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一氧化氮在人体长时间有节奏握力运动中的运动性充血中的作用。

Role of nitric oxide in exercise hyperaemia during prolonged rhythmic handgripping in humans.

作者信息

Dyke C K, Proctor D N, Dietz N M, Joyner M J

机构信息

Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

J Physiol. 1995 Oct 1;488 ( Pt 1)(Pt 1):259-65. doi: 10.1113/jphysiol.1995.sp020964.

Abstract
  1. We sought to determine whether the vasodilating molecule nitric oxide (NO) contributes to the forearm hyperaemia observed during prolonged rhythmic handgripping in humans. 2. Two bouts of exercise were performed during experimental protocols conducted on separate days. During each protocol the subject performed a 10 min and a 20 min bout of rhythmic (30 min-1) handgripping at 15% of maximum. Two exercise bouts were required to facilitate pharmacological interventions during the second protocol. Blood flow in the exercising forearm was measured every minute with plethysmography during brief pauses in the contractions. During both exercise bouts in the first protocol, forearm blood flow increased 2- to 3-fold above rest after 1 min of handgripping and remained constant at that level throughout the exercise. 3. During the 10 min bout of exercise in the second protocol, acetylcholine was given via a brachial artery catheter at 16 micrograms min-1 for 3 min to evoke NO release from the vascular endothelium. This caused forearm blood flow to increase above the values observed during exercise alone. 4. During the 20 min trial of handgripping in the second protocol, the NO synthase blocker NG-monomethyl-L-arginine (L-NMMA) was infused in the exercising forearm via the brachial catheter after 5 min of handgripping. The L-NMMA was infused at 4 mg min-1 for 10 min. 5. L-NMMA during exercise caused forearm blood flow to fall to values approximately 20-30% lower than those observed during exercise alone. When ACh was given during exercise after L-NMMA administration the rise in blood flow was also blunted, indicating blockade of NO synthase. These data suggest NO plays a role in exercise hyperaemia in humans.
摘要
  1. 我们试图确定血管舒张分子一氧化氮(NO)是否导致人类长时间有节奏的握力运动期间观察到的前臂充血。2. 在不同日期进行的实验方案中进行了两轮运动。在每个方案中,受试者以最大力量的15%进行10分钟和20分钟的有节奏(每分钟30次)握力运动。需要两轮运动以便在第二个方案中进行药物干预。在收缩的短暂间歇期间,用体积描记法每分钟测量一次运动前臂的血流。在第一个方案的两轮运动中,握力运动1分钟后,前臂血流比静息时增加2至3倍,并在整个运动过程中保持在该水平。3. 在第二个方案的10分钟运动期间,通过肱动脉导管以16微克/分钟的速度给予乙酰胆碱3分钟,以促使血管内皮释放NO。这导致前臂血流增加到单独运动期间观察到的值之上。4. 在第二个方案的20分钟握力试验中,在握力运动5分钟后,通过肱动脉导管将NO合酶阻滞剂N-甲基-L-精氨酸(L-NMMA)注入运动的前臂。以4毫克/分钟的速度注入L-NMMA 10分钟。5. 运动期间的L-NMMA导致前臂血流降至比单独运动期间观察到的值低约20-30%的值。在给予L-NMMA后运动期间给予乙酰胆碱时,血流的增加也减弱,表明NO合酶被阻断。这些数据表明NO在人类运动性充血中起作用。

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