Lauer Thomas, Heiss Christian, Preik Michael, Balzer Jan, Hafner Dieter, Strauer Bodo E, Kelm Malte
Department of Medicine, Division of Cardiology, Pulmonary Diseases and Angiology, Heinrich-Heine-University, Duesseldorf, Germany.
J Hypertens. 2005 Mar;23(3):563-9. doi: 10.1097/01.hjh.0000160213.40855.b7.
A diminished flow reserve in resistance vessels is a hallmark of hypertensive microvascular disease. Hypertension is associated with structural alterations in the microcirculation and a reduced endothelium-dependent dilation in conduit arteries. Both have been demonstrated to predict future cardiovascular events.
We hypothesized that a reduced peripheral flow reserve impairs endothelial function in upstream conduit arteries in patients with arterial hypertension.
In 43 hypertensive patients (HT) and 38 normotensive controls (NT) endothelial function of the brachial artery was assessed by measurement of flow-mediated dilatation (FMD), using high-resolution ultrasound. Peripheral flow reserve (FR) was determined via measurements of forearm blood flow at rest and during increments of reactive hyperaemia, using venous occlusion plethysmography.
FMD was markedly impaired in HT (3.6 +/- 0.3%) as compared with NT (10.2 +/- 0.3%), whereas maximum brachial artery diameter following endothelium-independent dilatation was similar in both groups. In hypertensive patients FR was significantly reduced (HT, 3.2 versus NT, 6.0) during reactive hyperaemia after 5 min of ischaemia. FR was associated with FMD (r = 0.68, P < 0.01). Multiple stepwise regression analysis identified FR as a strong independent variable determining the extent of FMD (r2 = 0.46, P < 0.01). In HT the dose-response curve of FMD upon stepwise increases of FR was shifted significantly to the right. Normalization of FR improved FMD in HT by more than 60%.
In essential hypertension a reduced FR contributes to the endothelial dysfunction of upstream conduit arteries. These findings may have therapeutic and prognostic implications in patients with arterial hypertension.
阻力血管中血流储备减少是高血压微血管疾病的一个标志。高血压与微循环结构改变以及传导动脉中内皮依赖性舒张功能降低有关。这两者均已被证明可预测未来心血管事件。
我们假设外周血流储备减少会损害高血压患者上游传导动脉的内皮功能。
采用高分辨率超声通过测量血流介导的血管舒张（FMD）来评估43例高血压患者（HT）和38例血压正常对照者（NT）肱动脉的内皮功能。使用静脉阻断体积描记法通过测量静息时和反应性充血增加期间的前臂血流量来确定外周血流储备（FR）。
与NT组（10.2±0.3%）相比，HT组的FMD明显受损（3.6±0.3%），而两组在非内皮依赖性舒张后肱动脉最大直径相似。在高血压患者中，缺血5分钟后反应性充血期间FR显著降低（HT组为3.2，NT组为6.0）。FR与FMD相关（r = 0.68，P < 0.01）。多元逐步回归分析确定FR是决定FMD程度的一个强有力的独立变量（r2 = 0.46，P < 0.01）。在HT组中，随着FR逐步增加，FMD的剂量反应曲线明显右移。FR正常化使HT组的FMD改善超过60%。
在原发性高血压中，FR降低导致上游传导动脉的内皮功能障碍。这些发现可能对高血压患者具有治疗和预后意义。
