Weber R, Stergiopulos N, Brunner H R, Hayoz D
Division d'Hypertension, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Hypertension. 1996 Mar;27(3 Pt 2):816-22. doi: 10.1161/01.hyp.27.3.816.
Isobaric compliance and distensibility of the radial artery were recently reported to be normal or slightly increased in untreated hypertensive patients. However, these findings provide no information on the intrinsic mechanical properties of the wall material. To address this question, we determined intima-media wall thickness, wall-to-lumen ratio, and incremental elastic modulus in the radial artery of 25 untreated hypertensive patients with blood pressure of 150 +/- 14/103 +/- 6 mm Hg (mean +/- SD) and 25 matched control subjects with blood pressure of 118 +/- 9/79 +/- 6 mm Hg. High-resolution echotracking for assessment of internal diameter and intima-media wall thickness was combined with measurements of blood flow velocity by Doppler and blood pressure by photoplethysmography. In addition, isobaric compliance and distensibility and incremental elastic modulus were measured at peak diameter during reactive hyperemia after a 5-minute brachial occlusion. No significant difference was found between the two groups for isobaric compliance or distensibility at baseline or during hyperemia. However, incremental elastic modulus at 100 mg Hg tended to be lower in hypertensive patients than control subjects (1.9 +/- 1.1 versus 2.5 +/- 1.2 mm Hg x 10(4), P = .1) in resting conditions. Hypertensive patients and control subjects had similar internal diameters (2.47 +/- 0.32 versus 2.41 +/- 0.35 microm), but intima-media wall thickness and wall-to-lumen ratio were significantly increased in hypertensive patients compared with control subjects (0.268 +/- 0.032 versus 0.236 +/- 0.025 mm -P < or = .01- and 0.220 +/- 0.038 versus 0.195 +/- 0.028 -P < or = .05-, respectively). Peak hyperemic blood flow response (hypertensive patients versus control subjects: 349% versus 360% increase from baseline) and reactive hyperemic dilation (7.2% versus 7.9%) were similar in amplitude and duration in the two groups. These results suggest that wall thickening is an adaptive process that reduces wall tension in hypertensive patients while preserving a normal mechanical behavior of the radial artery. This is most likely accomplished by modification of the incremental elastic modulus of wall components rather than by a change in vascular tone.
最近有报道称，未经治疗的高血压患者桡动脉的等压顺应性和扩张性正常或略有增加。然而，这些发现并未提供关于血管壁材料固有力学特性的信息。为了解决这个问题，我们测定了25名未经治疗的高血压患者（血压为150±14/103±6 mmHg，均值±标准差）和25名匹配的对照受试者（血压为118±9/79±6 mmHg）桡动脉的内膜中层厚度、壁腔比和增量弹性模量。通过高分辨率回声跟踪评估内径和内膜中层厚度，并结合多普勒测量血流速度和光电容积描记法测量血压。此外，在肱动脉闭塞5分钟后的反应性充血期间，于直径峰值处测量等压顺应性、扩张性和增量弹性模量。两组在基线或充血期间的等压顺应性或扩张性无显著差异。然而，在静息状态下，高血压患者的100 mmHg时的增量弹性模量往往低于对照受试者（1.9±1.1对2.5±1.2 mmHg×10⁴，P = 0.1）。高血压患者和对照受试者的内径相似（2.47±0.32对2.41±0.35微米），但与对照受试者相比，高血压患者的内膜中层厚度和壁腔比显著增加（分别为0.268±0.032对0.236±0.025毫米，P≤0.01；以及0.220±0.038对0.195±0.028，P≤0.05）。两组的峰值充血血流反应（高血压患者与对照受试者：较基线增加349%对360%）和反应性充血扩张（7.2%对7.9%）在幅度和持续时间上相似。这些结果表明，血管壁增厚是一种适应性过程，可在维持桡动脉正常力学行为的同时降低高血压患者的血管壁张力。这很可能是通过改变血管壁成分的增量弹性模量而非血管张力的变化来实现的。
