Department of Cardiology, Erasme University Hospital, Brussels, Belgium.
Clinica Medica, Department of Medicine and Surgery, University Milano-Bicocca, Milano.
J Hypertens. 2018 May;36(5):1188-1194. doi: 10.1097/HJH.0000000000001653.
Baroreceptor activation by a continuous infusion of phenylephrine selectively abolishes the muscle sympathetic nerve activity (MSNA) response to hypoxia in humans. Baroreceptor deactivation enhances the MSNA rise during hypoxia in animals. Whether this is true in humans is unknown and was tested in the present study.
We assessed MSNA responses elicited by isocapnic hypoxia (10% O2 in N2) during baroreflex loading and unloading with phenylephrine and nitroprusside, respectively, in 19 healthy volunteers. The study was randomized and placebo-controlled.
Phenylephrine and nitroprusside increased and decreased, respectively, blood pressure during normoxia and hypoxia, whereas the reverse occurred for heart rate and MSNA (all P < 0.001 vs. placebo). As compared with normoxia, cardiac barosensitivity decreased during the infusion of placebo and nitroprusside in the presence of hypoxia, as well as sympathetic barosensitivity during the infusion of nitroprusside (all P < 0.05). Three patients even disclosed a reduction in arterial pressure, which became apparent at the third minute of hypoxia and worsened steadily thereafter (SBP: 91 ± 7 mmHg; DBP 47 ± 9 mmHg), in spite of a gradual rise in heart rate of 20 ± 4 bpm. Changes in baroreceptor loading conditions did not affect ventilation during normoxia and hypoxia.
Cardiac and sympathetic baroreceptor sensitivity decrease during baroreceptor unloading in the presence of peripheral chemoreceptor activation. Normal humans have limited reflex capabilities to sustain simultaneous reductions in oxygen and pressure, and may experience hemodynamic instability episodes in such condition.
通过持续输注苯肾上腺素激活压力感受器可选择性消除人类对缺氧的肌肉交感神经活动（MSNA）反应。压力感受器失活增强了动物在缺氧期间的 MSNA 升高。这种情况在人类中是否真实尚不清楚，本研究对此进行了测试。
我们评估了 19 名健康志愿者在苯肾上腺素和硝普钠分别进行压力反射加载和卸载期间，等二氧化碳缺氧（氮气中的 10% O2）引起的 MSNA 反应。该研究是随机的和安慰剂对照的。
苯肾上腺素和硝普钠分别在正常氧合和缺氧期间升高和降低血压，而心率和 MSNA 则相反（与安慰剂相比，所有 P<0.001）。与正常氧合相比，在缺氧期间输注安慰剂和硝普钠时，心脏压力反射敏感性降低，以及在输注硝普钠时交感神经压力反射敏感性降低（所有 P<0.05）。三名患者甚至出现动脉压降低，这在缺氧的第三分钟变得明显，并在此后逐渐恶化（SBP：91±7mmHg；DBP 47±9mmHg），尽管心率逐渐升高 20±4bpm。压力感受器加载条件的变化不会影响正常氧合和缺氧期间的通气。
在周围化学感受器激活的情况下，压力感受器失载时心脏和交感神经压力感受器敏感性降低。正常人类对同时降低氧气和压力的反射能力有限，在这种情况下可能会经历血流动力学不稳定的发作。
