Responses of C fiber afferents of the rabbit airways and lungs to changes in extra-vascular fluid volume

Gunawardena, S.; Ravindran, Krishnan; Longhurst, John C.; Kaufman, Marc P.; Ma, Amy; Bravo, Milo; Kappagoda, C. T.

doi:10.1016/s1569-9048(02)00114-3

Cited by 20 publications

(10 citation statements)

References 20 publications

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“…The tonic activity was abolished by vagotomy (19; unpublished data).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airway immediately reduces the activity of the vagal efferents (20,21) and reduces the tonic activity of the diaphragm (unpublished data).…”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: 98%

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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Section: Discussionmentioning

confidence: 98%

Diaphragm Electrical Activity During Expiration in Mechanically Ventilated Infants

et al. 2006

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“…In our study, increasing PEEP likely increased functional residual capacity and recruited the lungs (1-38) and could thus have reduced the tonic activity produced by mechanisms related to the vagally mediated deflation reflex described by Hering and Breuer (39). It is also possible that a reduction or redistribution of lung edema (40) by PEEP may have played a role because changes in extravascular fluid affect the activity of vagally mediated receptors (9,10). Another possibility is that tracheobronchial instillation of hydrochloric acid acutely increases tonic diaphragm activity in part by stimulation of specific vagal "irritant" receptors (10).…”

Section: Discussionmentioning

confidence: 99%

Influence of neurally adjusted ventilatory assist and positive end-expiratory pressure on breathing pattern in rabbits with acute lung injury*

Allo

Beck

Brander

et al. 2006

Critical Care Medicine

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“…A second potential mechanism to contribute to the observed respiratory alkalosis would be augmentation of V E by edema-responsive neural afferent signals either from lung or from exercising muscle. In lung, the unmyelinated C fibers in airway mucosa respond to airway edema, triggering afferent ventilation stimuli in experimental animals (10). In muscle, Piepoli et al (24) described an increased ventilation stimulus from forearm exercise in chronic heart failure patients, attributed to afferent signals from the muscle.…”

Section: Discussionmentioning

confidence: 99%

Exercise response after rapid intravenous infusion of saline in healthy humans

Robertson¹,

Pellegrino²,

Pini³

et al. 2004

Journal of Applied Physiology

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Patients with chronic heart failure have an abnormal pattern of exercise ventilation (Ve), characterized by small tidal volumes (Vt), increased alveolar ventilation, and elevated physiological dead space (Vd/Vt). To investigate whether increased lung water in isolation could reproduce this pattern of exercise ventilation, 30 ml/kg of saline were rapidly infused into nine normal subjects, immediately before a symptom-limited incremental exercise test. Saline infusion significantly reduced forced vital capacity, 1-s forced expiratory volume, and alveolar volume (P < 0.01 for all). After saline, exercise ventilation assessed by the Ve/Vco(2) slope increased from 24.9 +/- 2.4 to 28.0 +/- 2.9 l/l, (P < 0.0002), associated with a small decrease in arterial Pco(2), but without changes in Vt, Vd/Vt, or alveolar-arterial O(2) difference. A reduction in maximal O(2) uptake of 175 +/- 184 ml/min (P < 0.02) was observed in the postsaline infusion exercise studies, associated with a consistent reduction in maximal exercise heart rate (8.1 +/- 5.9 beats/min, P < 0.01), but without a change in the O(2) pulse. Therefore, infusion of saline to normal subjects before exercise failed to reproduce either the increase in Vd/Vt or the smaller exercise Vt described in heart failure patients. The observed increase in Ve can be attributed to dilution acidosis from infusion of the bicarbonate-free fluid and/or to afferent signals from lung and exercising muscles. The reduction in maximal power output, maximal O(2) uptake, and heart rate after saline infusion may be linked to accumulation of edema fluid in exercising muscle, impairing the diffusion of O(2) to muscle mitochondria.

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Responses of C fiber afferents of the rabbit airways and lungs to changes in extra-vascular fluid volume

Cited by 20 publications

References 20 publications

Diaphragm Electrical Activity During Expiration in Mechanically Ventilated Infants

Diaphragm Electrical Activity During Expiration in Mechanically Ventilated Infants

Influence of neurally adjusted ventilatory assist and positive end-expiratory pressure on breathing pattern in rabbits with acute lung injury*

Exercise response after rapid intravenous infusion of saline in healthy humans

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