Sanders J S, Ferguson D W
Department of Internal Medicine, University of Iowa Hospitals, Iowa City 52242.
J Am Coll Cardiol. 1988 Nov;12(5):1241-51. doi: 10.1016/0735-1097(88)92607-1.
To further evaluate the reported interaction in animals and humans between cardiopulmonary baroreflexes and the somatic pressor reflex, studies were performed in 16 normal men using direct measurements of efferent sympathetic nerve activity to muscle (microneurography) during sustained isometric handgrip (30% maximal voluntary contraction). Forearm vasoconstrictor (plethysmography) and muscle sympathetic nerve activity responses to sustained handgrip were measured during cardiopulmonary baroreceptor deactivation (lower body negative pressure, n = 8) and activation (volume expansion, n = 8). In addition, responses to posthandgrip muscle ischemia were studied during these perturbations of cardiopulmonary baroreflexes. No evidence of an interaction between these two reflex pathways was found. When handgrip was performed during lower body negative pressure, the percent increase in muscle sympathetic nerve activity (+115 +/- 17%) was not different from the sum of the individual sympathetic responses to handgrip and lower body negative pressure performed separately (+106 +/- 19%, p = NS). Likewise, the change in forearm vascular resistance (+3.9 +/- 0.8 U) for sustained handgrip performed during lower body negative pressure was not different from the algebraic sum of the responses to handgrip and lower body negative pressure when these were performed separately (+4.7 +/- 2.7 U, p = NS). No difference was noted in forearm vasoconstrictor and sympathetic nerve activity responses to posthandgrip muscle ischemia and lower body negative pressure when these were performed alone or in combination. Volume expansion also failed to uncover an inhibitory interaction. Handgrip performed before volume expansion resulted in forearm vascular resistance responses (-1.2 +/- 0.9 U) that were not different from the responses when such handgrip was performed after volume infusion (+0.9 +/- 0.9 U, p = NS). Rather than producing the predicted inhibition of muscle sympathetic nerve activity responses to sustained handgrip, volume infusion actually increased these responses. During prevolume sustained handgrip, the increase in sympathetic nerve activity (+64.5 +/- 15.7%) was significantly less than the increase when handgrip was performed after volume infusion (+105.6 +/- 20.1%, p less than 0.01). A similar lack of inhibitory modulation was seen during posthandgrip muscle ischemia performed before and after volume expansion. These data indicate that the efferent sympathetic responses to the somatic pressor reflex are not modulated by the cardiopulmonary baroreflexes in normal humans.
为了进一步评估已报道的动物和人类心肺压力反射与躯体升压反射之间的相互作用,我们对16名正常男性进行了研究,在持续等长握力(最大自主收缩的30%)期间,使用直接测量肌肉传出交感神经活动(微神经ography)的方法。在心肺压力感受器失活(下体负压,n = 8)和激活(容量扩张,n = 8)期间,测量了前臂血管收缩(体积描记法)和肌肉交感神经活动对持续握力的反应。此外,在这些心肺压力反射的扰动期间,研究了对握力后肌肉缺血的反应。未发现这两种反射途径之间存在相互作用的证据。当下体负压期间进行握力时,肌肉交感神经活动的增加百分比(+115±17%)与分别进行握力和下体负压时个体交感反应的总和(+106±19%,p = 无显著性差异)没有差异。同样,下体负压期间进行持续握力时前臂血管阻力的变化(+3.9±0.8 U)与分别进行握力和下体负压时反应的代数和(+4.7±2.7 U,p = 无显著性差异)没有差异。单独或联合进行握力后肌肉缺血和下体负压时,前臂血管收缩和交感神经活动反应没有差异。容量扩张也未能揭示抑制性相互作用。在容量扩张前进行的握力导致前臂血管阻力反应(-1.2±0.9 U)与容量输注后进行该握力时的反应(+0.9±0.9 U,p = 无显著性差异)没有差异。容量输注非但没有对持续握力的肌肉交感神经活动反应产生预期的抑制作用,实际上反而增加了这些反应。在容量扩张前进行持续握力时,交感神经活动的增加(+64.5±15.7%)明显小于容量输注后进行握力时的增加(+105.6±20.1%,p < 0.01)。在容量扩张前后进行握力后肌肉缺血时,也观察到类似的缺乏抑制性调节的情况。这些数据表明,在正常人类中,躯体升压反射的传出交感反应不受心肺压力反射的调节。