Engelke K A, Halliwill J R, Proctor D N, Dietz N M, Joyner M J
Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
J Appl Physiol (1985). 1996 Oct;81(4):1807-14. doi: 10.1152/jappl.1996.81.4.1807.
We investigated the separate and combined contributions of nitric oxide (NO) and vasodilating prostaglandins as mediators of reactive hyperemia in the human forearm. Forearm blood flow (FBF) was measured with venous occlusion plethysmography after 5 min of ischemia. In one protocol (n = 12), measurements were made before and after intra-arterial administration of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) to one forearm. In a separate protocol (n = 7), measurements were made before and after systemic administration of the cyclooxygenase inhibitor ibuprofen and again after L-NMMA. L-NMMA reduced baseline FBF at rest (2.7 +/- 0.4 to 1.6 +/- 0.2 ml.100 ml-1.min-1; P < 0.05) and had a modest effect on peak forearm vascular conductance and flow (forearm vascular conductance = 31.1 +/- 3.1 vs. 25.7 +/- 2.5 ml.min-1.100 ml forearm-1.100 mmHg of perfusion pressure-1.min-1, P < 0.05; FBF = 26.6 +/- 2.9 vs. 22.8 +/- 2.6 ml.100 ml-1.min-1, P = 0.055). Total excess flow above baseline during reactive hyperemia was unaffected by L-NMMA (14.3 +/- 3.0 vs. 13.1 +/- 2.4 ml/100 ml; P < 0.05). Ibuprofen did not change FBF at rest, reduced peak FBF from 27.6 +/- 1.9 to 20.3 +/- 2.7 ml.100 ml-1.min-1 (P < 0.05), but had no effect on total excess flow above baseline, Infusion of L-NMMA after ibuprofen reduced FBF at rest by 40%, had no effect on peak flow, but reduced total excess flow above baseline from 12.0 +/- 2.5 to 7.6 +/- 1.3 ml/100 ml (P < 0.05). These date demonstrate that NO synthase inhibition has a modest effect on peak vasodilation during reactive hyperemia but plays a minimal role later. Prostaglandins appear to be important determinants of peak flow. The effects of NO synthase inhibition during reactive hyperemia may also be potentiated by concurrent cyclooxygenase inhibition.
我们研究了一氧化氮（NO）和血管舒张性前列腺素作为人体前臂反应性充血介质的单独及联合作用。在缺血5分钟后，用静脉阻塞体积描记法测量前臂血流量（FBF）。在一个方案中（n = 12），对一侧前臂在动脉内注射NO合酶抑制剂NG-单甲基-L-精氨酸（L-NMMA）前后进行测量。在另一个单独的方案中（n = 7），在全身给予环氧化酶抑制剂布洛芬前后以及再次给予L-NMMA后进行测量。L-NMMA降低了静息时的基线FBF（从2.7±0.4降至1.6±0.2 ml·100 ml⁻¹·min⁻¹；P < 0.05），并对峰值前臂血管传导率和血流量有适度影响（前臂血管传导率 = 31.1±3.1对25.7±2.5 ml·min⁻¹·100 ml前臂⁻¹·100 mmHg灌注压⁻¹·min⁻¹，P < 0.05；FBF = 26.6±2.9对22.8±2.6 ml·100 ml⁻¹·min⁻¹，P = 0.055）。反应性充血期间高于基线的总过量血流量不受L-NMMA影响（14.3±3.0对13.1±2.4 ml/100 ml；P < 0.05）。布洛芬未改变静息时的FBF，将峰值FBF从27.6±1.9降至20.3±2.7 ml·100 ml⁻¹·min⁻¹（P < 0.05），但对高于基线的总过量血流量无影响。布洛芬后输注L-NMMA使静息时的FBF降低40%，对峰值血流量无影响，但将高于基线的总过量血流量从12.0±2.5降至7.6±1.3 ml/100 ml（P < 0.05）。这些数据表明，抑制NO合酶对反应性充血期间的峰值血管舒张有适度影响，但在后期作用极小。前列腺素似乎是峰值血流量的重要决定因素。反应性充血期间抑制NO合酶的作用也可能因同时抑制环氧化酶而增强。
