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Effect of sodium nitrite on local control of contracting skeletal muscle microvascular oxygen pressure in healthy rats.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Colburn, Trenton D. Ferguson, Scott K. Holdsworth, Clark T. Craig, Jesse C. Musch, Timothy I. Poole, David C.
Description	Author Affiliation: Colburn TD ( Kansas State University.); Ferguson SK ( University of Colorado, Denver.); Holdsworth CT ( Kansas State University.); Craig JC ( Kansas State University.); Musch TI ( Kansas State University.); Poole DC ( Kansas State University poole@vet.ksu.edu.)
Abstract	Exercise intolerance characteristic of diseases such as chronic heart failure (CHF) and diabetes is associated with reduced nitric oxide (NO) bioavailability from nitric oxide synthase (NOS), resulting in an impaired microvascular O driving pressure (PO mv; O delivery / O utilization) and metabolic control. Infusions of the potent NO donor sodium nitroprusside augment NO bioavailability, yet decrease mean arterial pressure (MAP) thereby reducing its potential efficacy for patient populations. To eliminate or reduce hypotensive sequelae, NO was superfused onto the spinotrapezius muscle. It was hypothesized that local NO administration would elevate resting PO mv and slow PO mv kinetics (increased τ: time constant, MRT: mean response time) following the onset of muscle contractions without decreasing MAP. In 12 anesthetized male Sprague-Dawley rats, PO mv of the circulation-intact spinotrapezius muscle was measured by phosphorescence quenching during 180 s of electrically-induced twitch contractions (1 Hz) before and after superfusion of NaNO2 (30 mM). NO superfusion elevated resting PO mv (CON: 28.4 ± 1.1 vs NO : 31.6 ± 1.2 mmHg, P ≤ 0.05), τ (CON: 12.3 ± 1.2 vs NO : 19.7 ± 2.2 s, P ≤ 0.05) and MRT (CON: 19.3 ± 1.9 vs NO : 25.6 ± 3.3 s, P ≤ 0.05). Importantly, these effects occurred in the absence of any reduction in MAP (103 ± 4 vs 105 ± 4 mmHg, pre- and post-superfusion respectively; P Ë 0.05). These results indicate that NO supplementation delivered to the muscle directly through NO superfusion enhances the blood-myocyte oxygen driving pressure without compromising MAP at rest and following the onset of muscle contraction. This strategy has substantial clinical utility for a range of ischemic conditions.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
Journal	Journal of Applied Physiology
Language	English
Publisher	American Physiological Society
Publisher Date	2016-10-27
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Applied Physiology Molecular Biology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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