Tagawa T, Imaizumi T, Endo T, Shiramoto M, Harasawa Y, Takeshita A
Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Circulation. 1994 Nov;90(5):2285-90. doi: 10.1161/01.cir.90.5.2285.
The role of nitric oxide (NO) in reactive hyperemia (RH) is not well known. We investigated whether NO plays a role in RH in human forearm vessels by examining the effects of NG-monomethyl-L-arginine (L-NMMA), a blocker of NO synthesis, on reactive hyperemic flow.
Forearm blood flow (FBF) was measured by strain-gauge plethysmography with a venous occlusion technique. The left brachial artery was cannulated for drug infusion and direct measurement of arterial pressure. To produce RH, blood flow to the forearm was prevented by inflation of a cuff on the upper arm to suprasystolic pressure for intervals of 3 and 10 minutes. After the release of arterial occlusion (AO), FBF was measured every 15 seconds for 3 minutes. Resting FBF was 4.3 +/- 0.3 mL.min-1.100 mL-1 before 3 minutes of AO and 4.1 +/- 0.6 mL.min-1.100 mL-1 before 10 minutes of AO. FBF increased to 32.3 +/- 1.9 and 38.2 +/- 3.1 mL.min-1.100 mL-1 immediately after 3 and 10 minutes of AO, respectively, and gradually decayed (n = 13). Intra-arterial infusion of L-NMMA (4 mumol/min for 5 minutes) decreased baseline FBF (P < .01) without changes in arterial pressure. L-NMMA did not affect the peak reactive hyperemic FBF after 3 and 10 minutes of AO. L-NMMA significantly decreased total reactive hyperemic flow (flow debt repayment) by 20% to 30% after 3 and 10 minutes of AO. Simultaneous infusion of L-arginine (a precursor of NO) with L-NMMA reversed the effects of L-NMMA.
Our results suggest that NO plays a minimal role in vasodilation at peak RH but plays a modest yet significant role in maintaining vasodilation after peak vasodilation. Our results also suggest that reactive hyperemia in human forearms is caused largely by mechanisms other than NO.
一氧化氮（NO）在反应性充血（RH）中的作用尚不清楚。我们通过研究一氧化氮合成阻滞剂NG-单甲基-L-精氨酸（L-NMMA）对反应性充血血流的影响，来探讨NO在人体前臂血管反应性充血中是否发挥作用。
采用静脉阻断技术，通过应变片体积描记法测量前臂血流量（FBF）。将左肱动脉插管用于药物输注和直接测量动脉压。为诱导反应性充血，通过在上臂绑扎袖带使其充气至收缩压以上，持续3分钟和10分钟，以阻断前臂血流。解除动脉阻断（AO）后，每隔15秒测量一次FBF，共测量3分钟。静息FBF在AO 3分钟前为4.3±0.3 mL·min⁻¹·100 mL⁻¹，在AO 10分钟前为4.1±0.6 mL·min⁻¹·100 mL⁻¹。在AO 3分钟和10分钟后，FBF立即分别增加至32.3±1.9和38.2±3.1 mL·min⁻¹·100 mL⁻¹，并逐渐下降（n = 13）。动脉内输注L-NMMA（4 μmol/min，持续5分钟）可降低基础FBF（P < 0.01），而动脉压无变化。L-NMMA不影响AO 3分钟和10分钟后的反应性充血峰值FBF。L-NMMA显著降低AO 3分钟和10分钟后的总反应性充血血流（血流亏欠偿还）20%至30%。L-精氨酸（NO的前体）与L-NMMA同时输注可逆转L-NMMA的作用。
我们的结果表明，NO在反应性充血峰值时的血管舒张中作用极小，但在血管舒张峰值后维持血管舒张中起适度但显著的作用。我们的结果还表明，人体前臂的反应性充血主要由NO以外的机制引起。
