Responses to inflation of vagal afferents with endings in the lung of dogs.

Kaufman, Marc P.; Iwamoto, Gary A.; Ashton, J; Cassidy, S. S.

doi:10.1161/01.res.51.4.525

Cited by 76 publications

(32 citation statements)

References 23 publications

(31 reference statements)

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“…There are at least 4 different types of afferent stretch receptor fibers carried in the vagus: (1) slowly adapting myelinated afferents, which cause cardioacceleration at lower transpulmonary inflation pressure of Յ9 cm H 2 O (or 1/6 maximal lung expansion) 18 and inhibit the level of inspiration (Hering-Breuer reflex); (2) rapidly adapting myelinated fibers, some of which are from irritant receptors; (3) unmyelinated, slowly adapting bronchial C fibers; and (4) unmyelinated, slowly adapting pulmonary C fibers. The latter 2 are known to elicit the cardiovascular suppression reflex at higher inflation pressures from 10 to 30 cm H 2 O.…”

Section: Respiratory Influence On Sympathetic Nerve Activitymentioning

confidence: 99%

Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

et al. 2001

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Background-Sympathoexcitation and respiratory instability are closely related to worsening of chronic heart failure. To elucidate the dynamic nature of respiratory modulation of sympathetic activity in patients with heart failure, we studied within-breath variation of muscle sympathetic nerve activity (MSNA) under various ventilatory volumes. Methods and Results-MSNA, blood pressure, and respiratory flow were recorded in 23 patients with left ventricular ejection fraction Յ45%. Within-breath suppression of MSNA (neural silence) was found in 11 patients (MSNA bursts: 71Ϯ10/100 heartbeats) but not in the remaining 12 patients (MSNA bursts: 88Ϯ8/100 heartbeats). Patients without neural silence had a smaller tidal volume (391Ϯ70 versus 267Ϯ75 mL/m 2 , PϽ0.01) and a higher respiratory rate (15Ϯ2 versus 19Ϯ4 breaths/min, PϽ0.01) during spontaneous respiration than those with neural silence. The relationship between tidal volume and minimal amplitude of MSNA bursts in each breath was obtained during random-interval breathing and fitted by an exponential function. The curve of patients without neural silence was shifted to the right and upward, which suggests that a greater tidal volume was required to suppress MSNA (227Ϯ70 versus 437Ϯ195 mL/m 2 , PϽ0.01). Conclusions-Sympathoexcitation in patients with chronic heart failure is closely related to both a decrease in resting tidal volume and an attenuated sympathoinhibitory effect of lung inflation reflex.

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Section: Respiratory Influence On Sympathetic Nerve Activitymentioning

confidence: 99%

Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

et al. 2001

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“…Fourthly, there is considerable evidence in animals for a cardiac accelerator response to lung inflation with inflation pressure of less than 14 mmHg (Hainsworth, 1974;Angell-James & de Burgh Daly, 1978;Kauffman, Iwamoto, Ashton & Cassidy, 1982) and to distension of the pulmonary vein-atrial junction (Ledsome & Linden, 1964). The topic has been recently reviewed by de Burgh Daly (1985).…”

Section: Cardiac Output and Ventilation In Manmentioning

confidence: 99%

Ventilation and cardiac output during the onset of exercise, and during voluntary hyperventilation, in humans.

Cummin¹,

Iyawe²,

Mehta³

et al. 1986

The Journal of Physiology

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SUMMARY1. Three normal subjects performed rest-exercise transitions on a cycle ergometer, from rest to unloaded pedalling (0 W), 50, 100 and 150 W. Each experiment was performed in triplicate, with randomized work load order, in two sessions. Ventilation was obtained breath-to-breath by integration of a pneumotachygraph signal, and cardiac output beat-to-beat by a new development of the Doppler technique. Results were bin-averaged in 4 s bins over the first 20 s, and compared to resting values.2. Both ventilation and cardiac output increased significantly in the first 2 s. This initial rise in ventilation was due entirely to an increase in rate, the subsequent rise mainly to increase in tidal volume. Cardiac output increased predominantly through change in rate with smaller increases in stroke volume.3. A striking feature was a tendency for ventilation and cardiac output responses to be biphasic with an initial rise followed by a slight fall at the 14 s mark, and a subsequent rise, at all work loads. Overall correlation between ventilation and cardiac output was therefore high (r = 0 92).4. Six normal subjects hyperventilated for 45 s voluntarily, (a) at rate 24/min and normal tidal volume; (b) at normal rate and tidal volume of 1-5 1; (c) at rate 24/min and tidal volume of 1-5 1. Cardiac output, averaged over 10-45 s, rose by 0 4, 0 5, and 1-0 1 min-respectively, with falls in end-tidal PCO, of 4, 6, and 8 mmHg.5. Six normal subjects hyperventilated for 60 s with rate 24/min and tidal volume of 1-4 1, and end-tidal Pco, maintained at 38 + 2 mmHg. Cardiac output, averaged from 10-60 s, rose by 1-0 I min'.6. With increased rate and tidal volume, whether isocapnic or hypocapnic, cardiac output responses showed an overshoot with a peak value at about 30 s.7. The hypothesis of 'cardiodynamic hyperpnoea' considers a possible effect of increasing cardiac output on ventilation. The effects of ventilation on cardiac output must also be considered. We propose an extended hypothesis involving stable positive feed-back.

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“…The C-fiber hypersensitivity developed at the onset of the HH challenge increased progressively during HH and persisted even after the arterial blood pressure returned to the control level during recovery. The increased sensitivity was found in their responses to both Cap injection and HI; the latter is of particular interest because lung expansion is a natural physiological action, and pulmonary C-fibers normally have low sensitivity to HI (13,19). In addition, the increased chemical sensitivity induced by HH in these afferents was not limited to Cap but was also evident in their responses to other chemical stimulants of C-fibers tested in this study: Ado, PBG, and LA; each of them represents a selective activator of a specific type of receptor expressed in the pulmonary C-fiber sensory endings.…”

Section: Discussionmentioning

confidence: 99%

Hemorrhagic hypotension-induced hypersensitivity of vagal pulmonary C-fibers to chemical stimulation and lung inflation in anesthetized rats

Lin

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Lin RL, Lin YJ, Xu F, Lee LY. Hemorrhagic hypotensioninduced hypersensitivity of vagal pulmonary C-fibers to chemical stimulation and lung inflation in anesthetized rats. Am J Physiol Regul Integr Comp Physiol 308: R605-R613, 2015. First published January 14, 2015 doi:10.1152/ajpregu.00424.2014.-This study was carried out to investigate whether hemorrhagic hypotension (HH) altered the sensitivity of vagal pulmonary C-fibers. The fiber activity (FA) of single vagal pulmonary C-fiber was continuously recorded in anesthetized rats before, during, and after HH was induced by bleeding from the femoral arterial catheter into a blood reservoir and lowering the mean systemic arterial pressure (MSAP) to ϳ40 mmHg for 20 min. Our results showed the following. First, after MSAP reached a steady state of HH, the peak FA response to intravenous injection of capsaicin was elevated by approximately fivefold. The enhanced C-fiber sensitivity continued to increase during HH and sustained even after MSAP returned to baseline during the recovery, but slowly returned to control ϳ20 min later. Second, responses of FA to intravenous injections of other chemical stimulants of pulmonary C-fibers (phenylbiguanide, lactic acid, and adenosine) and a constantpressure lung hyperinflation were all significantly potentiated by HH. Third, infusion of sodium bicarbonate alleviated the systemic acidosis during HH, and it also attenuated, but did not completely prevent, the HH-induced C-fiber hypersensitivity. In conclusion, the pulmonary C-fiber sensitivity was elevated during HH, probably caused by the endogenous release of chemical substances (e.g., lactic acid) that were produced by tissue ischemia during HH. This enhanced C-fiber sensitivity may heighten the pulmonary protective reflexes mediated through these afferents (e.g., cough, J reflex) during hemorrhage when the body is more susceptible to other hazardous insults and pathophysiological stresses.hemorrhage; pulmonary; C-fiber; hypoxia; hypersensitivity VAGAL BRONCHOPULMONARY C-fibers represent ϳ75% of the vagal afferents arising from the lung and airways (17). These unmyelinated afferents innervate the entire respiratory tract and play an important role in regulating the respiratory functions under various physiological and pathophysiological conditions (5, 21). Activation of these afferents elicits centrally mediated protective reflex responses via the cholinergic pathway, which include laryngeal closure, bronchoconstriction and airway hypersecretion, accompanied by cough, airway irritation, dyspneic sensation, and J reflex (5, 21). Activation of these sensory nerves can also trigger release of tachykinins and calcitonin gene-related peptide from the sensory terminals, which can act on a number of effector cells in the respiratory tract (e.g., smooth muscles, cholinergic ganglia, mucous glands, immune cells), and elicit the local "axon reflexes" such as bronchoconstriction, protein extravasation, and inflammatory cell chemotaxis (5, 18, 21).Tissue ischemia is known to activate C-fib...

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Responses to inflation of vagal afferents with endings in the lung of dogs.

Cited by 76 publications

References 23 publications

Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

Respiratory Modulation of Muscle Sympathetic Nerve Activity in Patients With Chronic Heart Failure

Ventilation and cardiac output during the onset of exercise, and during voluntary hyperventilation, in humans.

Hemorrhagic hypotension-induced hypersensitivity of vagal pulmonary C-fibers to chemical stimulation and lung inflation in anesthetized rats

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