Penn State Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania.
Department of Surgery, Penn State College of Medicine, Hershey, Pennsylvania.
Am J Physiol Heart Circ Physiol. 2020 Apr 1;318(4):H916-H924. doi: 10.1152/ajpheart.00493.2019. Epub 2020 Feb 28.
Patients with peripheral artery disease (PAD) have an accentuated exercise pressor reflex (EPR) during exercise of the affected limb. The underlying hemodynamic changes responsible for this, and its effect on blood flow to the exercising extremity, are unclear. We tested the hypothesis that the exaggerated EPR in PAD is mediated by an increase in total peripheral resistance (TPR), which augments redistribution of blood flow to the exercising limb. Twelve patients with PAD and 12 age- and sex-matched subjects without PAD performed dynamic plantar flexion (PF) using the most symptomatic leg at progressive workloads of 2-12 kg (increased by 1 kg/min until onset of fatigue). We measured heart rate, beat-by-beat blood pressure, femoral blood flow velocity (FBV), and muscle oxygen saturation () continuously during the exercise. Femoral blood flow (FBF) was calculated from FBV and baseline femoral artery diameter. Stroke volume (SV), cardiac output (CO), and TPR were derived from the blood pressure tracings. Mean arterial blood pressure and TPR were significantly augmented in PAD compared with control during PF. FBF increased during exercise to an equal extent in both groups. However, of the exercising limb remained significantly lower in PAD compared with control. We conclude that the exaggerated pressor response in PAD is mediated by an abnormal TPR response, which augments redistribution of blood flow to the exercising extremity, leading to an equal rise in FBF compared with controls. However, this increase in FBF is not sufficient to normalize the SmO response during exercise in patients with PAD. In this study, peripheral artery disease (PAD) patients and healthy control subjects performed graded, dynamic plantar flexion exercise. Data from this study suggest that previously reported exaggerated exercise pressor reflex in patients with PAD is driven by greater vasoconstriction in nonexercising vascular territories which also results in a redistribution of blood flow to the exercising extremity. However, this rise in femoral blood flow does not fully correct the oxygen deficit due to changes in other mechanisms that require further investigation.
患有外周动脉疾病（PAD）的患者在受影响肢体运动时会出现增强的运动加压反射（EPR）。负责这种情况的潜在血液动力学变化及其对运动肢体血流的影响尚不清楚。我们检验了以下假设，即 PAD 中 EPR 的夸大是由总外周阻力（TPR）增加介导的，这会增加血流向运动肢体的再分配。12 名患有 PAD 的患者和 12 名年龄和性别匹配的无 PAD 患者在渐进性工作负荷下（以 1 公斤/分钟的速度增加，直到疲劳开始）使用最有症状的腿进行动态足底屈曲（PF）。我们在运动过程中连续测量心率、逐搏血压、股血流速度（FBV）和肌肉氧饱和度（）。股血流（FBF）是从 FBV 和基线股动脉直径计算得出的。SV、CO 和 TPR 是从血压描记图中得出的。与对照组相比，PF 期间 PAD 患者的平均动脉血压和 TPR 明显增加。两组的 FBF 在运动过程中均增加。然而，与对照组相比，运动肢体的仍明显较低。我们得出的结论是，PAD 中增强的加压反应是由异常 TPR 反应介导的，该反应增强了血流向运动肢体的再分配，导致与对照组相比 FBF 同等程度的增加。然而，这种 FBF 的增加不足以在 PAD 患者运动期间使 SmO 反应正常化。在这项研究中，外周动脉疾病（PAD）患者和健康对照组进行了分级、动态足底屈曲运动。来自这项研究的数据表明，以前报道的 PAD 患者增强的运动加压反射是由非运动血管区域的血管收缩增强驱动的，这也导致血流向运动肢体的再分配。然而，这种股血流的增加并没有完全纠正由于其他机制导致的氧气不足，这些机制需要进一步研究。
