Heart and Vascular Institute, Penn State College of Medicine , Hershey, Pennsylvania.
Am J Physiol Heart Circ Physiol. 2018 Jan 1;314(1):H114-H121. doi: 10.1152/ajpheart.00401.2017. Epub 2017 Oct 6.
Patients with atherosclerotic peripheral artery disease have an augmented pressor response to treadmill walking, but the underlying mechanisms remain poorly understood and difficult to isolate because of the confounding presence of numerous cardiovascular risk factors. In the present study, we tested the hypothesis that a chronic deficit in muscle blood flow capacity would be sufficient to trigger an exaggerated pressor response to dynamic exercise. Sprague-Dawley rats (5 male and 5 female) were instrumented with radiotelemetry devices to measure the cardiovascular responses to treadmill running before and after bilateral femoral artery ligation, which has been previously shown to reduce the blood flow capacity of distal hindlimb muscles by >60%. Treadmill running evoked reproducible increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly augmented 3 days after femoral artery ligation in both male rats [ΔMAP: +10 ± 1 (SE) vs. +18 ± 3 mmHg and ΔHR: +94 ± 12 vs. +148 ± 15 beats/min, P < 0.05] and female rats (ΔMAP: +16 ± 3 vs. +30 ± 5 mmHg and ΔHR: +128 ± 20 vs. +178 ± 19 beats/min, P < 0.05). Similar exaggerated MAP and HR responses were observed at repeated intervals between 3 and 65 days postligation. These findings indicate that a chronic deficit in muscle blood flow capacity is an important, persistent cause of the abnormal pressor and cardioaccelerator responses to dynamic exercise in both male and female rats with peripheral arterial insufficiency. NEW & NOTEWORTHY Using radiotelemetry to assess cardiovascular effects of exercise, we showed that femoral artery obstruction in male and female rats is an important, persistent cause of exaggerated pressor and cardioaccelerator responses to treadmill running. This translational model reproduces the abnormal cardiovascular response to exercise seen in patients with peripheral artery disease. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/ .
患有动脉粥样硬化外周动脉疾病的患者在进行跑步机行走时会出现增强的升压反应,但由于存在许多心血管危险因素,其潜在机制仍未得到很好的理解和难以分离。在本研究中,我们检验了这样一个假设,即肌肉血流容量的慢性缺陷足以引发对动态运动的夸张升压反应。雄性和雌性 Sprague-Dawley 大鼠(各 5 只)接受无线电遥测设备植入,以测量跑步机跑步前后的心血管反应,此前的研究表明,双侧股动脉结扎会使远侧后肢肌肉的血流容量减少超过 60%。跑步机跑步引起平均动脉压(MAP)和心率(HR)的可重复增加,在股动脉结扎后 3 天,雄性大鼠[ΔMAP:+10 ± 1(SE)对+18 ± 3mmHg 和 ΔHR:+94 ± 12 对+148 ± 15 次/分钟,P<0.05]和雌性大鼠[ΔMAP:+16 ± 3 对+30 ± 5mmHg 和 ΔHR:+128 ± 20 对+178 ± 19 次/分钟,P<0.05]显著增强。在结扎后 3 至 65 天的重复间隔内观察到类似的夸张 MAP 和 HR 反应。这些发现表明,肌肉血流容量的慢性缺陷是雄性和雌性大鼠外周动脉功能不全时对动态运动异常升压和心加速反应的重要持续原因。新的和值得注意的是,使用无线电遥测术评估运动的心血管效应,我们发现股动脉阻塞在雄性和雌性大鼠中是对跑步机跑步产生夸张升压和心加速反应的重要持续原因。这种转化模型再现了外周动脉疾病患者运动时异常的心血管反应。在 http://ajpheart.podbean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/ 上收听本文的相关播客。