Carotid chemoreceptors in ventilatory responses to changes in venous CO2 load

1981 ◽  
Vol 51 (6) ◽  
pp. 1398-1403 ◽  
Author(s):  
E. A. Phillipson ◽  
G. Bowes ◽  
E. R. Townsend ◽  
J. Duffin ◽  
J. D. Cooper
Keyword(s):  
Ventilatory Response ◽  
Venous Blood ◽  
Major Influence ◽  
Arterial Pco2 ◽  
Peripheral Venous Blood ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Co2 Excretion

We examined the role of the carotid chemoreceptors in the ventilatory response to changes in venous CO2 load in 12 awake sheep using a venovenous extracorporeal perfusion circuit and two carbon dioxide membrane lungs (CDML). Three of the sheep had undergone surgical denervation of the carotid bodies (CBD). In the nine intact sheep, as CO2 was removed from or added to the peripheral venous blood through the CDML under normoxic conditions, there was a linear relationship between the rate of pulmonary CO2 excretion (VCO2) and the resulting rate of ventilation over a VCO2 range of 0--800% of control, so that arterial PCO2 remained close to isocapnic. In contrast, in the three CBD sheep, the ventilatory response to changes in VCO2 was significantly decreased under normoxic conditions, resulting in marked hypercapnia. The results indicate that the carotid chemoreceptors exert a major influence on the ventilatory response to changes in venous CO2 load.

Awake baboon's ventilatory response to venous and inhaled CO2 loading

1975 ◽  
Vol 39 (3) ◽  
pp. 417-422 ◽  
Author(s):  
S. M. Lewis
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Venous Blood ◽  
Minute Volume ◽  
Arteriovenous Shunt ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Change In Mean

Steady-state ventilatory responses to CO2 in trained awake baboons were studied to determine the response to a venous CO2 load. CO2 was loaded either directly into the venous blood through an arteriovenous shunt or by addition to the inhaled air. The two modes of loading were adjusted to produce the same increase in minute volume. Minute volume, tidal volume respiratory frequency, end-tidal PCO2, PaCO2, and pHa were measured. PaCO2 and PETCO2 increased the same amount during the two modes of CO2 loading; thus, the response to changes in arterial PCO2, deltaVE/deltaPaCO2, was the same. I conclude that the ventilatory response to venous CO2 loading occurs only through the change in mean arterial PCO2 and thus it is unlikely that there are any important venous CO2 receptors.

Ventilatory responses to partial cardiopulmonary bypass at rest and exercise in dogs

1986 ◽  
Vol 61 (2) ◽  
pp. 575-583 ◽  
Author(s):  
A. Huszczuk ◽  
B. J. Whipp ◽  
A. Oren ◽  
E. C. Shors ◽  
M. Pokorski ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Peripheral Vascular ◽  
Descending Aorta ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Co2 Flow ◽  
Induced Changes ◽  
Different Levels ◽  
Rest And Exercise

We determined the role of blood flow-induced changes in CO2 load to the lungs on ventilatory control, at rest and in the steady-state of electrically induced exercise, in the anesthetized dog. A portion of the vena caval blood was diverted to the descending aorta following “arterialization” through an extracorporeal gas exchanger. Ventilation typically decreased, both at rest and during exercise (i.e., at 2 different levels of mixed venous CO2), in proportion to the CO2 loss; arterial PCO2 was consequently regulated. There were concomitant increases of the pulmonary and peripheral vascular resistance. Bilateral cervical vagosympathectomy markedly attenuated the ventilatory response at rest, thus disrupting arterial PCO2 homeostasis, but not so during exercise. The results therefore provide evidence for and support the suggestion of CO2 flow-related hyperpnea both at rest and during muscular exercise.

Role of carotid chemoreceptors and pulmonary vagal afferents during helium-oxygen breathing in ponies

1987 ◽  
Vol 62 (3) ◽  
pp. 1020-1027 ◽  
Author(s):  
L. G. Pan ◽  
H. V. Forster ◽  
G. E. Bisgard ◽  
T. F. Lowry ◽  
C. L. Murphy
Keyword(s):  
Treadmill Exercise ◽  
Work Load ◽  
Vagal Afferents ◽  
Breathing Frequency ◽  
Heavy Exercise ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Oxygen Breathing ◽  
Carotid Bodies

Our purpose was to assess compensatory breathing responses to airway resistance unloading in ponies. We hypothesized that the carotid bodies and hilar nerve afferents, respectively, sense chemical and mechanical changes caused by unloading, hence carotid body-denervated (CBD) and hilar nerve-denervated ponies (HND) might demonstrate greater ventilatory responses when decreasing resistance. At rest and during treadmill exercise, resistance was transiently reduced approximately 40% in five normal, seven CBD, and five HND ponies by breathing gas of 79% He-21% O2 (He-O2). In all groups at rest, He-O2 breathing did not consistently change ventilation (VE), breathing frequency (f), tidal volume (VT), or arterial PCO2 (PaCO2) from room air-breathing levels. During treadmill exercise at 1.8 mph-5% grade in normal and HND ponies, He-O2 breathing did not change PaCO2 but at moderate (6 mph-5% grade), and heavy (8 mph-8% grade) work loads, absolute PaCO2 tended to decrease by 1 min of resistance unloading. delta PaCO2 calculated as room air minus He-O2 breathing levels at 1 min demonstrated significant changes in PaCO2 during exercise resistance unloading (P less than 0.05). No difference between normal and HND ponies was found in exercise delta PaCO2 responses (P greater than 0.10); however, in CBD ponies, the delta PaCO2 during unloading was greater at any given work load (P less than 0.05), suggesting finer regulation of PaCO2 in ponies with intact carotid bodies. During heavy exercise VE and f increased during He-O2 breathing in all three groups of ponies (P less than 0.05), although there were no significant differences between groups (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

The essential role of carotid body chemoreceptors in sleep apnea

2003 ◽  
Vol 81 (8) ◽  
pp. 774-779 ◽  
Author(s):  
Curtis A Smith ◽  
Hideaki Nakayama ◽  
Jerome A Dempsey
Keyword(s):  
Sleep Apnea ◽  
Carotid Body ◽  
Respiratory Acidosis ◽  
Periodic Breathing ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
The Difference ◽  
Carotid Body Chemoreceptors

Sleep apnea is attributable, in part, to an unstable ventilatory control system and specifically to a narrowed "CO2 reserve" (i.e., the difference in PaCO2 between eupnea and the apneic threshold). Findings from sleeping animal preparations with denervated carotid chemoreceptors or vascularly isolated, perfused carotid chemoreceptors demonstrate the critical importance of peripheral chemoreceptors to the ventilatory responses to dynamic changes in PaCO2. Specifically, (i) carotid body denervation prevented the apnea and periodic breathing that normally follow transient ventilatory overshoots; (ii) the CO2 reserve for peripheral chemoreceptors was about one half that for brain chemoreceptors; and (iii) hypocapnia isolated to the carotid chemoreceptors caused hypoventilation that persisted over time despite a concomitant, progressive brain respiratory acidosis. Observations in both humans and animals are cited to demonstrate the marked plasticity of the CO2 reserve and, therefore, the propensity for apneas and periodic breathing, in response to changing background ventilatory stimuli.Key words: sleep apnea, carotid bodies, hypocapnia, apneic threshold, periodic breathing.

Effects of p-chlorophenylalanine on ventilatory control in goats

1983 ◽  
Vol 54 (1) ◽  
pp. 277-283 ◽  
Author(s):  
G. S. Mitchell ◽  
C. A. Smith ◽  
E. H. Vidruk ◽  
L. C. Jameson ◽  
J. A. Dempsey
Keyword(s):  
Tryptophan Hydroxylase ◽  
Ventilatory Response ◽  
Blood Gases ◽  
Co2 Production ◽  
Neural Pathways ◽  
Ventilatory Control ◽  
Arterial Pco2 ◽  
Carotid Bodies ◽  
Bilateral Carotid ◽  
O2 Concentration

The effects of tryptophan hydroxylase inhibition with p-chlorophenylalanine (PCPA; 100 mg/kg iv) on ventilatory control were studied in awake goats. Ventilation, CO2 production, and blood gases were measured 16–24 h after PCPA at rest and during mild exercise in normoxia and at rest in hypoxia and hypercapnia. PCPA increased ventilation 36% at rest, predominantly through an effect on respiratory frequency, and decreased arterial PCO2 (PaCO2) 6.5 Torr. Ventilatory gain in exercise (delta VI/deltaVCO2) was increased 20% by PCPA thereby maintaining PaCO2 at its new resting value. Hypoxia (fractional inspired O2 concentration = 0.12) had little effect on ventilation or PaCO2 at rest, either on control or on PCPA test days. Ventilatory sensitivity to CO2 at rest (delta VI/delta PaCO2) was unaffected by PCPA. Bilateral carotid body denervation (CBX) was performed in the animals, and experiments were repeated 3 mo after the first administration of PCPA. CBX alone decreased ventilation 29% and increased PaCO2 9.4 Torr. Administration of PCPA increased ventilation 35%, decreased PaCO2 by 10.2 Torr at rest, and increased ventilatory gain in exercise 26%. Thus carotid bodies are not necessary for the ventilatory response to PCPA. Furthermore, the primary neural pathways associated with exercise or hypercapnia are not specifically affected by inhibition of serotonin metabolism via PCPA.

Interaction between CO2 production and ventilation in the hypoxic kitten

1993 ◽  
Vol 74 (2) ◽  
pp. 905-910 ◽  
Author(s):  
J. P. Mortola ◽  
T. Matsuoka
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Co2 Production ◽  
Depressant Effect ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Parallel Increase ◽  
Shallow Breathing

We hypothesized that in the hypoxic newborn the drop in metabolic rate, and particularly in CO2 production (VCO2), contributes to the magnitude of the ventilatory response. Experiments were performed on unanesthetized newborn kittens in a warm [28–30 degrees C ambient temperature (Ta)] or cold (20 degrees C) environment. Breathing pattern and gaseous metabolism were measured by the barometric technique and the inflow-outflow O2 and CO2 difference, respectively. At 30 degrees C, hypoxia (10% O2) decreased VCO2 and induced rapid and shallow breathing, with little effect on minute ventilation (VE). Normoxic exposure to 20 degrees C determined a parallel increase in VE and metabolism; at this Ta, hypoxia decreased VCO2 more than at the higher Ta, and the drop in tidal volume (VT) was also proportionally larger; hence, at 20 degrees C, hypoxic VE was markedly below the normoxic values. Despite these changes in breathing pattern, at neither Ta during hypoxia did arterial PCO2 increase above the normoxic value; in fact, arterial PCO2 at 20 degrees C was slightly decreased because of the important drop in VCO2. Exposure to hypoxia with a CO2 load (inspired CO2 = 1, 3, or 5%) did not abolish the hypometabolic response; the hypoxic depressant effect on VT was either unchanged (by 1% CO2), completely offset (by 3% CO2), or reversed (by 5% CO2), with parallel effects on VE. The results are consistent with the hypothesis that in the newborn the level of CO2, by controlling VT, could represent a link between the metabolic and ventilatory responses to acute hypoxia.

Role of VCO2 in control of breathing of awake exercising dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1335-1339 ◽  
Author(s):  
F. M. Bennett ◽  
R. D. Tallman ◽  
F. S. Grodins
Keyword(s):  
Directional Statistics ◽  
Direct Signal ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
Ventilatory Responses ◽  
Co2 Output ◽  
Exercise Hyperpnea ◽  
Co2 Flow ◽  
End Tidal

Steady-state ventilatory responses to CO2 inhalation, intravenous CO2 loading (loading), and intravenous CO2 unloading (unloading) were measured in chronic awake dogs while they exercised on an air-conditioned treadmill at 3 mph and 0% grade. End-tidal PO2 was maintained at control levels by manipulation of inspired gas. Responses obtained in three dogs demonstrated that the response to CO2 loading [average increase in CO2 output (Vco2) of 216 ml/min or 35%] was a hypercapnic hyperpnea in every instance. Also, the response to CO2 unloading [average decrease in Vco2 of 90 ml/min or 15% decrease] was a hypocapnic hypopnea in every case. Also, the analysis of the data by directional statistics indicates that there was no difference in the slopes of the responses (change in expiratory ventilation divided by change in arterial Pco2) for loading, unloading, and inhalation. These results indicate that the increased CO2 flow to the lung that occurs in exercise does not provide a direct signal to the respiratory controller that accounts for the exercise hyperpnea. Therefore, other mechanisms must be important in the regulation of ventilation during exercise.

Ventilatory control during exercise in calves with artificial hearts

1990 ◽  
Vol 68 (6) ◽  
pp. 2604-2611 ◽  
Author(s):  
A. Huszczuk ◽  
B. J. Whipp ◽  
T. D. Adams ◽  
A. G. Fisher ◽  
R. O. Crapo ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Treadmill Exercise ◽  
Ventilatory Control ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Output Increase ◽  
Exercise Hyperpnea ◽  
Artificial Hearts ◽  
Arterial Po2

To determine the role of cardiac reflexes in mediating exercise hyperpnea, we investigated ventilatory responses to treadmill exercise in seven calves with artificial hearts and seven controls. In both groups, the ventilatory responses were adequate for the metabolic demands of the exercise; this resulted in regulation of arterial PCO2 and pH despite the absence of cardiac output increase in the implanted group. In this group, there was a small but significant reduction of arterial PO2 by 4 +/- 3 Torr and a rise of blood lactate by 1.1 +/- 1 mmol/l. When cardiac output was experimentally increased in the implanted calves to a level commensurate with that spontaneously occurring in the control calves, ventilation was not affected. However, experimental reductions of cardiac output led to an immediate augmentation of exercise hyperpnea by 4.56 +/- 4.3 l/min and a further significant lactate increase of 1.2 +/- 1.22 mmol/l that was associated with a significant decrease in the exercise O2 consumption (0.32 +/- 0.13 l/min). These observations indicate that neither cardiac nor hemodynamic effects of increased cardiac output constitute an obligatory cause of exercise hyperpnea in the calf.

Fibrinolysis and Fibrinogen Breakdown Products (Antithrombin VI) in Renal Venous Blood (RVB) in Dog

1964 ◽  
Vol 12 (01) ◽  
pp. 087-104 ◽  
Author(s):  
K Worowski ◽  
S Niewiarowski ◽  
J Prokopowicz
Keyword(s):  
Fibrinolytic Activity ◽  
General Circulation ◽  
Venous Blood ◽  
Kidney Injury ◽  
Mercury Chloride ◽  
Peripheral Venous Blood ◽  
Physiological Conditions ◽  
Natural Inhibitor ◽  
Coagulation And Fibrinolysis

SummaryThe authors investigated fibrinolytic system of renal venous blood (RVB) peripheral venous blood (PVB) in normal dogs and in those with kidney injury produced by mercury chloride. An increase of fibrinolytic activity as well as a decrease of the level of plasminogen and fibrinogen were found in RVB plasma of normal dogs. An inhibition of the fibrinolytic activity was found in intoxicated dogs in both RVB and PVB plasmas, followed by an increase of plasminogen and fibrinogen levels. The occurence of fibrinogen breakdown products, antithrombin VI, was demonstrated in RVB plasma of normal dogs. It does not appear in RVB plasma of intoxicated dogs.On the basis of experimental results an important role of urokinase, secreted by the kidney into the general circulation is suggested as regards the maintenance of the coagulation and fibrinolysis balance in the organism as well as in the fibrinogen and plasminogen catabolism.It has been also concluded that the antithrombin VI, formed in the kidney circulation is a natural inhibitor of blood coagulation appearing in physiological conditions.

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