Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506-5802, USA.
Acta Physiol (Oxf). 2010 Oct;200(2):159-69. doi: 10.1111/j.1748-1716.2010.02137.x.
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.
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 microm), Krebs-Henseleit (CONTROL) and l-NAME (1.5 mm) superfusion conditions.
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) ;
3471 ± 292 mmHg s; SNP: 4307 ± 282 mmHg s; P < 0.05) and faster off-kinetics as evidenced by the mean response time (MRToff;
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 ± 14.5s; P < 0.05).
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.
运动期间微血管 PO₂（PO₂mv）降低可能会损害肌肉代谢恢复，并限制重复任务的能力。目前的研究探讨了改变一氧化氮（NO）生物利用度对健康骨骼肌收缩后 PO₂mv 恢复的影响。我们假设增加 NO 生物利用度（硝普钠：SNP）会增强 PO₂mv 并加速其恢复动力学，而降低 NO 生物利用度（l-硝基精氨酸甲酯：l-NAME）会降低 PO₂mv 并减缓其恢复动力学。
在 Sprague-Dawley 大鼠的斜方肌中，通过磷光猝灭在过渡期间（休息-1 Hz 颤搐收缩 3 分钟-恢复）测量 PO₂mv，在 SNP（300 μm）、Krebs-Henseleit（对照）和 l-NAME（1.5 mM）灌注条件下。
与对照恢复相比，SNP 导致更大的整体微血管氧合，通过 PO₂mv 曲线下面积（PO₂AREA）评估；
3471±292 mmHg s；SNP：4307±282 mmHg s；P<0.05）和更快的离线动力学，表现为平均响应时间（MRToff）；
60.2±6.9 s；SNP：34.8±5.7 s；P<0.05），而 l-NAME 产生较低的 PO₂AREA（2339±444 mmHg s；P<0.05）和较慢的 MRToff（86.6±14.5 s；P<0.05）。
在健康的骨骼肌中，NO 生物利用度在决定 O₂输送与 O₂摄取的匹配以及毛细血管-肌细胞 O₂通量的上游 O₂压力（即 PO₂mv）方面起着关键作用。此外，这些数据支持了在衰老和患病人群中观察到的降低的 NO 生物利用度与肌肉代谢恢复延长之间的机制联系。
