Shen W, Xu X, Ochoa M, Zhao G, Bernstein R D, Forfia P, Hintze T H
Department of Physiology, New York Medical College, Valhalla, NY 10595, USA.
Acta Physiol Scand. 2000 Apr;168(4):675-86. doi: 10.1046/j.1365-201x.2000.00719.x.
Our previous studies uncovered an inhibitory effect of nitric oxide (NO) on leg skeletal muscle respiration in dogs at rest. The role of NO in the modulation of O2 consumption and O2 extraction in hindlimb muscle during elevated metabolic states was investigated in chronically instrumented dogs while walking and at three exercise intensities which markedly increased hindlimb blood flow. Walking resulted in increased O2 consumption by 17 +/- 4 mL min-1 and O2 extraction from 24 +/- 1 to 37 +/- 8%, with no alteration in hindlimb blood flow (BFLeg) and vascular resistance (VRLeg). Running at the highest speed (9.1 mph) resulted in an increase in BFLeg from 0.67 +/- 0.05 to 2.2 +/- 0.1 L min-1, a reduction of VRLeg and elevation of hindlimb O2 consumption from 33 +/- 3 to 226 +/- 21 mL min-1 and O2 extraction from 29 +/- 2 to 61 +/- 5%, with a decrease in leg venous PO2 from 38 +/- 1 to 25 +/- 1 mmHg. After nitro-L-arginine (NLA) (35 mg kg-1, i.v.) to inhibit endogenous NO synthesis, walking caused greater increases in hindlimb O2 consumption (29 +/- 5 mL min-1) and O2 extraction (43 +/- 1 to 60 +/- 3%) (both P < 0.05), with no significant change in BFLeg. During running at the highest speed, BFLeg was 1.9 +/- 0.1 L min-1 (P < 0. 05) and VRLeg was higher, accompanied by increases in hindlimb O2 consumption from 49 +/- 7 to 318 +/- 24 mL min-1 and O2 extraction from 41 +/- 2 to 79 +/- 4% (both P < 0.05), with a greater decrease in leg venous PO2 from 33 +/- 1 to 20 +/- 1 mmHg (P < 0.05). Similar results were found for intermediate levels of exercise. Our results indicate that NO modulates hindlimb skeletal muscle O2 extraction and O2 usage whether blood flow increased or not during exercise.
我们之前的研究发现，一氧化氮（NO）对静息状态下犬类腿部骨骼肌呼吸有抑制作用。在慢性植入仪器的犬类行走以及三种显著增加后肢血流量的运动强度下，研究了NO在高代谢状态下对后肢肌肉氧气消耗和氧气提取调节中的作用。行走导致氧气消耗增加17±4 mL·min⁻¹，氧气提取率从24±1%增加到37±8%，而后肢血流量（BFLeg）和血管阻力（VRLeg）无变化。以最高速度（9.1英里/小时）奔跑导致BFLeg从0.67±0.05 L·min⁻¹增加到2.2±0.1 L·min⁻¹，VRLeg降低，后肢氧气消耗从33±3 mL·min⁻¹增加到226±21 mL·min⁻¹，氧气提取率从29±2%增加到61±5%，腿部静脉血氧分压从38±1 mmHg降低到25±1 mmHg。静脉注射硝基-L-精氨酸（NLA）（35 mg·kg⁻¹）以抑制内源性NO合成后，行走导致后肢氧气消耗（29±5 mL·min⁻¹）和氧气提取率（43±1%到60±3%）进一步增加（均P<0.05），BFLeg无显著变化。在最高速度奔跑时，BFLeg为1.9±0.1 L·min⁻¹（P<0.05），VRLeg更高，同时后肢氧气消耗从49±7 mL·min⁻¹增加到318±24 mL·min⁻¹，氧气提取率从41±2%增加到79±4%（均P<0.05），腿部静脉血氧分压从33±1 mmHg更大幅度地降低到20±1 mmHg（P<0.05）。中等运动强度时也发现了类似结果。我们的结果表明，无论运动期间血流量是否增加，NO都能调节后肢骨骼肌的氧气提取和氧气利用。
