Engelke K A, Williams M M, Dietz N M, Joyner M J
Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905, USA.
Clin Auton Res. 1997 Apr;7(2):85-91. doi: 10.1007/BF02267752.
To determine if the vasodilating substance nitric oxide (NO) interferes with the ability of sympathetic nerves to regulate blood flow in humans, forearm blood flow (FBF) was measured during brachial artery infusions of acetylcholine (ACh) to evoke endothelial NO release, and during infusions of the NO donor nitroprusside (NTP) in five healthy volunteers. Sympathetic activity was increased by application of lower body suction and antagonized by brachial artery infusions of phentolamine. In the control condition, FBF was 2.4 +/- 0.4 ml/100 ml per min and rose by 16.9 +/- 3.6 ml/100 ml per min during ACh at 16 micrograms/min and by 17.0 +/- 4.3 ml/100 ml per min at 64 micrograms/min. With suction, FBF was 1.7 +/- 0.6 ml/100 ml per min (p < 0.05 versus control) and rose by 11.4 +/- 3.2 ml/100 ml per min during ACh at 16 micrograms/min (p < 0.05 versus control). After phentolamine, FBF was 3.8 +/- 0.5 ml/100 ml per min at baseline (p < 0.05 versus control) and the increases in flow with ACh at either 16 or 64 micrograms/min were identical to control. During the control NTP trial, FBF rose by 6.3 +/- 1.1 ml/100 ml per min with NTP at 2.5 micrograms/min and by 12.1 +/- 1.4 ml/100 ml per min at 10 micrograms/min. Suction blunted and phentolamine augmented the increases in flow with NTP by approximately 50% (p < 0.05). Due to the unexpected results with ACh, the effects of suction and pharmacological sympathectomy with both phentolamine and bretylium on ACh-mediated dilation were evaluated with lower doses of ACh (8 and 32 micrograms/min) in six additional studies. Again, altered sympathetic activity had inconsistent effects on the rise in FBF with ACh administration. The effects of altered sympathetic activity on the blood flow responses to NTP indicate that sympathetic activity can modulate NO-mediated vasodilation, suggesting that NO does not have a major sympatholytic effect in the human forearm. That sympathetic activity did not consistently alter ACh-mediated vasodilation suggests that vasodilating mechanisms, in addition to NO release, can be activated by arterial administration of ACh in the human forearm.
为了确定血管舒张物质一氧化氮（NO）是否会干扰交感神经调节人体血流的能力，在五名健康志愿者中，分别在输注乙酰胆碱（ACh）以诱发内皮源性NO释放期间以及输注NO供体硝普钠（NTP）期间，测量了前臂血流量（FBF）。通过施加下体负压增加交感神经活动，并通过肱动脉输注酚妥拉明来拮抗。在对照条件下，FBF为2.4±0.4 ml/100 ml per min，在16微克/分钟的ACh输注期间上升至16.9±3.6 ml/100 ml per min，在64微克/分钟时上升至17.0±4.3 ml/100 ml per min。施加负压时，FBF为1.7±0.6 ml/100 ml per min（与对照相比，p<0.05），在16微克/分钟的ACh输注期间上升至11.4±3.2 ml/100 ml per min（与对照相比，p<0.05）。给予酚妥拉明后，基线时FBF为3.8±0.5 ml/100 ml per min（与对照相比，p<0.05），16或64微克/分钟的ACh引起的血流量增加与对照相同。在对照NTP试验中，2.5微克/分钟的NTP使FBF上升6.3±1.1 ml/100 ml per min，10微克/分钟时上升12.1±1.4 ml/100 ml per min。负压减弱而酚妥拉明增强了NTP引起的血流量增加约50%（p<0.05）。由于ACh出现了意外结果，在另外六项研究中，使用较低剂量的ACh（8和32微克/分钟）评估了负压以及酚妥拉明和溴苄铵进行药理性交感神经切除对ACh介导的血管舒张的影响。同样，交感神经活动改变对ACh给药后FBF升高的影响并不一致。交感神经活动改变对NTP引起的血流反应的影响表明，交感神经活动可以调节NO介导的血管舒张，这表明NO在人前臂中没有主要的交感神经溶解作用。交感神经活动并未始终改变ACh介导的血管舒张，这表明除了NO释放外，血管舒张机制也可通过在人前臂动脉内给予ACh来激活。
