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Accepted (AM)Open Access (License Unspecified), Open
Journal article
A mathematical model for the role of N2O3 in enhancing nitric oxide bioavailability following nitrite infusion
Nitric oxide, v 60, pp 1-9
30 Nov 2016
PMID: 27565833
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Nitrite infusion into the bloodstream has been shown to elicit vasodilation and protect against ischemia-reperfusion injury through nitric oxide (NO) release in hypoxic conditions. However, the mechanism by which nitrite-derived NO escapes scavenging by hemoglobin in the erythrocyte has not been fully elucidated, owing in part to the difficulty in measuring the reactions and transport on NO in vivo. We developed a mathematical model for an arteriole and surrounding tissue to examine the hypothesis that dinitrogen trioxide (N2O3) acts as a stable intermediate for preserving NO. Our simulations predict that with hypoxia and moderate nitrite concentrations, the N2O3 pathway can significantly preserve the NO produced by hemoglobin nitrite reductase in the erythrocyte and elevate NO reaching the smooth muscle cells. Nitrite retains its ability to increase NO bioavailability even at varying flow conditions, but there is minimal effect under normoxia or very low nitrite concentrations. Our model demonstrates a viable pathway for reconciling experimental findings of potentially beneficial effects of nitrite infusions despite previous models showing negligible NO elevation associated with hemoglobin nitrite reductase. Our results suggest that additional mechanisms may be needed to explain the efficacy of nitrite-induced vasodilation at low infusion concentrations. (C) 2016 Elsevier Inc. All rights reserved.
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Details
- Title
- A mathematical model for the role of N2O3 in enhancing nitric oxide bioavailability following nitrite infusion
- Creators
- Yien Liu - Drexel UniversityDonald G. Buerk - Drexel UniversityKenneth A. Barbee - Drexel UniversityDov Jaron - Drexel University
- Publication Details
- Nitric oxide, v 60, pp 1-9
- Publisher
- Elsevier
- Number of pages
- 9
- Grant note
- HL 116256 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA U01HL116256 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems; [Retired Faculty]
- Web of Science ID
- WOS:000387197000001
- Scopus ID
- 2-s2.0-84984694191
- Other Identifier
- 991019169585304721
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InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Web of Science research areas
- Biochemistry & Molecular Biology
- Cell Biology