Responses of feline caudal hypothalamic cardiorespiratory neurons to hypoxia and hypercapnia.
Responses of feline caudal hypothalamic cardiorespiratory neurons to hypoxia and hypercapnia.
复制标题
猫尾部下丘脑心肺神经元对缺氧和高碳酸血症的反应。
DOI：
10.1007/bf00227106
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发表时间：
1993
影响因子：
2
通讯作者：
Waldrop,TG
中科院分区：
文献类型：
--
作者：
Dillon,GH;Waldrop,TG
一些研究表明，尾侧下丘脑调节对高碳酸血症和低氧的反应。此外，下丘脑的这个区域包含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缺氧刺激的下丘脑尾侧神经元的基底放电是否与心血管（交感放电和/或心脏周期）和/或呼吸活动（膈神经放电）有关。记录麻醉猫下丘脑单个单元活动、膈神经活动和颈交感神经活动。使用计算机平均技术比较下丘脑神经元放电与心血管和/或呼吸活动的时间。在正常猫、外周化学神经支配猫和气压神经支配猫中，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；在那些高碳酸血症刺激的患者中，所有患者都有与心血管和/或呼吸活动相关的基础放电。缺氧使完好动物下丘脑单位放电率显著提高21%；其中90%的人有心血管和/或呼吸相关节律。只有13%的神经元受到缺氧和高碳酸血症的刺激。类似的结果也被发现在气压神经，周围化学神经的猫。在未受刺激的猫和去神经的猫中，被这些刺激激发的神经元都集中在下丘脑后区。本研究结果表明，一组尾状下丘脑神经元对缺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，来自外周压力感受器和化学感受器传入的输入不需要这种调制。
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.