Regulation of arterial PCO2 during intravenous CO2 loading

Wasserman, Karlman; Whipp, Brian J.; Casaburi, Richard; Huntsman, D. J.; Castagna, John; Lugliani, Robert

doi:10.1152/jappl.1975.38.4.651

Cited by 58 publications

(22 citation statements)

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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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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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“…The suggestion that in man sensitivity to alternate breaths of high and low C02 mixtures depends on the background tension (Marsh et al 1973) is not borne out in the work reported here. Yamamoto (1960) suggested that oscillations in PaI,02 could give rise to an effect on ventilation different from that expected from the mean value of the Pa co, Cunningham, Elliott, Lloyd, Miller & Young (1965) (1974,1976) and Wasserman, Whipp, Casaburi, Huntsman, Castagna & Lugliani. (1975) have suggested that larger oscillations in Pa co than occur at rest may be responsible for increased ventilation during intravenous infusion of C02 enriched blood.…”

Section: Discussionmentioning

confidence: 97%

The effects of breathing of alternate breaths of air and a carbon dioxide rich gas mixture in anaesthetized cats

Wolff

1977

The Journal of Physiology

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SUMMARY1. An in vivo pH electrode was used to assess the effect in anaesthetized cats of the administration of 5 % CO2 (21 % 02, balance N2) and air as alternate inspirates upon the time course of the carotid arterial pH, and by inference, the Pco2.2. This method of administration of CO2 and air resulted in a lowering of the recorded pH with the production of oscillations of twice the duration seen on air alone. These larger oscillations had a period of two respiratory cycles and their amplitude was approximately twice that of normal oscillations.3. The respiratory response consisted in all cases of an increase in mean tidal volume and ventilation, and in 50-60 % of recorded runs, of a highly specific sequence of tidal volume changes. The specific sequence was composed of alternately larger and smaller breaths which persisted while the larger oscillations continued.4. The use of the in vivo pH electrode made it possible to determine whether or not the tidal volume alternation was a result of sensitivity to carotid arterial Pco, oscillations. By diverting the carotid arterial blood through a mixing chamber the amplitude of the double (respiratory) period oscillations was, in some cases, reduced but not eliminated. In these cases the specific pattern of tidal volume changes was still present in 60 % of trials. In the cases where the pH fluctuations were completely eliminated the specific respiratory pattern was never present.5. Average breath to breath differences in tidal volume seen during control runs with large oscillations present ranged in size from 3X6 to 8-6 % of the mean tidal volume. When the oscillations were completely eliminated by means of the mixing chamber the breath by breath differences * Present address: Physiology Department, Guy's Hospital Medical School, London, S.E.1. only ranged from 0.2 to 2*7 % of mean tidal volume. The change was highly significant.

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“…In mild to mod erate exercise, such as done in our study, ventilation is closely associated with VCO2. In fact, CO2 flow in the central circulation (via postpulmonary capillary chemoreceptors) may be a controlling stimulus for ventilation under these conditions [17][18][19], 1Vasserman et al [18] demonstrated that CO2 addition to the blood via a mem brane gas exchanger in dogs resulted in a proportional increase in Va and VCO2 with PaCC>2 remaining un changed. When similar studies were done in sheep with CO2 removed, there was a proportional decrease in VA and VCO2.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Hemodialysis-Induced Fall in PaO<sub>2</sub> with Exercise

Germain¹,

Burke²,

Braden³

et al. 1985

Am J Nephrol

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The hypoxemia of acetate hemodialysis may result from a decrease in alveolar ventilation (V_A) related to a reduction in pulmonary carbon dioxide excretion (VCO₂). To test this theory, ventilation was increased by exercise during dialysis on 6 patients and the effect on arterial oxygen tension (PaCO₂) measured. With hemodialysis the PaCO₂ fell from 102 to 92 mm Hg and with exercise rose to 102 mm Hg. These changes in PaO2 paralleled changes in Va and VCO₂ induced by acetate dialysis and then exercise. The correlation coefficient between V_A and VCO₂ was 0.997. This close correlation suggests that CO₂ load may be the main controlling factor for ventilation under these conditions. We conclude that the fall in PaCO₂ that occurs with acetate hemodialysis is due to decreased ventilation secondary to decreased VCO₂ and that exercise can ameliorate the fall in PaO₂ by increasing ventilation.

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Regulation of arterial PCO2 during intravenous CO2 loading

Cited by 58 publications

References 0 publications

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

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

The effects of breathing of alternate breaths of air and a carbon dioxide rich gas mixture in anaesthetized cats

Amelioration of Hemodialysis-Induced Fall in PaO<sub>2</sub> with Exercise

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