Phasic volume-related feedback on upper airway muscle activity

Abstract

The effects of vagally mediated volume-related feedback on the activity of upper airway muscles was assessed in nine pentobarbital-anesthetized, tracheostomized, spontaneously breathing dogs. Moving average electrical activity was recorded before and during single-breath airway occlusions from the genioglossus, posterior cricoarytenoid, and alae nasi muscles and compared with simultaneously recorded tidal volume and electrical activity of the phrenic nerve (6 dogs) or diaphragm (3 dogs). The normally early peak of upper airway muscle activity during unoccluded breaths was delayed to late or end inspiration during occluded breaths. Inspiratory depression started at a lower volume above end-expiratory volume and at an earlier time after inspiratory onset for the upper airway muscles than for the phrenic nerve and the diaphragm. The amount of depression at the end of inspiratory airflow was larger for all of the upper airway muscles than for the phrenic nerve and diaphragm. Depressive effects were most prominent in the genioglossus, followed by the posterior cricoarytenoid and the alae nasi. After vagotomy, depressive effects of volume-related feedback were no longer seen. These results suggest that activity of the upper airway muscles is modulated by vagally mediated feedback, apparently to a larger extent than that of the diaphragm and phrenic nerve.

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

“…Mechanical feedback from lung stretch receptors is relayed by vagus nerve afferents to the neural circuits that drive breathing (van Lunteren et al, 1984;Kuna, 1986). Lung mechanoreceptors function to couple lung mechanics with respiratory motor drive.…”

“…Mechanical feedback from lung mechanoreceptors is relayed by vagus nerve afferents to the brainstem circuitry that controls breathing (van Lunteren et al, 1984;Kuna, 1986;Ezure et al, 2002;Kubin et al, 2006). We predict that repeated modulation of mechanical feedback will trigger respiratory motor plasticity, and we base this assertion on three lines of evidence.…”

“…Obstructive apneas not only cause hypoxemia (Guilleminault and Abad, 2004), they also affect mechanical vagal afferent feedback (van Lunteren et al, 1984;Strohl, 1985;Milsom, 1990;Bailey and Fregosi, 2006). The following set of experiments was therefore designed to determine how each of these variables contributes to apnea-induced LTF.…”

“…5A), suggesting that vagal feedback, which normally suppresses respiratory activity, was either reduced or absent (van Lunteren et al, 1984;Kubin et al, 2006). To further demonstrate that nerve cooling blocked vagal feedback, we activated the vagus-dependent Hering-Breuer lung-inflation reflex (Cohen, 1975;Mellen and Feldman, 2000) before and dur- A, An EMG trace of genioglossus (GG) activity before, during, and after repeated apneas under vagotomy.…”

Determinants of effective ventilation during nasal intermittent positive pressure ventilation

“…We suggest that volume receptors reacting to an increase in lung volume induced glottic narrowing and attenuated the distension of the lungs. Volume information can be originated in slowly adapting receptors from the lung [25], in joint receptors from the thorax [26] or in intercostal muscles receptors [27]. Any or all of these receptors could have mediated the glottic response we postulate, in response to increases in delivered VT.…”