Dillon G H, Waldrop T G
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Exp Brain Res. 1993;96(2):260-72. doi: 10.1007/BF00227106.
Several studies have suggested that the caudal hypothalamus modulates responses to hypercapnia and hypoxia. In addition, this area of the hypothalamus contains neurons that have a sympathoexcitatory discharge. The purpose of the present study was to determine whether the basal discharge of caudal hypothalamic neurons that are stimulated by hypercapnia or hypoxia is related to cardiovascular (sympathetic discharge and/or the cardiac cycle) and/or respiratory activity (phrenic nerve discharge). Hypothalamic single unit activity, phrenic nerve activity, and cervical sympathetic nerve activity were recorded in anesthetized cats. Computer averaging techniques were used to compare temporally the discharge of hypothalamic neurons with cardiovascular and/or respiratory activity. Cardiorespiratory and hypothalamic neuronal responses to ventilation with hypoxic (10% O2/90% N2) and hypercapnic (5% CO2/95% O2) gases were determined in intact and in peripherally-chemodenervated, barodenervated cats. Thirty-two percent of hypothalamic neurons were stimulated by a hypercapnic stimulus in intact cats; of those that were stimulated by hypercapnia, all had a basal discharge related to cardiovascular and/or respiratory activity. Hypoxia significantly increased the discharge rate of 21% of hypothalamic units in intact animals; 90% of those had a cardiovascular and/or respiratory-related rhythm. Only 13% of the neurons were stimulated by both hypoxia and hypercapnia. Similar results were found in barodenervated, peripherally chemodenervated cats. Neurons excited by these stimuli in both the intact and denervated cats were found to be concentrated in the posterior hypothalamic area. The results of this study suggest that a group of caudal hypothalamic neurons contribute to the cardiorespiratory responses to hypoxia and hypercapnia, but via separate subpopulations of neurons. In addition, input from peripheral baroreceptor and chemoreceptor afferents is not required for this modulation.
多项研究表明，下丘脑尾部可调节对高碳酸血症和低氧血症的反应。此外，下丘脑的这一区域含有具有交感兴奋放电的神经元。本研究的目的是确定受高碳酸血症或低氧血症刺激的下丘脑尾部神经元的基础放电是否与心血管（交感放电和/或心动周期）和/或呼吸活动（膈神经放电）有关。在麻醉的猫身上记录下丘脑单单位活动、膈神经活动和颈交感神经活动。使用计算机平均技术在时间上比较下丘脑神经元的放电与心血管和/或呼吸活动。在完整的和外周化学去神经、压力感受器去神经的猫身上，测定了心肺和下丘脑神经元对低氧（10% O2/90% N2）和高碳酸（5% CO2/95% O2）气体通气的反应。在完整的猫中，32%的下丘脑神经元受到高碳酸刺激；在那些受到高碳酸血症刺激的神经元中，所有神经元都有与心血管和/或呼吸活动相关的基础放电。低氧显著增加了完整动物中21%的下丘脑单位的放电率；其中90%具有与心血管和/或呼吸相关的节律。只有13%的神经元同时受到低氧和高碳酸血症的刺激。在外周压力感受器去神经、化学感受器去神经的猫中也发现了类似的结果。在完整和去神经的猫中，受这些刺激兴奋的神经元都集中在下丘脑后部区域。本研究结果表明，一组下丘脑尾部神经元对低氧和高碳酸血症的心肺反应有贡献，但通过不同的神经元亚群。此外，这种调节不需要外周压力感受器和化学感受器传入的输入。
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