Joannides R, Haefeli W E, Linder L, Lüscher T F, Richard V, Thuillez C
Service de phármacologie, VACOMED, IFRMP, CHU de Rouen.
Arch Mal Coeur Vaiss. 1995 Aug;88(8):1149-52.
Although several experiments have demonstrated the existence of a basal NO-dependent vasodilatory tone at the arteriolar level, the contribution of NO to the mechanical properties of large arteries has not been investigated in humans. To evaluate the effect of NO-synthase inhibition on these mechanical properties, radial artery internal diameter (d, mm) and wall thickness (h, mm) were measured continuously in 11 healthy volunteers (age: 24 +/- 1 years), using an A-mode echo-tracking system coupled to a Doppler device for the measurement of radial blood flow (RBF, ml/min). A catheter was inserted in the brachial artery for measurement of arterial pressure (AP, mmHg), and infusion of the inhibitor of NO synthesis NG-monomethyl L-arginine (L-NMMA: 4 mumol/min for 5 min, infusion rate 0.8 ml/min). Arterial compliance C, 10(-3) mm2/mmHg), distensibility (D, 10(-3)/mmHg), mid-wall stress (sigma, 10(5) dynes/mm2) and incremental modulus (Ei, 10(7) dynes/mm2) were calculated before and after L-NMMA. After L-NMMA, RBF decreased from 31 +/- 6 to 23 +/- 4 (p < 0.05), radial vascular resistance increased from 2.70 +/- 0.35 to 3.77 +/- 0.55 (p < 0.05), without changes in AP or heart rate. Table shows mechanical parameters, assessed at fixed AP (80 mmHg) (*: p < 0.05 vs baseline): [table: see text] Thus, the L-NMMA-induced decrease in radial arterial wall stiffness (Ei) without changes in arterial diameter or stress demonstrates that NO-synthase inhibition induces an isometric relaxation of vascular muscle cells, which explains the increase of arterial compliance at constant mid-wall stress. These results demonstrate that NO contributes to the regulation of peripheral muscular arterial mechanics in humans. At the level of large arteries, the isometric relaxation observed after NO-synthase inhibition is probably the consequence of compensatory vasodilator mechanisms.
尽管多项实验已证明在小动脉水平存在基础的一氧化氮（NO）依赖性血管舒张张力，但NO对大动脉力学特性的作用尚未在人体中进行研究。为评估一氧化氮合酶抑制对这些力学特性的影响，使用与多普勒装置耦合的A型回声跟踪系统连续测量了11名健康志愿者（年龄：24±1岁）的桡动脉内径（d，mm）和壁厚（h，mm），以测量桡动脉血流量（RBF，ml/min）。将一根导管插入肱动脉以测量动脉压（AP，mmHg），并输注一氧化氮合成抑制剂N-甲基-L-精氨酸（L-NMMA：4 μmol/min，持续5分钟，输注速率0.8 ml/min）。在输注L-NMMA前后计算动脉顺应性C（10⁻³ mm²/mmHg）、扩张性（D，10⁻³/mmHg）、中膜应力（σ，10⁵达因/mm²）和增量模量（Ei，10⁷达因/mm²）。输注L-NMMA后，RBF从31±6降至23±4（p<0.05），桡动脉血管阻力从2.70±0.35增至3.77±0.55（p<0.05），而AP或心率无变化。表显示了在固定AP（80 mmHg）下评估的力学参数（*：与基线相比p<0.05）：[表：见原文] 因此，L-NMMA诱导的桡动脉壁硬度（Ei）降低而动脉直径或应力无变化表明，一氧化氮合酶抑制诱导血管平滑肌细胞等长舒张，这解释了在恒定中膜应力下动脉顺应性的增加。这些结果表明，NO有助于调节人体外周肌性动脉的力学特性。在大动脉水平，一氧化氮合酶抑制后观察到的等长舒张可能是代偿性血管舒张机制的结果。
