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戊巴比妥钠诱导完整、迷走神经切断及呼吸调整中枢损伤猫出现长吸式呼吸。

Pentobarbital-induced apneusis in intact, vagotomized, and pneumotaxic-lesioned cats.

作者信息

Webber C L, Peiss C N

出版信息

Respir Physiol. 1979 Sep;38(1):37-57. doi: 10.1016/0034-5687(79)90005-7.

Abstract

While recording several respiratory parameters, sodium pentobarbital (PB) was infused into the inferior vena cava of spontaneously breathing, PB anesthetized cats. Three cat groups were investigated: intact control (group A); vagotomized (group B); pneumotaxic center-lesioned (group C). With a few exceptions, all cats developed PB-induced inspiratory apneusis. Groups B and C exhibited 10-sec inspiratory hold pattern at significantly lower PB levels than group A cats. All groups developed apnea at different PB levels. Ventilation was consistently depressed, predominantly by breathing frequently attenuation. Tidal volume remained comparable to control, but decreased in vagotomized cats at high PB levels. These results are interpreted to signify that (1) inspiratory inhibitory inputs are more susceptible to depression by PB than inspiratory drive mechanisms; (2) the breathing pattern of apneusis results when summed inspiratory inhibition is reduced below a critical minimum level; (3) vagal and pneumotaxic center inhibitions on inspiration are equally weighted at apneusis, but not at apnea. These results are further discussed in terms of the inspiratory off-switch model. A possible model of Biot respiration is also introduced.

摘要

在记录多个呼吸参数的同时,将戊巴比妥钠(PB)注入自主呼吸、经PB麻醉的猫的下腔静脉。研究了三组猫:完整对照组(A组);迷走神经切断组(B组);呼吸调节中枢损伤组(C组)。除少数例外,所有猫均出现PB诱导的吸气性呼吸暂停。B组和C组在显著低于A组猫的PB水平时表现出10秒的吸气暂停模式。所有组在不同的PB水平下均出现呼吸暂停。通气持续受到抑制,主要是通过呼吸频率的衰减。潮气量与对照组相当,但在高PB水平时,迷走神经切断的猫的潮气量减少。这些结果被解释为表明:(1)吸气抑制性输入比吸气驱动机制更容易受到PB的抑制;(2)当总的吸气抑制降低到临界最低水平以下时,就会出现呼吸暂停的呼吸模式;(3)迷走神经和呼吸调节中枢对吸气的抑制在呼吸暂停时权重相等,但在呼吸停止时不相等。根据吸气切断模型对这些结果进行了进一步讨论。还介绍了一种比奥呼吸的可能模型。

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