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Journal of applied physiology v.122 no.1, 2017년, pp.153 - 160   SCI SCIE
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Effect of sodium nitrite on local control of contracting skeletal muscle microvascular oxygen pressure in healthy rats

Colburn, Trenton D. ; Ferguson, Scott K. ; Holdsworth, Clark T. ; Craig, Jesse C. ; Musch, Timothy I. ; Poole, David C. ;

  • 초록  

    Ischemic conditions as diverse as chronic heart failure (CHF) and frostbite inflict tissue damage via inadequate O 2 delivery. Herein we demonstrate that direct application of sodium nitrite enhances the O 2 supply-O 2 demand relationship, raising microvascular O 2 pressure in healthy skeletal muscle. This therapeutic action of nitrite-derived nitric oxide occurred without inducing systemic hypotension and has the potential to relieve focal ischemia and preserve tissue vitality by enhancing O 2 delivery. 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 2 driving pressure (P O 2 mv ; O 2 delivery/O 2 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, [Formula] was superfused onto the spinotrapezius muscle. It was hypothesized that local [Formula] administration would elevate resting P O 2 mv and slow P O 2 mv kinetics [increased time constant (τ) and mean response time (MRT)] following the onset of muscle contractions without decreasing MAP. In 12 anesthetized male Sprague-Dawley rats, P O 2 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 sodium nitrite (NaNO 2 30 mM). [Formula] superfusion elevated resting P O 2 mv (control: 28.4 ± 1.1 vs. [Formula]: 31.6 ± 1.2 mmHg; P ≤ 0.05), τ (control: 12.3 ± 1.2 vs. [Formula]: 19.7 ± 2.2 s; P ≤ 0.05), and MRT (control: 19.3 ± 1.9 vs. [Formula]: 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 postsuperfusion respectively; P > 0.05). These results indicate that [Formula] supplementation delivered to the muscle directly through [Formula] 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. NEW & NOTEWORTHY Ischemic conditions as diverse as chronic heart failure (CHF) and frostbite inflict tissue damage via inadequate O 2 delivery. Herein we demonstrate that direct application of sodium nitrite enhances the O 2 supply-O 2 demand relationship, raising microvascular O 2 pressure in healthy skeletal muscle. This therapeutic action of nitrite-derived nitric oxide occurred without inducing systemic hypotension and has the potential to relieve focal ischemia and preserve tissue vitality by enhancing O 2 delivery.


  • 주제어

    beetroot .   nitrate .   nitric oxide .   microcirculation .   oxygen delivery .   blood flow .   exercise .   vascular control.  

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