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猫通过咽部刺激在平静呼吸时对延髓喘息机制的反射性募集。

Reflex recruitment of medullary gasping mechanisms in eupnoea by pharyngeal stimulation in cats.

作者信息

Fung M L, St John W M, Tomori Z

机构信息

Department of Physiology, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center, Lebanon, NH 03755.

出版信息

J Physiol. 1994 Mar 15;475(3):519-29. doi: 10.1113/jphysiol.1994.sp020090.

DOI:10.1113/jphysiol.1994.sp020090
PMID:8006833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1160402/
Abstract
  1. Mechanical stimulation of the naso- and oropharynx causes the replacement of the eupnoeic ventilatory pattern by a brief, but large, burst of activity of the phrenic nerve. Our purpose was to define whether these changes in phrenic activity represent a switch to gasping. 2. In decerebrate, vagotomized, paralysed and ventilated cats, mechanical stimulation of the pharynx was performed during eupnoea, apneusis and gasping. The latter two ventilatory patterns were produced by ventilating the experimental animal with 1.0% carbon monoxide in air or with 100% nitrogen. Eupnoea could be re-established by a recommencement of ventilation with oxygen. 3. The rate of rise of phrenic activity and its peak height were much greater following mechanical stimulation of the pharynx than the phrenic bursts of eupnoea or apneusis. The durations of phrenic burst and the period between these were much less following pharyngeal stimulation. In contrast, these variables of phrenic activity were the same during pharyngeal stimulation and in gasping. 4. Previous studies had established that activity within a region of the lateral tegmental field of medulla is critical for the manifestation of gasping. Hence, electrical stimulation of this region during gasping elicits premature gasps whereas its ablation irreversibly eliminates gasping. 5. We positioned a multibarrelled pipette in the critical medullary region for gasping. Its location was verified, once gasping was established in hypoxia or anoxia, by the elicitation of premature gasps following electrical stimulation. Neurons in this region were destroyed by microinjections of the neurotoxin kainic acid; in a few experiments the region was destroyed by electrolytic lesions. 6. Following destruction of the region of the lateral tegmental field, gasping could no longer be provoked in anoxia. In contrast, the eupnoeic pattern of phrenic activity continued. However, mechanical stimulation of the pharynx no longer caused any changes in the on-going pattern of phrenic activity. 7. We conclude that mechanical stimulation of the pharynx elicits a powerful reflex by which eupnoea is suppressed and gasping is elicited. Stated differently, the changes in phrenic activity during this pharyngeal stimulation in fact represent gasps. 8. Gasps are dependent upon activity within a region of the lateral tegmental field of the medulla. This region plays no role in the neurogenesis of eupnoea. Hence, our results provide additional support for the concept that there are multiple sites for ventilatory neurogenesis in the mammalian brainstem.
摘要
  1. 对鼻咽部和口咽部进行机械刺激会导致膈神经活动短暂但强烈地爆发,从而取代平静呼吸的通气模式。我们的目的是确定膈神经活动的这些变化是否代表着转变为喘息。2. 在去大脑、切断迷走神经、麻痹并进行通气的猫身上,在平静呼吸、长吸式呼吸和喘息期间对咽部进行机械刺激。后两种通气模式是通过用含1.0%一氧化碳的空气或100%氮气对实验动物进行通气产生的。通过重新用氧气通气可恢复平静呼吸。3. 咽部受到机械刺激后,膈神经活动的上升速率及其峰值高度比平静呼吸或长吸式呼吸时的膈神经爆发要大得多。咽部刺激后,膈神经爆发的持续时间及其间隔时间要短得多。相比之下,咽部刺激期间和喘息时膈神经活动的这些变量是相同的。4. 先前的研究已经证实,延髓外侧被盖区的一个区域内的活动对于喘息的表现至关重要。因此,在喘息期间对该区域进行电刺激会引发过早的喘息,而对其进行损毁则会不可逆地消除喘息。5. 我们将一个多管移液管放置在延髓中对喘息至关重要的区域。一旦在缺氧或无氧状态下建立了喘息,通过电刺激引发过早的喘息来验证其位置。通过微量注射神经毒素 kainic 酸破坏该区域的神经元;在一些实验中通过电解损伤破坏该区域。6. 破坏外侧被盖区后,在缺氧状态下不再能引发喘息。相比之下,膈神经活动的平静呼吸模式仍在继续。然而,咽部的机械刺激不再引起正在进行的膈神经活动模式的任何变化。7. 我们得出结论,咽部的机械刺激引发了一种强大的反射,通过这种反射抑制平静呼吸并引发喘息。换句话说,在这种咽部刺激期间膈神经活动的变化实际上代表着喘息。8. 喘息依赖于延髓外侧被盖区一个区域内的活动。该区域在平静呼吸的神经发生中不起作用。因此,我们的结果为哺乳动物脑干中存在多个通气神经发生位点这一概念提供了额外的支持。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f307/1160402/2e5db96c2d45/jphysiol00406-0157-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f307/1160402/bb34895cfbb0/jphysiol00406-0156-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f307/1160402/2e5db96c2d45/jphysiol00406-0157-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f307/1160402/bb34895cfbb0/jphysiol00406-0156-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f307/1160402/2e5db96c2d45/jphysiol00406-0157-a.jpg

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J Appl Physiol Respir Environ Exerc Physiol. 1984 Apr;56(4):1008-19. doi: 10.1152/jappl.1984.56.4.1008.
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