Ventilatory response to CO2 Inhalation and intravenous infusion of hypercapnic blood

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

doi:10.1016/0034-5687(76)90008-6

Cited by 31 publications

(13 citation statements)

References 18 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: 99%

“…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: 99%

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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“…The second hypothesis maintains that the hyperpnea of exercise is completely attributable to the increased delivery of CO2 to the lungs (16); but because arterial hypercapnia is absent, the precise C02-related stimulus linking ventilation and pulmonary CO2 excretion, and its site of detection have not been specified. Support for this hypothesis has been derived from a number of studies in which CO2 was infused into the venous blood of experimental animals (venous CO2 loading), resulting in an increase in ventilation, but no measurable increase in Paco2 (i.e., isocapnic hyperpnea) (17)(18)(19)(20). The demonstration of isocapnic hyperpnea in response to venous CO2 loading has been extrapolated to imply that the isocapnic hyperpnea of exercise may also be attributable solely to the associated increase in Vco2.…”

Section: Introductionmentioning

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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“…Experiments designed to change the amplitude have produced conflicting results (Lamb, 1966;Sylvester, Whipp & Wasserman, 1973;Lewis, 1975;Linton, Miller & Cameron, 1976;Grant & Semple, 1976;Fordyce, Greco, Gonzalez, Reischl & Grodins, 1977;Ponte & Purves, 1978;Stremel, Huntsman, Casaburi, Whip & Wasserman, 1978).…”

Section: Introductionmentioning

confidence: 99%

Dependence of phrenic motoneurone output on the oscillatory component of arterial blood gas composition.

Cross¹,

Grant²,

Guz³

et al. 1979

The Journal of Physiology

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SUMMARY1. The hypothesis that respiratory oscillations of arterial blood gas composition influence ventilation has been examined.2. Phrenic motoneurone output recorded in the C5 root of the left phrenic nerve and the respiratory oscillations of arterial pH in the right common carotid artery were measured in vagotomized anaesthetized dogs which had been paralysed and artificially ventilated.3. The effect of a change in tidal volume for one or two breaths on phrenic motoneurone output was measured with the inspiratory pump set at a constant frequency similar to, and in phase with, the animal's own respiratory frequency. A reduction of tidal volume to zero or an increase by 30 % led to a corresponding change of mean carotid artery pH level. The changes of carotid artery pH resulted in a change of phrenic motoneurone output, predominantly of expiratory time (Te) but to a lesser extent of inspiratory time (TI) and also peak amplitude of 'integrated' phrenic motoneurone output (Phr). Denervation of the carotid bifurcation blocked this response.4. The onset of movement of the inspiratory pump was triggered by the onset of phrenic motoneurone output. When a time delay was interposed between them, the phase relationship between respiratory oscillations of arterial pH and phrenic motoneurone output altered. The dominant effect was to alter Te; smaller and less consistent changes of Phr and Ti were observed.5. When the inspiratory pump was maintained at a constant frequency but independent of and slightly different from the animal's own respiratory frequency (as judged by phrenic motoneurone output), the phase relationship between phrenic motoneurone output and the respiratory oscillations of pH changed breath by breath over a sequence of 100-200 breaths, without change of the mean level of arterial blood gas composition. Te varied by up to 30 % about its mean value depending on the phase relationship. Ti and Phr were also dependent on the phase relationship but varied to a lesser extent. The changes were comparable to the results obtained in paragraph 4.6. It was concluded that phrenic motoneurone output is dependent in part on its relationship to the respiratory oscillations of arterial blood gas composition.

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Ventilatory response to CO2 Inhalation and intravenous infusion of hypercapnic blood

Cited by 31 publications

References 18 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.

Dependence of phrenic motoneurone output on the oscillatory component of arterial blood gas composition.

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