Somers V K, Mark A L, Abboud F M
Department of Internal Medicine, University of Iowa, Iowa City 55242.
J Clin Invest. 1991 Jun;87(6):1953-7. doi: 10.1172/JCI115221.
Animal studies have demonstrated that activation of the baroreflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroreflex activation on the sympathetic response to stimulation of PC and central chemoreceptors in humans. PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal reflex control to determine the selectivity of the interactive influence of baroreflex activation. Baroreflex activation was achieved by raising mean blood pressure by greater than 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 +/- 92 to 354 +/- 107 U/min (P less than 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 +/- 45 U/min (P less than 0.05). With hypoxia during baroreflex activation with PE, SNA did not increase (50 +/- 23 U/min). During hypercapnia alone, SNA increased from 116 +/- 39 to 234 +/- 72 U/min (P less than 0.01). Hypercapnia during baroreflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroreflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroreflex and the peripheral chemoreflex may be explained by convergence of baroreceptor and peripheral chemoreceptor afferents on neurons in the medulla.
动物研究表明,动脉血压升高激活压力反射可抑制心血管和通气对低氧激活外周化学感受器(PC)的反应。在本研究中,我们检测了压力反射激活对人体中PC和中枢化学感受器刺激的交感反应的影响。通过低氧(10% O₂/90% N₂)刺激PC(n = 6),通过高碳酸血症(7% CO₂/93% O₂)刺激中枢化学感受器(n = 6)。还获得了对冷加压刺激的反应作为内部反射对照,以确定压力反射激活的交互影响的选择性。通过静脉输注去氧肾上腺素(PE)使平均血压升高超过10 mmHg来实现压力反射激活。从腓总神经(微神经图)记录对肌肉的交感神经活动(SNA)。仅在低氧期间,SNA从255±92增加到354±107 U/min(P<0.05)。仅在使用PE期间,平均血压升高且SNA降至87±45 U/min(P<0.05)。在使用PE进行压力反射激活期间低氧时,SNA未增加(50±23 U/min)。仅在高碳酸血症期间,SNA从116±39增加到234±72 U/min(P<0.01)。在使用PE进行压力反射激活期间高碳酸血症使SNA从仅使用PE时的32±25 U/min增加到高碳酸血症和PE期间的61±26 U/min(P<0.05)。与高碳酸血症一样(但与低氧不同),冷加压试验在使用PE期间也增加了SNA。我们得出结论,压力反射激活选择性地消除了对低氧的SNA反应,但对高碳酸血症或冷加压试验没有影响。压力反射和外周化学反射的抑制性相互作用可能由压力感受器和外周化学感受器传入纤维在延髓神经元上的汇聚来解释。