接受过治疗的高血压患者在运动时,外周化学反射抑制骨骼肌血流。

Ana Luiza C Sayegh,Michael J Plunkett,Thalia Babbage,Mathew Dawes,Julian F R Paton,James P Fisher
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引用次数: 0

摘要

我们对以下假设进行了测试:在人类高血压患者中,外周化学反射的强直性/敏感性增加会导致由交感神经介导的对运动肌肉营养血流的抑制。在静脉注射 0.9% 生理盐水(对照组)和低剂量多巴胺(2 µg kg-1 min-1)以抑制外周化学反射的条件下,对 14 名接受过治疗的高血压患者(年龄 69 ± 11 岁,136 ± 12/80 ± 11 mmHg;平均值 ± SD)进行了研究。基线时,多巴胺不会改变平均血压(95 ± 10 vs. 98 ± 10 mmHg,P = 0.155),但会增加肱动脉血流(59 ± 20 vs. 48 ± 16 ml min-1,P = 0.030)和血管传导(0.565 ± 0.246 vs. 0.483 ± 0.160 ml min-1 mmHg-1;P = 0.039)。多巴胺可减轻等压缺氧再呼吸时平均血压的升高(∆3 ± 4 vs. ∆8 ± 6 mmHg,P = 0.007),并使外周化学反射敏感性降低 28 ± 37% (P = 0.044)。有节奏的手握运动可诱导肱动脉血流和血管传导的增加(与 45 秒后的静息相比,P 均<0.05),多巴胺的作用大于生理盐水(例如,在 60 秒时,分别为 Δ76 ± 54 对 Δ60 ± 43 ml min-1 和 Δ0.730 ± 0.440 对 Δ0.570 ± 0.424 ml min-1 mmHg-1;条件的主效应 P 均<0.0001)。我们的研究结果表明,外周化学反射在静息状态下处于强直性活跃状态,在治疗人类高血压时可抑制运动时血流量和血管传导性的增加。要点:假设在人类高血压患者中,外周化学反射的强直性/敏感性增加会导致交感神经介导的营养性血流流向运动肌肉的抑制。在静脉注射 0.9% 生理盐水(对照组)和低剂量多巴胺(2 µg kg-1 min-1)以抑制外周化学反射的条件下,对接受治疗的高血压患者(n = 14)进行了研究。低剂量多巴胺降低了静息通气和外周化学反射的敏感性,虽然平均血压没有变化,但肱动脉血流和血管传导却增加了。小剂量多巴胺增强了肱动脉血流和血管传导对节律性握手的反应。这些研究结果表明,外周化学反射在静息状态下处于强直性活跃状态,可抑制血流,在治疗人类高血压时,血管传导会随着运动而增加。
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Peripheral chemoreflex restrains skeletal muscle blood flow during exercise in participants with treated hypertension.
We tested the hypothesis that in human hypertension, an increased tonicity/sensitivity of the peripheral chemoreflex causes a sympathetically mediated restraint of nutritive blood flow to the exercising muscles. Fourteen patients with treated hypertension (age 69 ± 11 years, 136 ± 12/80 ± 11 mmHg; mean ± SD) were studied under conditions of intravenous 0.9% saline (control) and low-dose dopamine (2 µg kg-1 min-1) to inhibit the peripheral chemoreflex, at baseline, during isocapnic hypoxic rebreathing and during rhythmic handgrip exercise (3 min, 50% maximum voluntary contraction). At baseline, dopamine did not change mean blood pressure (95 ± 10 vs. 98 ± 10 mmHg, P = 0.155) but increased brachial artery blood flow (59 ± 20 vs. 48 ± 16 ml min-1, P = 0.030) and vascular conductance (0.565 ± 0.246 vs. 0.483 ± 0.160 ml min-1 mmHg-1; P = 0.039). Dopamine attenuated the increase in mean blood pressure (∆3 ± 4 vs. ∆8 ± 6 mmHg, P = 0.007) to isocapnic hypoxic rebreathing and reduced peripheral chemoreflex sensitivity by 28 ± 37% (P = 0.044). Rhythmic handgrip exercise induced increases in brachial artery blood flow and vascular conductance (both P < 0.05 vs. rest after 45 s) that were greater with dopamine than saline (e.g. Δ76 ± 54 vs. Δ60 ± 43 ml min-1 and Δ0.730 ± 0.440 vs. Δ0.570 ± 0.424 ml min-1 mmHg-1, respectively, at 60 s; main effect of condition both P < 0.0001). Our results indicate that the peripheral chemoreflex is tonically active at rest and restrains the blood flow and vascular conductance increases to exercise in treated human hypertension. KEY POINTS: It was hypothesised that in human hypertension, an increased tonicity/sensitivity of the peripheral chemoreflex causes a sympathetically mediated restraint of nutritive blood flow to the exercising muscles. Treated patients with hypertension (n = 14) were studied under conditions of intravenous 0.9% saline (control) and low-dose dopamine (2 µg kg-1 min-1) to inhibit the peripheral chemoreflex. Low-dose dopamine reduced resting ventilation and peripheral chemoreflex sensitivity, and while mean blood pressure was unchanged, brachial artery blood flow and vascular conductance were increased. Low-dose dopamine augmented the brachial artery blood flow and vascular conductance responses to rhythmic handgrip. These findings indicate that the peripheral chemoreflex is tonically active at rest and restrains the blood flow, and vascular conductance increases to exercise in treated human hypertension.
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