NITRIC-OXIDE CONTRIBUTES TO THE RISE IN FOREARM BLOOD-FLOW DURING MENTAL STRESS IN HUMANS
NITRIC-OXIDE CONTRIBUTES TO THE RISE IN FOREARM BLOOD-FLOW DURING MENTAL STRESS IN HUMANS
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DOI：
10.1113/jphysiol.1994.sp020366
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发表时间：
1994-10-15
影响因子：
5.5
通讯作者：
JOYNER, MJ
中科院分区：
文献类型：
--
作者：
DIETZ, NM;RIVERA, JM;JOYNER, MJ
1.我们的目的是确定血管舒张物质一氧化氮（NO）是否有助于在人类精神压力期间观察到的前臂血流量上升。我们还确定了NO是否可能作为胆碱能刺激血管内皮的结果而释放.在几次3-5分钟的色词测试中，使用体积描记法测量两个前臂的血流量。在一侧前臂，通过肱动脉导管输注一氧化氮合酶阻断剂N-G-单甲基-L-精氨酸（L-NMMA）和其他药物。对侧前臂作为对照.当在精神压力之前给予L-NMMA时，它几乎完全减弱了治疗前臂血流量的上升。在洗脱期后进行的第二轮压力期间，正常的血流反应恢复。在第三轮精神压力期间，给予更多的L-NMMA再次减弱了对精神压力的血流反应。在精神紧张之前给予阿托品，治疗组前臂血流量的增加减少。随后给予阿托品和L-NMMA引起的血流反应比单独给予阿托品时的血流反应减少更大。这些数据表明，NO在人类精神应激时前臂血管舒张中起作用。很可能大部分NO是通过血管内皮的胆碱能刺激释放的。
1. Our aim was to determine whether the vasodilating substance nitric oxide (NO) contributes to the rise in forearm blood flow observed during mental stress in humans. We also determined whether the NO might be released as a result of cholinergic stimulation of the vascular endothelium.2. Blood flow was measured in both forearms using plethysmography during several 3-5 min bouts of a colour word test. In one forearm the nitric oxide synthase blocker N-G-monomethyl-L-arginine (L-NMMA) and other drugs were infused via a brachial artery catheter. The contralateral forearm served as a control.3. When L-NMMA was given prior to mental stress it blunted the rise in blood flow in the treated forearm almost completely. The normal blood flow response returned during a second bout of stress conducted after a wash-out period. During a third bout of mental stress, administration of more L-NMMA again blunted the blood flow responses to mental stress.4. When atropine was given prior to mental stress, the increases in blood flow were reduced in the treated forearm. Subsequent administration of both atropine and L-NMMA caused a somewhat greater reduction in the blood flow responses than those observed with atropine alone.5. These data demonstrate that NO plays a role in forearm vasodilatation during mental stress in humans. It is likely that most of the NO is released by cholinergic stimulation of the vascular endothelium.