Vitamins C and E Inhibit O
            <sub>2</sub>
            <sup>−</sup>
            Production in the Pig Coronary Artery

Nunes, Gilberto L.; Robinson, Keith A.; Kalynych, Anna; King, Spencer B.; Sgoutas, Demetrios S.; Berk, Bradford C.

doi:10.1161/01.cir.96.10.3593

Cited by 147 publications

(108 citation statements)

References 48 publications

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“…30 Bassenge et al 4 found oral ascorbate supplementation completely prevented the development of hemodynamic tolerance and upregulation of platelet activity in healthy volunteers. With the treatment and dosing regimes used in our subjects, a residual hemodynamic action of organic nitrates could be identified that was unaffected by oral ascorbate administration.…”

Section: Discussionmentioning

confidence: 99%

Platelet Nitric Oxide and Superoxide Release During the Development of Nitrate Tolerance

et al. 2002

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Background-The therapeutic benefits that accompany the continuous administration of organic nitrates are attenuated by the development of tolerance to the compounds. Altered superoxide production and NO bioavailability have been implicated in contributing to the development of tolerance, an effect that may be ameliorated by the administration of antioxidants. Methods and Results-We studied the effect of 3 days of continuous transdermal administration of nitroglycerin (NTG) (10 mg/24 hours) on platelet free radical (NO and superoxide anion [O 2 ·Ϫ ] activity) with and without coadministration of supplemental ascorbate (2.4 g/24 hours). NAD(P)H oxidase activity, nitric oxide synthase (NOS) activity, and cyclic guanosine monophosphate (cGMP) content were also assessed. Radial artery pressure pulse waveforms were used to track the hemodynamic actions of NTG. Three days of NTG/placebo was associated with a significant increase in platelet NO and O 2 ·Ϫ production from 1.0Ϯ1.17 to 2.52Ϯ0.88 pmol/10 8 platelets and 13.2Ϯ4.8 to 72.5Ϯ34.4 pmol/10

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Section: Discussionmentioning

confidence: 99%

Platelet Nitric Oxide and Superoxide Release During the Development of Nitrate Tolerance

et al. 2002

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“…O xidative stress and production of both reactive oxygen species (ROS) and reactive nitrogen species (RNS) are thought to contribute to the pathophysiology of vascular diseases such as atherosclerosis (1,2) and restenosis (3)(4)(5)(6)(7)(8)(9). ROS have been implicated in many aspects of vascular injury and neointimal formation, including endothelial cell dysfunction, inflammatory cell recruitment, foam cell formation, and smooth muscle cell (SMC) proliferation (reviewed in ref.…”

mentioning

confidence: 99%

Decreased neointimal formation in Nox2-deficient mice reveals a direct role for NADPH oxidase in the response to arterial injury

Chen

Keaney

Schulz

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced, in part, from NADPH oxidase in response to host invasion and tissue injury. Defects in NADPH oxidase impair host defense; however, the role of ROS and RNS in the response to tissue injury is not known. We addressed this issue by subjecting leukocyte oxidase (Nox2)-deficient (Nox2 ؊/؊ ) mice to arterial injury. Femoral artery injury was associated with increased Nox2 expression, ROS͞RNS production, and oxidative protein and lipid modification in wild-type mice. In Nox2 ؊/؊ mice, RNS-mediated protein oxidation, as monitored by protein nitrotyrosine content, was significantly diminished. This was accompanied by reduced neointimal proliferation, as monitored by intimal thickness and intimal͞medial ratio, in Nox2 ؊/؊ compared to wild-type mice. In addition, Nox2 deficiency led to reduced cellular proliferation and leukocyte accumulation. These data indicate that Nox2-mediated oxidant production has a requisite role in the response to tissue injury.

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“…23,24 In addition, a dysfunctional interaction between the endothelium, platelets, and leukocytes results in a proinflammatory state with free radical production and microvascular plugging. 25,26 Attenuation of Ach-mediated increases in CBF with preserved responses to adenosine would imply a defect at the level of the endothelium. However, this does not clarify whether the diminished Ach response is attributable to abnormalities in stimulated NO production, decreased endothelium-derived hyperpolarizing factor or prostacyclin production, enhanced vasoconstrictors such as serotonin, 22 thromboxane, 27 and endothelin-1, 28 or a combination of these mechanisms.…”

Section: Vasomotor Responses After Pcimentioning

confidence: 99%

Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting

et al. 2002

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Background-Platelet glycoprotein IIb/IIIa receptor blockade with abciximab decreases ischemic events after percutaneous coronary intervention (PCI); however, the mechanism of this benefit has not been fully elucidated. The present study was designed to assess endothelium-dependent vasomotion after coronary stenting and to determine if abciximab alters this response. Methods and Results-The study group consisted of 48 patients (59Ϯ10 years of age) with discrete coronary stenoses who underwent stenting alone (nϭ28) or stenting plus abciximab (nϭ20). A control group consisted of 31 additional patients who had vasomotor testing on a non-PCI vessel. Coronary blood flow (CBF) was measured (0.014-inch Doppler wire) 30 minutes after uncomplicated PCI and in response to the intracoronary infusion of acetylcholine (Ach) (10 Ϫ7 , 10 Ϫ6 mol/L Ach) and adenosine (24 g). Ach-mediated increase in CBF was impaired after stent insertion when compared with the control group (41Ϯ52% versus 70Ϯ48%; PϽ0.05). The stenting plus abciximab group demonstrated a superior CBF response to Ach compared with the stenting alone group (83Ϯ93% versus 41Ϯ52%; PϽ0.05), with no difference between groups in the peak flow or percent change in flow to adenosine. By multivariate analysis, concomitant administration of abciximab was strongly predictive of the change in CBF to Ach (PϽ0.005). Conclusions-Abciximab preserves the CBF response to Ach after coronary stenting. The preservation of microvascular endothelial function may help explain the beneficial clinical effect of this agent in patients undergoing PCI.

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Vitamins C and E Inhibit O ₂ ⁻ Production in the Pig Coronary Artery

Cited by 147 publications

References 48 publications

Platelet Nitric Oxide and Superoxide Release During the Development of Nitrate Tolerance

Platelet Nitric Oxide and Superoxide Release During the Development of Nitrate Tolerance

Decreased neointimal formation in Nox2-deficient mice reveals a direct role for NADPH oxidase in the response to arterial injury

Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting

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Vitamins C and E Inhibit O 2 − Production in the Pig Coronary Artery

Cited by 147 publications

References 48 publications

Platelet Nitric Oxide and Superoxide Release During the Development of Nitrate Tolerance

Platelet Nitric Oxide and Superoxide Release During the Development of Nitrate Tolerance

Decreased neointimal formation in Nox2-deficient mice reveals a direct role for NADPH oxidase in the response to arterial injury

Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting

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Product

Resources

About

Vitamins C and E Inhibit O ₂ ⁻ Production in the Pig Coronary Artery