Endo T, Imaizumi T, Tagawa T, Shiramoto M, Ando S, Takeshita A
Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Circulation. 1994 Dec;90(6):2886-90. doi: 10.1161/01.cir.90.6.2886.
We wished to determine the role of NO in exercise-induced metabolic forearm vasodilation.
Young healthy volunteers (n = 11) underwent static handgrip exercise (4 to 5 kg, 3 minutes). Forearm blood flow (FBF) measured by strain plethysmography increased from 4.1 +/- 0.7 mL.min-1.100 mL-1 at rest to 9.8 +/- 1.2 mL.min-1.100 mL-1 immediately after exercise and gradually decreased thereafter. Exercise was repeated after intrabrachial artery infusion of NG-monomethyl-L-arginine (L-NMMA) at 4.0 mumol/min for 5 minutes. L-NMMA did not alter blood pressure and heart rate. L-NMMA decreased FBF at rest to 2.9 +/- 0.4 mL.min-1.100 mL-1 (P < .01), peak FBF immediately after exercise to 7.2 +/- 0.7 mL.min-1.100 mL-1 (P < .01), and FBF during the mid to late phase of metabolic vasodilation (P < .01). Calculated oxygen consumption during peak exercise was comparable before and after L-NMMA. Intra-arterially infused L-arginine (10 mg/min, 5 minutes) reversed the inhibitory effect of L-NMMA. To determine the effect of the decrease in resting FBF on exercise-induced hyperemia, we normalized FBF after exercise by resting FBF. The percent increases in FBF after exercise from resting FBF were similar before and after L-NMMA. Furthermore, we examined the effect of intra-arterially infused angiotensin II on FBF at rest and after exercise (n = 7). Angiotensin II decreased FBF at rest from 3.1 +/- 0.3 to 1.8 +/- 0.3 mL.min-1.100 mL-1 (P < .01), peak FBF after exercise from 8.1 +/- 0.5 to 5.6 +/- 0.5 mL.min-1.100 mL-1 (P < .01), and FBF during the mid to late phase of metabolic vasodilation. The effects of L-NMMA and angiotensin II on FBF at rest and exercise were similar.
Our results suggest that L-NMMA decreased FBF after exercise largely by decreasing resting FBF. These results suggest that NO may not play a significant role in exercise-induced metabolic arteriolar vasodilation in the forearm of healthy humans.
我们希望确定一氧化氮（NO）在运动诱导的代谢性前臂血管舒张中的作用。
年轻健康志愿者（n = 11）进行静态握力运动（4至5千克，3分钟）。通过应变容积描记法测量的前臂血流量（FBF）从静息时的4.1±0.7毫升·分钟⁻¹·100毫升⁻¹增加到运动后即刻的9.8±1.2毫升·分钟⁻¹·100毫升⁻¹，随后逐渐下降。在肱动脉内以4.0微摩尔/分钟的速度输注N⁻甲基⁻L⁻精氨酸（L⁻NMMA）5分钟后重复运动。L⁻NMMA未改变血压和心率。L⁻NMMA将静息时的FBF降至2.9±0.4毫升·分钟⁻¹·100毫升⁻¹（P <.01），运动后即刻的峰值FBF降至7.2±0.7毫升·分钟⁻¹·100毫升⁻¹（P <.01），以及代谢性血管舒张中晚期的FBF（P <.01）。L⁻NMMA前后运动峰值时计算的耗氧量相当。动脉内输注L⁻精氨酸（10毫克/分钟，5分钟）可逆转L⁻NMMA的抑制作用。为了确定静息FBF降低对运动诱导的充血的影响，我们通过静息FBF对运动后的FBF进行标准化。L⁻NMMA前后运动后FBF相对于静息FBF的增加百分比相似。此外，我们研究了动脉内输注血管紧张素II对静息和运动后FBF的影响（n = 7）。血管紧张素II将静息时的FBF从3.1±0.3降至1.8±0.3毫升·分钟⁻¹·100毫升⁻¹（P <.01），运动后峰值FBF从8.1±0.5降至5.6±0.5毫升·分钟⁻¹·100毫升⁻¹（P <.01），以及代谢性血管舒张中晚期的FBF。L⁻NMMA和血管紧张素II对静息和运动时FBF的影响相似。
我们的结果表明，L⁻NMMA主要通过降低静息FBF来降低运动后的FBF。这些结果表明，NO在健康人前臂运动诱导的代谢性小动脉血管舒张中可能不起重要作用。
