Role of PCO2 oscillations and chemoreceptors in ventilatory response to inhaled and infused CO2

Linton, R. A. F.; Miller, R.; Cameron, I. R.

doi:10.1016/0034-5687(77)90093-7

Cited by 13 publications

(8 citation statements)

References 12 publications

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“…There was no evidence of a fluctuation of arterial pH or of peripheral chemoreceptor discharge with the same period as the lung-to-brain circulation time and any theoretical increase in the amplitude of the chemical signal in arterial blood within each breath was more than offset by the accompanying increase in respiratory frequency. This progressive attenuation of the within-breath fluctuation of the chemical signal is identical to that which occurs when C02 is inhaled (Biscoe & Purves, 1967a, b Linton et al (1976Linton et al ( , 1977 and Grant & Semple (1976): but in addition, these workers used a method involving the infusion of tonometered blood for brief periods and measuring the respiratory response for equally brief periods during the 'on' transient. As is shown in Fig.…”

Section: Discussionmentioning

confidence: 83%

“…First, we have searched for unusual forms of the C02 signal in arterial blood which might provide an additional stimulus to respiration when C02 is perfused such as has been suggested by Yamamoto & Edwards (1960) and by Linton (1976Linton ( , 1977. We have found none.…”

Section: Discussionmentioning

confidence: 97%

“…This allowed isometabolic curves to be plotted at two levels of inspired CO2 PI C02 = 0 and 17 mm Hg. (c) Because it has been suggested that an important stimulus to respiration in arterial blood derives, in addition to the mean level of P EC02 from fluctuations of Pa C2 with a period either similar to the lung-to-brain circulation time (Yamamoto & Edwards, 1961) or of the respiratory cycle (Linton et al 1976(Linton et al , 1977 and which would be detected by peripheral or central chemoreceptors, we measured in a number of experiments in parallel arterial pH using a rapid, continuous, through-flow pH electrode placed in an external carotid artery-to-external jugular venous loop (Cragg, Patterson & Purves, 1977) and the afferent discharge from the carotid body chemoreceptors in single-or few-fibre strands of the sinus nerve. Action potentials were recorded with platinum electrodes in a pool of liquid paraffin at 37 'C, amplified, monitored on an oscilloscope face and stored on magnetic tape in parallel with a record of tracheal air flow.…”

Section: Introductionmentioning

confidence: 99%

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Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

Ponte¹,

Purves²

1978

The Journal of Physiology

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

Ponte¹,

Purves²

1978

The Journal of Physiology

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“…Studies were performed in four adult sheep, weighing [35][36][37][38][39][40] kg, that were selected for study on the basis of being in good health (by veterinarian examination) and of calm temperament, and of a demonstrated ability to run on a treadmill. The sheep were trained to stand quietly in place and to run on the treadmill at speeds of0.7-2.0 mph for 20-30 min at each speed.…”

Section: Methodsmentioning

confidence: 99%

Role of metabolic CO2 production in ventilatory response to steady-state exercise.

Phillipson¹,

Bowes²,

Townsend³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We examined the role of metabolic CO2 production in the hyperpnea of muscular exercise by comparing the response of alveolar ventilation to moderate levels ofexercise with the response to venous infusion of CO2 at rest. Studies were performed in four awake sheep that were trained to run on a treadmill. The sheep had been cannulated for veno-venous extracorporeal perfusion so that CO2 could be infused into the peripheral venous blood through membrane lungs in the perfusion circuit. The sheep breathed room air through an endo-tracheal tube inserted through a tracheostomy, and samples of expired gas were collected for measurement of the rates of CO2 production and 02 consumption. All measurements were made in the steady state. In each of the four sheep, the relationship between alveolar ventilation and the rate of CO2 production could be described by a single linear function (r > 0.99; P < 0.001), regardless of whether CO2 production was increased by exercise, venous CO2 infusion, or combinations of both procedures. This relationship applied for values of CO2 production up to 350% of control. In contrast, no unique relationship was found between the rate of alveolar ventilation and either the rate of 02 consumption, cardiac output, or mixed venous blood gas pressures. The findings indicate that the hyperpnea of mild to moderate steady-state exercise can be attributed to the associated increase in the rate of CO2 production. Therefore, there is no need to invoke obligatory nonmetabolic stimuli to account for the ventilatory response to steady-state exercise.

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“…Also in a steady state, carotid body denervation abolishs the isocapnic response to the venous C02 loading in unanesthetized sheep (PHILLIPs0N et al, 1981a). Moreover, attenuation of Paco2 oscillation with the mixing chamber connected to the carotid artery diminished ventilation in venous C02 loading (LINTON et al, 1977). Hence, the contribution of the Paco2 oscillation to the control of respiration may be superimposed on the usual humoral drive derived from the peripheral and the central receptors.…”

Section: Discussionmentioning

confidence: 99%

Open-loop analysis of Pax(x=CO2) oscillation in the dog.

1984

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Venous C02 loading and/or unloading using an artificial lung was performed on dogs to evaluate whether changes in the rate of carbon dioxide output (V002) can be involved in the control of respiration. As the signal providing J'2 information, small fluctuations in arterial Pco2 (4Paco2) which synchronized with the respiratory cycle were estimated from both the mean Pa002 and the fluctuations in arterial pH (4pH) measured with a catheter tip ISFET (ion sensitive field-effect transistor) pH sensor inserted in the common carotid artery. The open-loop method was used to analyze the effects of various respiratory parameters such as j02, tidal volume, and respiratory frequency on the changes in dpH and 4Paco2. Findings are: (1) 4Paco2 was linearly proportional to VC02 while the correlation between 4pH and VC02 was less linear, (2) magnitude of 4pH was dependent on the changes in tidal volume while 4Pa0O2 was not, (3) both the amplitude and the positive slope of Pa002 oscillation were functions of respiratory frequency. These results suggest the possibility that if Vco2 itself takes part in the control of ventilation, it will be C02 oscillation which links ventilation with Vco2.

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Role of PCO2 oscillations and chemoreceptors in ventilatory response to inhaled and infused CO2

Cited by 13 publications

References 12 publications

Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

Carbon dioxide and venous return and their interaction as stimuli to ventilation in the cat

Role of metabolic CO2 production in ventilatory response to steady-state exercise.

Open-loop analysis of Pax(x=CO2) oscillation in the dog.

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