Department of Anesthesiology, Mayo Clinic Rochester, MN 55905, USA.
J Appl Physiol (1985). 2011 May;110(5):1181-9. doi: 10.1152/japplphysiol.00836.2010. Epub 2011 Feb 3.
We previously demonstrated that nitric oxide (NO) contributes to compensatory vasodilation in the contracting human forearm subjected to acute hypoperfusion. We examined the potential role of an adenosine-NO interaction to this response in 17 male subjects (25 ± 2 yr). In separate protocols subjects performed rhythmic forearm exercise (20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included exercise before inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and local [brachial artery catheter pressure (BAP)] and systemic [mean arterial pressure (MAP); Finometer] arterial pressure were measured. In protocol 1 (n = 10), exercise was repeated during nitric oxide synthase inhibition [N(G)-monomethyl-L-arginine (L-NMMA)] alone and during L-NMMA-aminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-L-NMMA. Forearm vascular conductance (FVC; ml·min(-1)·100 mmHg(-1)) was calculated from blood flow (ml/min) and BAP (mmHg). Percent recovery in FVC during inflation was calculated as (steady-state inflation + exercise value - nadir)/[steady-state exercise (control) value - nadir]. In protocol 1, percent recovery in FVC was 108 ± 8% during the control (no drug) trial. Percent recovery in FVC was attenuated with inhibition of NO formation alone (78 ± 9%; P < 0.01 vs. control) and was attenuated further with combined inhibition of NO and adenosine (58 ± 9%; P < 0.01 vs. L-NMMA). In protocol 2, percent recovery was reduced with adenosine receptor blockade (74 ± 11% vs. 113 ± 6%, P < 0.01) compared with control drug trials. Percent recovery in FVC was attenuated further with combined inhibition of adenosine and NO (48 ± 11%; P < 0.05 vs. aminophylline). Our data indicate that adenosine contributes to compensatory vasodilation in an NO-independent manner during exercise with acute hypoperfusion.
我们之前已经证明，一氧化氮（NO）有助于在急性低灌注状态下收缩的人类前臂中的代偿性血管扩张。我们在 17 名男性受试者（25±2 岁）中研究了腺苷-NO 相互作用对这种反应的潜在作用。在单独的方案中，受试者在肘上方肱动脉的球囊充气时进行节律性前臂运动（最大的 20%）。每个试验包括充气前的运动、充气时的运动和充气后的运动（各 3 分钟）。前臂血流量（FBF；超声）和局部[肱动脉导管压（BAP）]和全身[平均动脉压（MAP）；Finometer]动脉压均进行了测量。在方案 1（n=10）中，在单独给予一氧化氮合酶抑制剂[N（G）-单甲基-L-精氨酸（L-NMMA）]和给予 L-NMMA-氨茶碱（腺苷受体阻断）时重复运动。在方案 2 中，单独给予氨茶碱和氨茶碱-L-NMMA 时重复运动。从血流量（ml/min）和 BAP（mmHg）计算前臂血管传导率（FVC；ml·min-1·100mmHg-1）。充气时 FVC 的恢复百分比计算为（充气时的稳态+运动值-最低点）/[（对照）运动时的稳态值-最低点]。在方案 1 中，在对照（无药物）试验中，FVC 的恢复百分比为 108±8%。单独抑制 NO 形成（78±9%；P<0.01 与对照）和进一步抑制 NO 和腺苷（58±9%；P<0.01 与 L-NMMA）会减弱 FVC 的恢复百分比。在方案 2 中，与对照药物试验相比，腺苷受体阻断会降低 FVC 的恢复百分比（74±11%与 113±6%，P<0.01）。进一步抑制腺苷和 NO（48±11%；P<0.05 与氨茶碱）会进一步减弱 FVC 的恢复百分比。我们的数据表明，在急性低灌注时的运动中，腺苷以一种不依赖于 NO 的方式参与代偿性血管扩张。
