Division of Sleep Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
J Appl Physiol (1985). 2012 Mar;112(5):695-703. doi: 10.1152/japplphysiol.00136.2011. Epub 2011 Nov 3.
Obstructive sleep apnea patients experience recurrent upper airway (UA) collapse due to decreases in the UA dilator muscle activity during sleep. In contrast, activation of UA dilators reduces pharyngeal critical pressure (Pcrit, an index of pharyngeal collapsibility), suggesting an inverse relationship between pharyngeal collapsibility and dilator activity. Since most UA muscles display phasic respiratory activity, we hypothesized that pharyngeal collapsibility is modulated by respiratory drive via neuromuscular mechanisms. Adult male Sprague-Dawley rats were anesthetized, vagotomized, and ventilated (normocapnia). In one group, integrated genioglossal activity, Pcrit, and maximal airflow (V(max)) were measured at three expiration and five inspiration time points within the breathing cycle. Pcrit was closely and inversely related to phasic genioglossal activity, with the value measured at peak inspiration being the lowest. In other groups, the variables were measured during expiration and peak inspiration, before and after each of five manipulations. Pcrit was 26% more negative (-15.0 ± 1.0 cmH(2)O, -18.9 ± 1.2 cmH(2)O; n = 23), V(max) was 7% larger (31.0 ± 1.0 ml/s, 33.2 ± 1.1 ml/s), nasal resistance was 12% bigger [0.49 ± 0.05 cmH(2)O/(ml/s), 0.59 ± 0.05 cmH(2)O/(ml/s)], and latency to induced UA closure was 14% longer (55 ± 4 ms, 63 ± 5 ms) during peak inspiration vs. expiration (all P < 0.005). The expiration-inspiration difference in Pcrit was abolished with neuromuscular blockade, hypocapnic apnea, or death but was not reduced by the superior laryngeal nerve transection or altered by tracheal displacement. Collectively, these results suggest that pharyngeal collapsibility is moment-by-moment modulated by respiratory drive and this phasic modulation requires neuromuscular mechanisms, but not the UA negative pressure reflex or tracheal displacement by phasic lung inflation.
阻塞性睡眠呼吸暂停患者在睡眠期间上呼吸道 (UA) 扩张肌活动减少，导致 UA 反复塌陷。相比之下，UA 扩张肌的激活降低了咽临界压 (Pcrit，咽塌陷指数)，这表明咽塌陷性和扩张肌活性之间存在反比关系。由于大多数 UA 肌肉呈现出相位性呼吸活动，我们假设通过神经肌肉机制，呼吸驱动调节咽塌陷性。成年雄性 Sprague-Dawley 大鼠被麻醉、迷走神经切断并进行通气（正常碳酸血症）。在一组实验中，在呼吸周期内的三个呼气点和五个吸气点测量颏舌肌综合活动、Pcrit 和最大气流 (V(max))。Pcrit 与相位性颏舌肌活动密切相关且呈反比关系，吸气峰时测量的值最低。在其他组中，在呼气和吸气峰时测量变量，在五次操作前后各测量一次。在吸气峰时，Pcrit 更负（-15.0 ± 1.0 cmH(2)O，-18.9 ± 1.2 cmH(2)O；n = 23），V(max) 更大（31.0 ± 1.0 ml/s，33.2 ± 1.1 ml/s），鼻阻力更大[0.49 ± 0.05 cmH(2)O/（ml/s），0.59 ± 0.05 cmH(2)O/（ml/s）]，诱导 UA 关闭的潜伏期更长（55 ± 4 ms，63 ± 5 ms），吸气时与呼气时相比（所有 P < 0.005）。神经肌肉阻滞、低碳酸血症性呼吸暂停或死亡可消除呼气-吸气 Pcrit 差异，但上喉神经切断或气管移位均未减少差异，也未改变差异。综上所述，这些结果表明，呼吸驱动时刻调节咽塌陷性，这种相位调节需要神经肌肉机制，而不是 UA 负压反射或通过相位性肺充气导致的气管移位。
