Victor R G, Mark A L
J Clin Invest. 1985 Oct;76(4):1592-8. doi: 10.1172/JCI112142.
Previous studies in experimental animals indicate an important inhibitory interaction between cardiopulmonary and arterial baroreflexes. In the dog, for example, cardiopulmonary vagal afferents modulate carotid baroreflex control of vascular resistance. On the other hand, previous studies in human subjects have not produced convincing evidence of a specific interaction between these baroreceptor reflexes. The purpose of this study was to determine whether unloading of cardiopulmonary baroreceptors in humans with nonhypotensive lower body negative pressure selectively augments the reflex vasoconstrictor responses to simulated carotid hypotension produced by neck pressure. In nine healthy subjects, we measured forearm vascular responses with plethysmography during lower body negative pressure alone (cardiopulmonary baroreflex), during neck pressure alone (carotid baroreflex), and during concomitant lower body negative pressure and neck pressure (baroreflex interaction). Lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure. This increase in resistance was significantly greater (P less than 0.05) than the algebraic sum of the increase in resistance from lower body negative pressure alone plus that from neck pressure alone. In contrast, lower body negative pressure did not potentiate the forearm vasoconstrictor responses either to intra-arterial norepinephrine or to the cold pressor test. Thus, the potentiation of the vasoconstrictor response to neck pressure by lower body negative pressure cannot be explained by augmented reactivity to the neurotransmitter or to a nonspecific augmentation of responses to all reflex vasoconstrictor stimuli. In conclusion, nonhypotensive lower body negative pressure selectively augments carotid baroreflex control of forearm vascular resistance. These experiments demonstrate a specific inhibitory cardiopulmonary-carotid baroreflex interaction in humans.
先前对实验动物的研究表明,心肺压力反射和动脉压力反射之间存在重要的抑制性相互作用。例如,在狗身上,心肺迷走神经传入纤维可调节颈动脉压力反射对血管阻力的控制。另一方面,先前对人类受试者的研究尚未产生令人信服的证据证明这些压力感受器反射之间存在特定的相互作用。本研究的目的是确定在非低血压性下肢负压状态下,人体心肺压力感受器的卸载是否会选择性增强对颈部压力所产生的模拟颈动脉低血压的反射性血管收缩反应。在9名健康受试者中,我们通过体积描记法测量了单独下肢负压(心肺压力反射)、单独颈部压力(颈动脉压力反射)以及同时施加下肢负压和颈部压力(压力反射相互作用)时的前臂血管反应。下肢负压使前臂对颈部压力的血管收缩反应增强了两倍多。这种阻力增加显著大于(P<0.05)单独下肢负压引起的阻力增加与单独颈部压力引起的阻力增加的代数和。相比之下,下肢负压并未增强前臂对动脉内去甲肾上腺素或冷加压试验的血管收缩反应。因此,下肢负压对颈部压力的血管收缩反应的增强作用不能用对神经递质反应性增强或对所有反射性血管收缩刺激的非特异性反应增强来解释。总之,非低血压性下肢负压选择性增强了颈动脉压力反射对前臂血管阻力的控制。这些实验证明了人类中存在特定的心肺-颈动脉压力反射抑制性相互作用。