Nitric oxide bioavailability modulates the dynamics of microvascular oxygen exchange during recovery from contractions
Nitric oxide bioavailability modulates the dynamics of microvascular oxygen exchange during recovery from contractions
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DOI：
10.1111/j.1748-1716.2010.02137.x
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发表时间：
2010-10-01
影响因子：
6.3
通讯作者：
Poole, D. C.
中科院分区：
文献类型：
--
作者：
Hirai, D. M.;Copp, S. W.;Poole, D. C.
目的：运动非瞬态期间微血管PO(2) （PO(2)mv）降低可能会损害肌肉代谢恢复并限制执行重复性任务的能力。本研究探讨了健康骨骼肌收缩恢复过程中一氧化氮（NO）生物利用度改变对PO(2)mv的影响。我们假设增加的NO生物利用度（硝普钠：SNP）会增加PO(2)mv并加速其恢复动力学，而降低的NO生物利用度（l-硝基精氨酸甲酯：l-NAME）会降低PO(2)mv并减慢其恢复动力学。方法：在SNP （300 μ m）、Krebs-Henseleit（对照）和l-NAME （1.5 mm）灌注条件下，采用荧光猝灭法测定Sprague-Dawley大鼠斜方肌在过渡（休息-1 Hz抽搐-收缩3 min-恢复）过程中的PO(2)mv。结果：与对照组相比，通过PO(2)mv曲线下面积（PO(2 area)）评估，SNP导致整体微血管氧合水平提高；对照：3471 +/- 292 mmHg s；SNP: 4307 +/- 282 mmHg s；平均反应时间（MRToff; Control: 60.2 +/- 6.9 s; SNP: 34.8 +/- 5.7 s; P < 0.05）表明，l-NAME产生较低的PO(2 AREA) （2339 +/- 444 mmHg s; P < 0.05）和较慢的MRToff （86.6 +/- 14.5 s; P < 0.05）。结论：NO的生物利用度在确定O(2)递送与O(2)摄取的匹配以及在健康骨骼肌收缩停止后，上游O(2)压力驱动毛细血管-肌细胞O(2)通量（即PO(2)mv）方面起关键作用。此外，这些数据支持一氧化氮生物利用度降低与肌肉代谢恢复延长之间的机制联系，这在衰老和患病人群中很常见。
Aim:Lowered microvascular PO(2) (PO(2)mv) during the exercise off-transient likely impairs muscle metabolic recovery and limits the capacity to perform repetitive tasks. The current investigation explored the impact of altered nitric oxide (NO) bioavailability on PO(2)mv during recovery from contractions in healthy skeletal muscle. We hypothesized that increased NO bioavailability (sodium nitroprusside: SNP) would enhance PO(2)mv and speed its recovery kinetics while decreased NO bioavailability (l-nitro arginine methyl ester: l-NAME) would reduce PO(2)mv and slow its recovery kinetics.Methods:PO(2)mv was measured by phosphorescence quenching during transitions (rest-1 Hz twitch-contractions for 3 min-recovery) in the spinotrapezius muscle of Sprague-Dawley rats under SNP (300 mu m), Krebs-Henseleit (Control) and l-NAME (1.5 mm) superfusion conditions.Results:Relative to recovery in Control, SNP resulted in greater overall microvascular oxygenation as assessed by the area under the PO(2)mv curve (PO(2 AREA); Control: 3471 +/- 292 mmHg s; SNP: 4307 +/- 282 mmHg s; P < 0.05) and faster off-kinetics as evidenced by the mean response time (MRToff; Control: 60.2 +/- 6.9 s; SNP: 34.8 +/- 5.7 s; P < 0.05), whereas l-NAME produced lower PO(2 AREA) (2339 +/- 444 mmHg s; P < 0.05) and slower MRToff (86.6 +/- 14.5 s; P < 0.05).Conclusion:NO bioavailability plays a key role in determining the matching of O(2) delivery-to-O(2) uptake and thus the upstream O(2) pressure driving capillary-myocyte O(2) flux (i.e. PO(2)mv) following cessation of contractions in healthy skeletal muscle. Additionally, these data support a mechanistic link between reduced NO bioavailability and prolonged muscle metabolic recovery commonly observed in ageing and diseased populations.