Responses of bronchial C-fiber afferents of the rabbit to changes in lung compliance

Ma, Amy; Bravo, Milo; Kappagoda, C. T.

doi:10.1016/s1569-9048(03)00189-7

Cited by 18 publications

(8 citation statements)

References 19 publications

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“…The second response is likely in part vagally mediated. 10,18 Although the NAVAhigh for the group was more than twice NAVAal, the increases in mean inspiratory Paw (approximately 1 cm H 2 O) and Vt (approximately 0.8 mL/kg PBW) were relatively small. If the EAdi had not been down-regulated between NAVAal and NAVAhigh, the Paw delivered at NAVAhigh would have been more than double the Paw delivered at NAVAal.…”

Section: Discussionmentioning

confidence: 91%

Titration and Implementation of Neurally Adjusted Ventilatory Assist in Critically Ill Patients

Brander

Leong‐Poi

Beck

et al. 2009

Chest

156

166

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Section: Discussionmentioning

confidence: 91%

Titration and Implementation of Neurally Adjusted Ventilatory Assist in Critically Ill Patients

Brander

Leong‐Poi

Beck

et al. 2009

Chest

156

166

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“…The tonic activity was abolished by vagotomy (19; unpublished data). Animal models have also been used to demonstrate that lung deflation (20,21) and pulmonary edema (22) increase the activity of vagal efferents and that direct stimulation of vagal afferents causes tonic activation of the diaphragm (23). Application of PEEP to the intubated airway immediately reduces the activity of the vagal efferents (20,21) and reduces the tonic activity of the diaphragm (unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Diaphragm Electrical Activity During Expiration in Mechanically Ventilated Infants

et al. 2006

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ABSTRACT:The presence of diaphragm electrical activity (EAdi) during expiration is believed to be involved in the maintenance of end-expiratory lung volume (EELV) and has never been studied in intubated and mechanically ventilated infants. The aim of this study was to quantify the amplitude of diaphragm electrical activity present during expiration in mechanically ventilated infants and to measure the impact of removing positive end-expiratory pressure (PEEP) on this activity. We studied the EAdi in 16 ready-to-be weaned intubated infants who were breathing on their prescribed ventilator and PEEP settings. In all 16 patients, 5 min of data were collected on the prescribed ventilator settings. In a subset of eight patients, the PEEP was briefly reduced to zero PEEP (ZEEP). EAdi was recorded with miniaturized sensors placed on a conventional nasogastric feeding tube. Airway pressure (Paw) was also measured. For each spontaneous breath, we identified the neural inspiration and neural expiration. Neural expiration was divided into quartiles (Q1, Q2, Q3, and Q4), and the amplitude of EAdi calculated for each Q1-Q4 represented 95 Ϯ 29%, 31 Ϯ 15%, 15 Ϯ 8%, and 12 Ϯ 7%, respectively, of the inspiratory EAdi amplitude. EAdi for Q3-Q4 significantly increased during ZEEP, and decreased after reapplication of PEEP. These findings confirm that the diaphragm remains partially active during expiration in intubated and mechanically ventilated infants and that removal of PEEP affects this tonic activity. This could have potential implications on the management of PEEP in intubated infants. T he diaphragm is primarily known as an inspiratory muscle that is active during inspiration and relaxed during expiration. However, in healthy premature and full-term newborns, it has been demonstrated that electrical activity of the diaphragm, measured with electrodes on the surface of the chest wall, may persist throughout expiration, suggesting a "tonic" activity of the respiratory muscles (1-4). Lopes et al.(2) demonstrated that changes in tonic activity of the diaphragm were associated with changes in EELV and provided the original physiologic explanation that persistent diaphragmatic activity during the exhalation period helps to regulate EELV in infants . In healthy full-term or premature infants, the EELV is higher than the relaxation volume, the latter being determined by the passive mechanical properties of the respiratory system (1,3,5). It is only after 1 y of age that the EELV coincides with the relaxed lung volume (6); before this age, adapting reflexes must compensate for the reduced EELV. In newborns, persistence of diaphragm activity during expiration, in combination with the flow-braking action of the laryngeal adductor muscles (7), a high respiratory rate, and a reduced time-constant of the respiratory system, has been suggested to contribute to an active elevation of EELV (5,8 -11). However, in intubated and mechanically ventilated infants, the presence of an endotracheal tube does not allow for expiratory flow braking via...

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“…Most of the nodose ganglion afferent fiber express markers of nociceptors, including TRP channels (TRPA1, TRPV1, and TRPM8) ( 84 ), voltage-gated sodium channels (NaV1.7, NaV1.8, and NaV1.9), voltage-gated calcium channels (CaV2.2) and mechanosensitive channels (Piezo2) ( 85 ). While these nociceptors mostly serve a defensive role by detecting chemical, mechanical, or thermal threats and initiate essential, protective airway reflexes such as cough and bronchoconstriction ( 86 ), they may also directly respond to decreases in lung compliance leading to subconscious sighs or deep inspirations ( 87 ). Physiologically, airway nociceptors can evoke both cough and neurogenic inflammation, the latter being a consequence of the axon reflex discussed above ( 8 , 88 , 89 ).…”

Section: Airway Immunity: a Model System For Delineating Neuro-immunementioning

confidence: 99%

Sense and Immunity: Context-Dependent Neuro-Immune Interplay

et al. 2017

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The sensory nervous and immune systems, historically considered autonomous, actually work in concert to promote host defense and tissue homeostasis. These systems interact with each other through a common language of cell surface G protein-coupled receptors and receptor tyrosine kinases as well as cytokines, growth factors, and neuropeptides. While this bidirectional communication is adaptive in many settings, helping protect from danger, it can also become maladaptive and contribute to disease pathophysiology. The fundamental logic of how, where, and when sensory neurons and immune cells contribute to either health or disease remains, however, unclear. Our lab and others’ have begun to explore how this neuro-immune reciprocal dialog contributes to physiological and pathological immune responses and sensory disorders. The cumulative results collected so far indicate that there is an important role for nociceptors (noxious stimulus detecting sensory neurons) in driving immune responses, but that this is highly context dependent. To illustrate this concept, we present our findings in a model of airway inflammation, in which nociceptors seem to have major involvement in type 2 but not type 1 adaptive immunity.

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Responses of bronchial C-fiber afferents of the rabbit to changes in lung compliance

Cited by 18 publications

References 19 publications

Titration and Implementation of Neurally Adjusted Ventilatory Assist in Critically Ill Patients

Titration and Implementation of Neurally Adjusted Ventilatory Assist in Critically Ill Patients

Diaphragm Electrical Activity During Expiration in Mechanically Ventilated Infants

Sense and Immunity: Context-Dependent Neuro-Immune Interplay

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