Gorini M, Spinelli A, Gigliotti F, Duranti R, Arcangeli P, Scano G
Istituto di Clinica Medica III, Università degli Studi, Firenze, Italy.
Eur Respir J. 1988 Aug;1(8):691-7.
This study was undertaken in order to assess the neural drive to the respiratory muscles and the inspiratory neuromuscular coupling in patients with bronchial asthma during histamine-induced bronchoconstriction. Bronchoconstriction was produced in a graded fashion, with histamine phosphate aerosol of increasing dose, in twelve asymptomatic asthmatic patients and was measured by FEV1. Inspiratory drive was measured by electromyographic activity of the diaphragm (EMGd) and the coupling of the neural drive to the respiratory muscles was assessed by the relationship of mouth occlusion pressure (P0.1) to EMGd. During the test we also measured electromyographic activity of the inspiratory intercostal (EMGint), sternomastoid (EMGsm) and expiratory abdominal (EMGab) muscles. Histamine caused a significant decrease in FEV1, a significant increase in P0.1, EMGd, EMGint, and a relevant increase in EMGsm, with no substantial increase in EMGab. An inverse significant relationship between the change in FEV1 and changes in P0.1, EMGd and EMGint and a significant correlation between the change in FEV1 and in the P0.1/EMGd ratio were observed. We conclude that a progressive increase in bronchospasm is accompanied by a progressive increase in respiratory neural drive and decrease in neuromuscular coupling. This could be caused both by an increase in lung volume and a lack of abdominal expiratory muscle recruitment.
本研究旨在评估组胺诱导支气管收缩期间支气管哮喘患者呼吸肌的神经驱动及吸气神经肌肉耦联。对12例无症状哮喘患者，以递增剂量的磷酸组胺气雾剂以分级方式诱导支气管收缩，并通过第1秒用力呼气量（FEV1）进行测量。吸气驱动通过膈肌肌电图活动（EMGd）进行测量，神经驱动与呼吸肌的耦联通过口腔阻断压（P0.1）与EMGd的关系进行评估。在测试过程中，我们还测量了吸气肋间肌（EMGint）、胸锁乳突肌（EMGsm）和呼气腹肌（EMGab）的肌电图活动。组胺导致FEV1显著降低，P0.1、EMGd、EMGint显著增加，EMGsm有相应增加，而EMGab无显著增加。观察到FEV1变化与P0.1、EMGd和EMGint变化之间存在显著负相关，以及FEV1变化与P0.1/EMGd比值变化之间存在显著相关性。我们得出结论，支气管痉挛的逐渐加重伴随着呼吸神经驱动的逐渐增加和神经肌肉耦联的降低。这可能是由肺容积增加和呼气腹肌募集不足共同导致的。
