Effect of upper airway negative pressure on inspiratory drive during sleep.

Effect of upper airway negative pressure on inspiratory drive during sleep.
复制标题

上呼吸道负压对睡眠期间吸气驱动的影响。

DOI:
10.1152/jappl.1998.84.3.1063
复制
发表时间:
1998
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Dempsey,JA
Dempsey,JA
中科院分区:
--
文献类型:
--
作者:
Eastwood,PR;Curran,AK;Smith,CA;Dempsey,JA

文献摘要

被引文献

相似文献

为了确定吸气时上呼吸道负压和塌陷对呼吸调节的影响,我们研究了4只清醒和睡眠时未麻醉的雌性犬,它们通过一个封闭在永久气管造口周围的有窗口的气管造口管进行呼吸。口鼻用密闭面罩密封,从而在关闭窗口(Fen)时隔离UA,并使UA在Fen打开时暴露于胸腔内压力变化,但不暴露于流量变化。在Fen闭合时,吸气时间(Ti)在清醒、非快速眼动(NREM)睡眠和快速眼动(REM)睡眠时增加(分别为155±8、164±11和161±32%),反映抑制性肺膨胀反射的消失。在Fen开放(与Fen闭合)的气管阻断中:1)UA保持开放;2)Tifurther在觉醒和NREM时增加(分别为215±52和197±28%),但在REM睡眠时不明显(196±42%);3)隔膜肌电平均上升速率(EMGdi/Ti)和气管压力下降速率(PTR/Ti)降低,反映来自UA受体的额外抑制输入;4)随着吸气的进行,EMGdi/Tii和PTR/Ti值均按比例降低,提示更大的反射抑制。在清醒和睡眠期间,当吸气阻力负荷在几次呼吸中施加时,将尿酸暴露在负压下(通过开放的气管分流)也可以看到类似的抑制效果。即使面对不断上升的化学刺激,这些抑制作用也会持续存在。这种对吸气运动输出的抑制在吸气中是线性的,反映了UA扭曲激活了UA压力敏感受体,更大的扭曲可能发生在努力的后期。
To determine the effect of upper airway (UA) negative pressure and collapse during inspiration on regulation of breathing, we studied four unanesthetized female dogs during wakefulness and sleep while they breathed via a fenestrated tracheostomy tube, which was sealed around the permanent tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration (Fen) was closed and exposing the UA to intrathoracic pressure changes, but not to flow changes, when Fen was open. During tracheal occlusion with Fen closed, inspiratory time (Ti) increased during wakefulness, non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep (155 ± 8, 164 ± 11, and 161 ± 32%, respectively), reflecting the removal of inhibitory lung inflation reflexes. During tracheal occlusion with Fen open (vs. Fen closed):1) the UA remained patent;2) Tifurther increased during wakefulness and NREM (215 ± 52 and 197 ± 28%, respectively) but nonsignificantly during REM sleep (196 ± 42%);3) mean rate of rise of diaphragm EMG (EMGdi/Ti) and rate of fall of tracheal pressure (Ptr/Ti) were decreased, reflecting an additional inhibitory input from UA receptors; and4) both EMGdi/Tiand Ptr/Tiwere decreased proportionately more as inspiration proceeded, suggesting greater reflex inhibition later in the effort. Similar inhibitory effects of exposing the UA to negative pressure (via an open tracheal Fen) were seen when an inspiratory resistive load was applied over several breaths during wakefulness and sleep. These inhibitory effects persisted even in the face of rising chemical stimuli. This inhibition of inspiratory motor output is alinear within an inspiration and reflects the activation of UA pressure-sensitive receptors by UA distortion, with greater distortion possibly occurring later in the effort.