aDepartment of Kinesiology and Nutrition, Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois, USA bDepartment of General Practice, Erasmus MC University Medical Center, Rotterdam, The Netherlands cDepartment of Biology, University of Houston-Victoria, Victoria, Texas, USA.
J Hypertens. 2017 Dec;35(12):2454-2461. doi: 10.1097/HJH.0000000000001481.
To evaluate changes in arterial stiffness with positional change and whether the stiffness changes are due to hydrostatic pressure alone or if physiological changes in vasoconstriction of the conduit arteries play a role in the modulation of arterial stiffness.
Thirty participants' (male = 15, 24 ± 4 years) upper bodies were positioned at 0, 45, and 72° angles. Pulse wave velocity (PWV), cardio-ankle vascular index, carotid beta-stiffness index, carotid blood pressure (cBP), and carotid diameters were measured at each position. A gravitational height correction was determined using the vertical fluid column distance (mmHg) between the heart and carotid artery. Carotid beta-stiffness was calibrated using three methods: nonheight corrected cBP of each position, height corrected cBP of each position, and height corrected cBP of the supine position (theoretical model). Low frequency systolic blood pressure variability (LFSAP) was analyzed as a marker of sympathetic activity.
PWV and cardio-ankle vascular index increased with position (P < 0.05). Carotid beta-stiffness did not increase if not corrected for hydrostatic pressure. Arterial stiffness indices based on Method 2 were not different from Method 3 (P = 0.65). LFSAP increased in more upright positions (P < 0.05) but diastolic diameter relative to diastolic pressure did not (P > 0.05).
Arterial stiffness increases with a more upright body position. Carotid beta-stiffness needs to be calibrated accounting for hydrostatic effects of gravity if measured in a seated position. It is unclear why PWV increased as this increase was independent of blood pressure. No difference between Methods 2 and 3 presumably indicates that the beta-stiffness increases are only pressure dependent, despite the increase in vascular sympathetic modulation.
评估体位变化时动脉僵硬程度的变化，以及这种僵硬变化是仅仅由于静水压力引起，还是管腔动脉的血管收缩的生理变化在调节动脉僵硬程度中起作用。
30 名参与者（男性 15 名，24±4 岁）的上半身分别处于 0°、45°和 72°三个角度。在每个体位下测量脉搏波速度（PWV）、心踝血管指数、颈动脉β-僵硬指数、颈动脉血压（cBP）和颈动脉直径。使用心脏和颈动脉之间的垂直液柱距离（mmHg）确定重力高度校正值。使用三种方法校准颈动脉β-僵硬度：每个体位的未校正 cBP、每个体位的校正 cBP 和仰卧位的校正 cBP（理论模型）。低频收缩压变异性（LFSAP）被分析为交感神经活动的标志物。
PWV 和心踝血管指数随体位增加而增加（P<0.05）。如果不校正静水压力，颈动脉β-僵硬度不会增加。基于方法 2 的动脉僵硬指数与方法 3 没有差异（P=0.65）。LFSAP 在更直立的体位增加（P<0.05），但舒张压与舒张压的比值没有增加（P>0.05）。
动脉僵硬随身体更直立的姿势而增加。如果在坐姿下测量，颈动脉β-僵硬度需要校正重力的静水压力效应。PWV 增加的原因尚不清楚，因为这种增加与血压无关。方法 2 和 3 之间没有差异，可能表明β-僵硬度的增加仅与压力有关，尽管血管交感神经调节增加。
