Respiratory responses to intravenous and intrapulmonary CO2 in awake dogs

Greco, E. C.; Fordyce, Wayne E.; González, Francisco Martel; Reischl, Peter; Grodins, Fred S.

doi:10.1152/jappl.1978.45.1.109

Cited by 34 publications

(14 citation statements)

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“…In several studies on anesthetized animals, it was claimed thatV E changed in proportion to the change in CO 2 delivery to maintain homeostasis of PaCO 2 (206,214,274,314,338). In contrast, in an equal number of studies, there was a change in PaCO 2 sufficient to account for the hyperpnea or hypopnea during CO 2 loading and unloading (39,118,138,171,209,277,284,300). Similar studies on awake sheep found that venous CO 2 loading that increased pulmonary CO 2 excretion up to 350% also increasedV E to the same extent as exercise induced increases in CO 2 excretion (275).…”

Section: Venous Co 2 Content As a Signal For The Exercise Hyperpneamentioning

confidence: 99%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.

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Section: Venous Co 2 Content As a Signal For The Exercise Hyperpneamentioning

confidence: 99%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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“…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. However, an equally large number of other studies have been unable to demonstrate isocapnic hyperpnea in response to venous CO2 loading; and have therefore concluded that an increase in Vco2 alone cannot account for the isocapnic hyperpnea of exercise (21)(22)(23)(24)(25)(26).…”

Section: Introductionmentioning

confidence: 98%

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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“…Experimental studies in animals have shown that changes in the venous blood 1 This work was supported by a grant from CNPq, Brazil. composition through C 0 2 remotion or infusion cause alterations in the pulmonary ventilation with no variation in the composition of the arterial blood [15][16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Central Venous Blood Composition and the Pulmonary Ventilation during Hemodialysis

Faro¹,

C²,

Santos³

et al. 1985

Nephron

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The elimination of CO₂ across the dialyzer has been reported as the cause of the pulmonary hypoventilation during hemodialysis. There are some evidences that the venous line blood composition could influence the central venous blood and this one the pulmonary ventilation. Our purpose was to analyze (1) the influence of the changes in composition of the venous line blood on the central venous blood and (2) the possible role of the central venous blood composition on the pulmonary ventilation of 10 chronic renal failure patients during hemodialysis performed twice in the same patients in two different conditions: acetate dialysate without (condition I) and with (condition II) constant addition of 100% CO₂ bubbling into the dialysis bath. During condition I the venous line blood pH was kept in a normal range, and the PCO₂ was low, whereas during condition II the pH was very low and the PCO₂ extremely high. The patients during condition I decreased their pulmonary ventilation and lost CO₂ across the dialyzer as the central venous blood pH and HCO^-₃ increased, and PCO₂ did not change. The same patients during condition II increased their pulmonary ventilation and absorbed CO₂ across the dialyser as the central venous blood pH decreased and PCO₂ increased. Thus, the venous line blood has influence on the central venous blood composition, and this plays a role on the control of pulmonary ventilation of these patients.

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Respiratory responses to intravenous and intrapulmonary CO2 in awake dogs

Cited by 34 publications

References 0 publications

Control of Breathing During Exercise

Control of Breathing During Exercise

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

Central Venous Blood Composition and the Pulmonary Ventilation during Hemodialysis

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