Martin Elizabeth A, Nicholson Wayne T, Eisenach John H, Charkoudian Nisha, Joyner Michael J
Dept. of Anesthesiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905, USA.
J Appl Physiol (1985). 2006 Aug;101(2):492-9. doi: 10.1152/japplphysiol.00684.2005. Epub 2006 Apr 13.
To gain insight into the role of adenosine (Ado) in exercise hyperemia, we compared forearm vasodilation induced by intra-arterial infusion of three doses of Ado with vasodilation during three workloads of forearm handgrip exercise in 27 human subjects. We measured forearm blood flow (FBF) using Doppler ultrasound and mean arterial pressure (MAP) via brachial artery catheters and calculated forearm vascular conductance (FVC = FBF/MAP) during each infusion dose or workload. We found that about half of the subjects demonstrated robust vasodilator responsiveness to both Ado infusion and exercise, and the other half demonstrated blunted vasodilator responsiveness to Ado infusion compared with exercise. In 15 subjects (identified as "Ado responders"), the change in FVC above baseline was 209 +/- 33, 419 +/- 57, and 603 +/- 75 ml.min(-1).100 mmHg(-1) for the low, medium, and high doses of Ado, respectively, and 221 +/- 35, 413 +/- 54, and 582 +/- 70 ml.min(-1).100 mmHg(-1) for the low, medium, and high exercise workloads, respectively. In the other 12 subjects (identified as "Ado nonresponders"), the change in FVC above baseline was 102 +/- 36, 113 +/- 42, and 151 +/- 54 ml.min(-1).100 mmHg(-1) for the low, medium, and high doses of Ado, respectively (P < 0.05 vs. Ado responders), whereas exercise hyperemia was not different from Ado responders (P > 0.05). Furthermore, infusion of NG-monomethyl-L-arginine (L-NMMA) blunted vasodilator responses to Ado infusion only in Ado responders (P < 0.01 vs. post-L-NMMA) and had no effect on exercise in either group. We also found differences in vasodilator responses to isoproterenol at all doses, but acetylcholine only at one dose, between Ado responders and nonresponders. We conclude that vasodilator responsiveness to Ado exhibits a bimodal distribution among human subjects involving differences in the contribution of nitric oxide to Ado-mediated vasodilation. Finally, our data support the concept that neither Ado nor nitric oxide is obligatory for exercise hyperemia.
为深入了解腺苷（Ado）在运动性充血中的作用，我们比较了27名健康受试者在动脉内输注三种剂量Ado所诱导的前臂血管舒张情况与前臂握力运动三种负荷下的血管舒张情况。我们使用多普勒超声测量前臂血流量（FBF），通过肱动脉导管测量平均动脉压（MAP），并计算每次输注剂量或负荷期间的前臂血管传导率（FVC = FBF/MAP）。我们发现，约一半受试者对Ado输注和运动均表现出强烈的血管舒张反应，另一半受试者与运动相比，对Ado输注的血管舒张反应减弱。在15名受试者（被认定为“Ado反应者”）中，低、中、高剂量Ado时，FVC相对于基线的变化分别为209±33、419±57和603±75 ml·min⁻¹·100 mmHg⁻¹，低、中、高运动负荷时，FVC相对于基线的变化分别为221±35、413±54和582±70 ml·min⁻¹·100 mmHg⁻¹。在另外12名受试者（被认定为“Ado无反应者”）中，低、中、高剂量Ado时，FVC相对于基线的变化分别为102±36、113±42和151±54 ml·min⁻¹·100 mmHg⁻¹（与Ado反应者相比，P<0.05），而运动性充血与Ado反应者无差异（P>0.05）。此外，输注N⁻单甲基⁻L⁻精氨酸（L⁻NMMA）仅使Ado反应者对Ado输注的血管舒张反应减弱（与L⁻NMMA注射后相比，P<0.01），对两组的运动均无影响。我们还发现，Ado反应者和无反应者对所有剂量异丙肾上腺素的血管舒张反应存在差异，但对乙酰胆碱的血管舒张反应仅在一个剂量上存在差异。我们得出结论，人类受试者对Ado的血管舒张反应呈双峰分布，这涉及一氧化氮对Ado介导的血管舒张作用贡献的差异。最后，我们的数据支持以下观点，即Ado和一氧化氮都不是运动性充血所必需的。
