Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2.
Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2.
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神经肌肉活动对最大吸气气流的调节：CO2 的作用。
DOI：
10.1152/jappl.1993.74.4.1597
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Smith,PL
中科院分区：
文献类型：
--
作者：
Schwartz,AR;Thut,DC;Brower,RG;Gauda,EB;Roach,D;Permutt,S;Smith,PL
为了确定最大吸气气流（VImax）是如何被气道神经肌肉活动的变化所调节的，我们分析了不同二氧化碳水平麻醉的高氧狗在离体上呼吸道吸气和呼气时的压力-流量关系。记录吸入气流（VI）、下咽压（Php）、限流部位咽压（FLS）、鼻翼（AN）和颏舌肌（GG）肌电图（EMG）活动，同时通过快速降低Php产生VI限制，直到VI在VImax处趋于平稳。测量VImax及其力学决定因素，即FLS上游咽临界压（Pcrit）和鼻阻力（Rn）。在高碳酸血症（高CO2）时，吸气（217.3）和呼气（184.1%）时VImax显著升高。这些增加与相性而非强直性AN和GG活性的显著增加有关。它们还与呼气和吸气时Pcrit分别从低碳酸血症时的-6.2 +/- 1.6 （SE）降低到高CO2时的-9.3 +/- 3.0和-11.8 +/- 3.4 cmH2O相关。Rn未发生显著变化。当3只狗的相性神经肌肉活动被完全阻断时，高CO2时VImax的增加和Pcrit的降低被消除。当4只迷走神经切除犬的相相肌电图活动增强时，在高二氧化碳吸气和呼气时，VImax显著增加，prcrit显著减少。这些结果表明，当高碳酸血症刺激神经肌肉活动时，上呼吸道神经肌肉活动通过降低FLS部位的湿陷性（Pcrit）而增加离体上呼吸道的VImax。
To determine how maximal inspiratory airflow (VImax) is modulated by changes in airway neuromuscular activity, we analyzed pressure-flow relationships obtained during inspiration and expiration in isolated upper airways of anesthetized hyperoxic dogs at different levels of CO2. Inspiratory airflow (VI), hypopharyngeal pressure (Php), pharyngeal pressure at the flow-limiting site (FLS), and alae nasi (AN) and genioglossus (GG) electromyographic (EMG) activity were recorded while VI limitation was produced by rapidly lowering Php until VI plateaued at VImax. VImax and its mechanical determinants, pharyngeal critical pressure (Pcrit) and nasal resistance (Rn) upstream to the FLS, were measured. During hypercapnia (high CO2), VImax increased significantly during inspiration (217.3) and expiration (184.1%). These increases were associated with significant increases in phasic but not tonic AN and GG activity. They were also associated with decreases in Pcrit from -6.2 +/- 1.6 (SE) at hypocapnia to -9.3 +/- 3.0 and -11.8 +/- 3.4 cmH2O at high CO2 during expiration and inspiration, respectively. No significant changes in Rn occurred. When phasic neuromuscular activity was abolished by complete neuromuscular blockade in three dogs, these increases in VImax and decreases in Pcrit at high CO2 were eliminated. When phasic EMG activity was accentuated in four vagotomized dogs, significant increases in VImax and decreases in Pcrit were demonstrated during inspiration vs. expiration at high CO2. These findings indicate that upper airway neuromuscular activity increases VImax in the isolated upper airway by decreasing collapsibility (Pcrit) at the FLS site when neuromuscular activity is stimulated by hypercapnia.