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化学去神经支配猫在缺氧期间呼吸神经元的活动

Activity of respiratory neurons during hypoxia in the chemodenervated cat.

作者信息

England S J, Melton J E, Douse M A, Duffin J

机构信息

Department of Pediatrics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick 08903, USA.

出版信息

J Appl Physiol (1985). 1995 Mar;78(3):856-61. doi: 10.1152/jappl.1995.78.3.856.

Abstract

Exposure of anesthetized paralyzed vagotomized peripherally chemodenervated cats to hypoxia results in initial depression and subsequent loss of the phrenic neurogram. To determine whether hypoxic respiratory depression results from the inhibition of respiratory premotor neurons by bulbospinal neurons of the Bötzinger complex (Böt-E neurons), extracellular recordings were made of dorsal and ventral respiratory group bulbospinal inspiratory neurons and Böt-E neurons during acute hypoxic hypoxia. All neurons recorded decreased firing rate during hypoxia. Böt-E neurons became silent before the loss of phasic phrenic activity during hypoxia and commenced firing before or coincident with the return of the phrenic neurogram during reoxygenation. Inspiratory neurons ceased firing coincident with phrenic silence. Dorsal respiratory group and ventral respiratory group neurons that had a late onset of firing with respect to the phrenic neurogram during normoxia fired progressively earlier in inspiration during hypoxia, an effect that was reversed during reoxygenation. These data are consistent with inhibition and/or disfacilitation as the mechanism of hypoxic respiratory depression but suggest that Böt-E neurons are not the source of this inhibition.

摘要

将麻醉、麻痹、切断迷走神经且外周化学去神经支配的猫暴露于低氧环境中,会导致膈神经电图最初出现抑制,随后消失。为了确定低氧性呼吸抑制是否由Bötzinger复合体的延髓脊髓神经元(Böt-E神经元)对呼吸前运动神经元的抑制所致,在急性低氧性低氧期间,对背侧和腹侧呼吸组延髓脊髓吸气神经元以及Böt-E神经元进行了细胞外记录。在低氧期间,所有记录的神经元放电频率均降低。在低氧期间,Böt-E神经元在膈神经相性活动消失之前就停止放电,而在复氧期间,在膈神经电图恢复之前或与之同时开始放电。吸气神经元在膈神经沉默时停止放电。在正常氧合期间相对于膈神经电图放电起始较晚的背侧呼吸组和腹侧呼吸组神经元,在低氧期间吸气时放电逐渐提前,而复氧期间这种效应则相反。这些数据与抑制和/或去易化作为低氧性呼吸抑制的机制一致,但表明Böt-E神经元不是这种抑制的来源。

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