The importance of timing on the respiratory effects of intermittent carotid body chemoreceptor stimulation

Eldridge, Frederíc L.

doi:10.1113/jphysiol.1972.sp009799

Cited by 104 publications

(26 citation statements)

References 11 publications

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“…Dependence of respiratory center output on the timing of carotid body stimulation within a respiratory cycle has been demonstrated (ELDRIDGE, 1972;CROSS et al, 1979;TEPPEMA et al, 1985). In the present experiment, vagotomy changed the phase relationship between mechanical ventilation (hence arterial C02 oscillation) and the respiratory center output of the dog.…”

Section: Resultssupporting

confidence: 46%

Role of carbon dioxide oscillation in the control of respiration in the anesthetized dog.

Takahashi

Ashe

1989

Jpn.J.Physiol

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In order to examine the role of respiratory oscillation of Paco2 (CO2 oscillation) in the control of respiration, we performed veno-venous bypass using a membrane lung in 10 anesthetized paralyzed dogs, where the dog was put on fixed mechanical ventilation so that we could keep average Paco2 and Pa02 constant by adjusting FIco2 and Fio2 during CO2 loading/unloading. By venous CO2 loading/unloading we could widely change the CO2 output from the lung (11-440 of the control) resulting in large changes in the arterial CO2 oscillations (50-280% of the control for the maximum rate of rise of Paco2 and 40-350°c of the control for the maximum rate of fall of Paco2), which was measured by a rapidly responding intra-arterial pH electrode. Despite such wide variations in CO2 oscillations we did not find any consistent change in the respiratory center output (minute phrenic activity). This held true after compensating the changes in the minute phrenic activity for the CO2 sensitivity of each individual dog. Thus, the present results may suggest that the CO2 oscillation plays little role in the control of respiration in mild increase in Vco2.

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Section: Resultssupporting

confidence: 46%

Role of carbon dioxide oscillation in the control of respiration in the anesthetized dog.

Takahashi

Ashe

1989

Jpn.J.Physiol

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“…of warmed, physiological saline through which 100 % C02 had been bubbled (002 saline: cf. Black & Torrance, 1971;Eldridge, 1972). These injections produced only slight transient alterations, if any, in carotid sinus pressure as measured from the lingual artery.…”

Section: Methodsmentioning

confidence: 99%

“…When a similar stimulus is delivered during the expiratory phase of a respiratory cycle, it has little effect, or simply prolongs the expiratory pause (Black & Torrance, 1971;Eldridge, 1972). The effects upon the heart rate of similar stimuli to the chemoreceptors, and of brief stimuli to the carotid baroreceptors, were investigated here in anaesthetized dogs.…”

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confidence: 99%

Baroreceptor and chemoreceptor influences on heart rate during the respiratory cycle in the dog.

Haymet¹,

McCloskey²

1975

The Journal of Physiology

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SUMMARY1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with pentobarbitone or chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0-2-05 ml. warmed, CO2-equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline, or of freshly drawn arterial blood, into the external carotid artery after first clamping the common carotid artery.2. Brief baroreceptor stimuli had no noticeable effect on breathing. Brief chemoreceptor stimuli had no effect on breathing in some dogs, but in many produced a reflex increase in the depth of inspiration when delivered during inspiration. In these same dogs, brief chemoreceptor stimuli delivered in expiration either prolonged the expiratory pause or evoked an active expiratory effort.3. Prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered during inspiration. If the carotid sinus nerve or the vagus nerves were cut the responses were abolished. 4. Brief chemoreceptor or baroreceptor stimuli remained effective in evoking prompt decreases in heart rate during periods of apnoea in the end-inspiratory position (Hering-Breuer inflation reflex). In periods of apnoea after prolonged artificial hyperventilation the stimuli were sometimes ineffective at first, but were always effective late in the period of apnoea, again producing prompt cardiac slowing.5. After denervation of the lungs, brief baroreceptor and chemoreceptor stimuli continued to evoke prompt falls in heart rate when given during B. T. HAYMET AND D. I. McCLOSKEY expiration. When delivered during inspiration the same stimuli were either ineffective, or less effective.

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“…In this context, it must be noted that Eldridge (1972) found that a variety of chemical stimuli to the carotid chemoreceptors (including NaCN) caused no inspiratory movements if delivered during the expiratory phase. However, in some animals, this carotid chemoreceptor stimulation 'was associated with a small brust of tiny phrenic nerve action potentials' (Eldridge, 1972 The second unusual observation was the positive response of a single animal to saline injected into the external carotid artery cannulae. Systemic saline injections produced no effect upon ventilation in this animal and, moreover, carotid sinus nerve section eliminated the response to intra-arterial saline and also NaCN injections.…”

Section: Discussionmentioning

confidence: 99%

Differential alteration by hypercapnia and hypoxia of the apneustic respiratory pattern in decerebrate cats

John

1979

The Journal of Physiology

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SUMMARY1. A combination of bilateral lesions within the nucleus parabrachialis medialis complex (n.p.b.m.) and bilateral vagotomy typically resulted in an apneustic respiratory pattern in decerebrate and paralysed cats. Integrated efferent phrenic nerve activity was recorded as an index of the respiratory rhythm.2. Changes in components of this apneustic breathing cycle were evaluated in response to steady-state hypercapnia and hypoxia. The components evaluated were (a) the period of phrenic discharge (inspiratory time, TI), (b) the period of no detectable phrenic activity (expiratory time, TE), (c) the total duration of the apneustic respiratory cycle (TTOT, the sum of T, and TE), and (d) the average height of the integrated phrenic nerve activity (apneustic depth).3. Elevations of PA, co. from values below 45 torr to 50-60 torr, under both hyperoxic and normoxic conditions, resulted in significant elevations of TI, TE, TTOT and depth. Further PA, CO, elevations to approximately 70 torr caused no change, or frequently, a decrease in TI, TE and TTOT; the apneustic depth increased in most animals.4. Diminutions in PA, 0, from normoxic to hypoxic levels at isocapnia typically caused an increase in apneustic depth and, concomitantly, significant decreases in TI, TE and TTOT.5. Pharmacological stimulation of the carotid chemoreceptors by intracarotid administration of 1*0-20,sg NaCN produced a premature onset of phrenic nerve activity if delivered during the expiratory period. Such NaCN administrations, delivered during the inspiratory phase, resulted in an augmentation of the integrated phrenic discharge and a premature termination of phrenic activity. Carotid sinus nerve section eliminated the response to NaCN administration.6. In experimental animals having bilateral carotid sinus nerve section, normoxic hypercapnia caused similar changes in the apneustic breathing pattern to those recorded in cats having intact carotid chemoreceptors. However, isocapnic hypoxia induced time-dependent changes in the pattern of phrenic discharge including diminutions in depth, an onset of gasping-type activity, or expiratory apnea.7. In a few animals, bilateral n.p.b.m. lesions and bilateral vagotomy resulted in expiratory apnea which was continuous as long as ventilation with air was maintained. This expiratory apnea was replaced by an apneustic breathing pattern

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The importance of timing on the respiratory effects of intermittent carotid body chemoreceptor stimulation

Cited by 104 publications

References 11 publications

Role of carbon dioxide oscillation in the control of respiration in the anesthetized dog.

Role of carbon dioxide oscillation in the control of respiration in the anesthetized dog.

Baroreceptor and chemoreceptor influences on heart rate during the respiratory cycle in the dog.

Differential alteration by hypercapnia and hypoxia of the apneustic respiratory pattern in decerebrate cats

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