 1C). 34 The present study was not without limitations. First, endothelial cell biopsies in the present study were performed on an arm vein versus an arm artery.…”

Section: Discussionmentioning

confidence: 77%

Flow-mediated dilation is associated with endothelial oxidative stress in human venous endothelial cells

et al. 2014

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Endothelial dysfunction (ED) is the first pathophysiological step that produces atherosclerosis, which is responsible for ≈90% of all cardiovascular diseases. 1-4 ED is generally defined as the decrease in nitric oxide (NO) bio-availability within the endothelium, normally attributed to an increased endothelial oxidative stress. [1][2][3]5,6 In humans, early stages 7 and changes after interventions 8-10 of ED can be assessed non-invasively via flow-mediated dilation (FMD). [11][12][13][14][15] Briefly, FMD measures the dilatory capacity of a blood vessel, typically the brachial artery, which is exposed to a blood flow-induced stimulus (i.e. shear stress) elicited by reactive hyperemia. 12,13 Although FMD is recognized as a bioassay for ED, [11][12][13][14][15] with excellent clinical significance, 16,17 few studies have shown a relationship between FMD and endothelial oxidative stress in humans. 18 FMD is based on two physiological principles: (1) blood flow-induced shear stress activates the endothelium to produce NO; and (2) NO elicits vascular dilation via relaxation of vascular smooth muscle. 12,14 When there is an increased endothelial oxidative stress, endothelial NO synthase (eNOS) is uncoupled, producing a decrease in NO production and bioavailability. 5,6,19 Thus, an increased endothelial oxidative stress should decrease endothelial reactivity to shear stress, which will negatively impact FMD.Accordingly, the purpose of the present study was to determine if FMD is associated with endothelial oxidative Abstract Flow-mediated dilation (FMD) is recognized as a non-invasive endothelial function bioassay. However, FMD's relationship with endothelial cell oxidative stress in humans is yet to be determined. Here, we sought to determine if FMD was associated with endothelial nitric oxide synthase (eNOS) and endothelial oxidative stress in humans. Twenty-seven apparently healthy young men (26.5±5.9 years) underwent brachial artery FMD testing and endothelial cell biopsy from a forearm vein. Non-normalized FMD (%) and three different brachial artery FMD normalizations were performed: (1) peak shear rate (%/SR); (2) area under the SR curve until peak dilation (%/AUC); and (3) AUC 30 seconds before peak dilation (%/AUC30). Immunofluorescence quantification was used to assess eNOS expression and nitrotyrosine (NT), a criterion marker of endothelial oxidative stress. Values for eNOS and NT expression were reported as a ratio of endothelial cell to human umbilical vein endothelial cell average pixel intensity. NT expression was significantly correlated with FMD normalized by AUC30 (r = −0.402, p<0.05). Other FMD normalizations and non-normalized FMD were not significantly correlated with NT expression (r range = −0.364 to −0.142, all p>0.05). There were no significant correlations between eNOS expression and normalized and non-normalized FMD (r range = −0.168 to −0.066, all p>0.05). In conclusion, brachial artery FMD is associated with venous endothelial cell oxidative stress. However, this association is observed onl...

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Half-life of nitric oxide in aqueous solutions with and without haemoglobin

Cited by 141 publications

References 27 publications

Reduction in thrombosis and bacterial adhesion with 7 day implantation of S-nitroso-N-acetylpenicillamine (SNAP)-doped Elast-eon E2As catheters in sheep

Reduction in thrombosis and bacterial adhesion with 7 day implantation of S-nitroso-N-acetylpenicillamine (SNAP)-doped Elast-eon E2As catheters in sheep

Inhibition of human platelet aggregation by a novel S‐nitrosothiol is abolished by haemoglobin and red blood cells in vitro: implications for anti‐thrombotic therapy

Flow-mediated dilation is associated with endothelial oxidative stress in human venous endothelial cells

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