Eikermann Matthias, Vogt Florian M, Herbstreit Frank, Vahid-Dastgerdi Mehdi, Zenge Michael O, Ochterbeck Christof, de Greiff Armin, Peters Jürgen
Oberarzt der Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
Am J Respir Crit Care Med. 2007 Jan 1;175(1):9-15. doi: 10.1164/rccm.200512-1862OC. Epub 2006 Oct 5.
Partial neuromuscular transmission failure by acetylcholine receptor blockade (neuromuscular blockade) or antibody-mediated functional loss (myasthenia gravis), even with a magnitude of muscle weakness that does not evoke respiratory symptoms, can evoke dysphagia and decreased inspiratory airflow, and increases the risk of susceptible patients to develop severe pulmonary complications.
To assess whether impaired neuromuscular transmission predisposes individuals to inspiratory upper airway collapse, we assessed supraglottic airway diameter and volume by respiratory-gated magnetic resonance imaging, upper airway dilator muscle function (genioglossus force and EMG), and changes in lung volume, respiratory timing, and peripheral muscle function before, during, and after partial neuromuscular blockade in healthy, awake volunteers.
Partial neuromuscular blockade (train-of-four [TOF] ratio: 0.5 and 0.8) was associated with the following: (1) a decrease of inspiratory retropalatal and retroglossal upper airway volume to 66 +/- 22 and 82 +/- 12% of baseline, which was significantly more intense in the retropalatal area; (2) an attenuation of the normal increase in anteroposterior upper airway diameter during forced inspiration to 74 +/- 18% of baseline; (3) a decrease in genioglossus activity during maximum voluntary tongue protrusion to 39 +/- 19% (TOF, 0.5) and 73 +/- 29% (TOF, 0.8) of baseline; and (4) no effects on upper airway size during expiration, lung volume, and respiratory timing.
Thus, impaired neuromuscular transmission, even to a degree insufficient to evoke respiratory symptoms, markedly impairs upper airway dimensions and function. This may be explained by an impairment of the balance between upper airway dilating forces and negative intraluminal pressure generated during inspiration by respiratory "pump" muscles.
通过乙酰胆碱受体阻滞导致的部分神经肌肉传递失败（神经肌肉阻滞）或抗体介导的功能丧失（重症肌无力），即使肌肉无力程度未引发呼吸道症状，也可引起吞咽困难和吸气气流减少，并增加易感患者发生严重肺部并发症的风险。
为评估神经肌肉传递受损是否会使个体易发生吸气性上气道塌陷，我们通过呼吸门控磁共振成像评估了声门上气道直径和容积、上气道扩张肌功能（颏舌肌力量和肌电图），以及健康清醒志愿者在部分神经肌肉阻滞前、期间和之后肺容积、呼吸时间和外周肌肉功能的变化。
部分神经肌肉阻滞（四个成串刺激[TOF]比值：0.5和0.8）与以下情况相关：（1）吸气时软腭后和舌后上气道容积分别降至基线的66±22%和82±12%，软腭后区域的下降更为明显；（2）用力吸气时上气道前后径的正常增加减弱至基线的74±18%；（3）最大自主伸舌时颏舌肌活动降至基线的39±19%（TOF为0.5）和73±29%（TOF为0.8）；（4）对呼气时上气道大小、肺容积和呼吸时间无影响。
因此，即使神经肌肉传递受损程度不足以引发呼吸道症状，也会显著损害上气道尺寸和功能。这可能是由于上气道扩张力与呼吸“泵”肌肉在吸气时产生的管腔内负压之间的平衡受损所致。
