scholarly journals Effects of potassium, oxygen and carbon dioxide on the steady-state discharge of cat carotid body chemoreceptors.

1988 ◽  
Vol 401 (1) ◽  
pp. 519-531 ◽  
Author(s):  
R E Burger ◽  
J A Estavillo ◽  
P Kumar ◽  
P C Nye ◽  
D J Paterson
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Carotid Body ◽  
Carotid Body Chemoreceptors

Interaction of dopamine and haloperidol with O2 and CO2 chemoreception in carotid body

1980 ◽  
Vol 49 (1) ◽  
pp. 45-51 ◽  
Author(s):  
S. Lahiri ◽  
T. Nishino ◽  
A. Mokashi ◽  
E. Mulligan
Keyword(s):  
Carbon Dioxide ◽  
Carotid Body ◽  
Intravenous Infusion ◽  
Dopamine Release ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Carotid Body Chemoreceptors

Effects of dopamine and of a dopaminergic blocker, haloperidol, on the responses of carotid body chemoreceptors to hypoxia and hypercapnia were investigated in 16 anesthetized cats. Intravenous infusion of dopamine (10-20 micrograms.min-1) decreased carotid body chemoreceptor responses to hypoxia and hypercapnia. The effect was greater at higher levels of arterial oxygen and carbon dioxide tension (PaO2 and PaCO2) stimulus. Thus, the magnitude of the dopamine effect depended on the degree of both PO2- and PCO2-mediated excitation of the receptors. Haloperidol potentiated responses to both hypoxia and hypercapnia but apparently did not stimulate the receptors in the absence of these stimuli. Potentiation by haloperidol and inhibition by dopamine of excitatory effects due to PaO2 decrease and PaCO2 increase are complementary. The data suggest that chemoreception of dopamine, O2, and CO2 converge at some site in the carotid body. Persistence of hypoxic and hypercapnic responses, following dopamine-blocking doses of haloperidol, does not support the theory that regulation of dopamine release is responsible for O2 and CO2 chemoreception in carotid body of the cat.

scholarly journals Contribution of the carotid body chemoreceptors to eupneic ventilation in the intact, unanesthetized dog

2009 ◽  
Vol 106 (5) ◽  
pp. 1564-1573 ◽  
Author(s):  
Grégory M. Blain ◽  
Curtis A. Smith ◽  
Kathleen S. Henderson ◽  
Jerome A. Dempsey
Keyword(s):  
Steady State ◽  
Carotid Body ◽  
Sensory Input ◽  
Carotid Sinus ◽  
Respiratory Acidosis ◽  
Tonic Activity ◽  
Inspiratory Flow Rate ◽  
Compensatory Response ◽  
Per Se ◽  
Carotid Body Chemoreceptors

We used extracorporeal perfusion of the reversibly isolated carotid sinus region to determine the effects of specific carotid body (CB) chemoreceptor inhibition on eupneic ventilation (V̇i) in the resting, awake, intact dog. Four female spayed dogs were studied during wakefulness when CB was perfused with 1) normoxic, normocapnic blood; and 2) hyperoxic (>500 mmHg), hypocapnic (∼20 mmHg) blood to maximally inhibit the CB tonic activity. We found that CB perfusion per se (normoxic-normocapnic) had no effect on V̇i. CB inhibition caused marked reductions in V̇i (−60%, range 49–80%) and inspiratory flow rate (−58%, range 44–87%) 24–41 s following the onset of CB perfusion. Thereafter, a partial compensatory response was observed, and a steady state in V̇i was reached after 50–76 s following the onset of CB perfusion. This steady-state tidal volume-mediated hypoventilation (∼31%) coincided with a significant reduction in mean diaphragm electromyogram (−24%) and increase in mean arterial pressure (+12 mmHg), which persisted for 7–25 min until CB perfusion was stopped, despite a substantial increase in CO2 retention (+9 Torr, arterial Pco2) and systemic respiratory acidosis. We interpret these data to mean that CB chemoreceptors contribute more than one-half to the total eupneic drive to breathe in the normoxic, intact, awake animal. We speculate that this CB contribution consists of both the normal tonic sensory input from the CB chemoreceptors to medullary respiratory controllers, as well as a strong modulatory effect on central chemoreceptor responsiveness to CO2.

Response time and sensitivity of the ventilatory response to CO2 in unanesthetized intact dogs: central vs. peripheral chemoreceptors

2006 ◽  
Vol 100 (1) ◽  
pp. 13-19 ◽  
Author(s):  
C. A. Smith ◽  
J. R. Rodman ◽  
B. J. A. Chenuel ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Steady State ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Periodic Breathing ◽  
Ventilatory Responses ◽  
Central Chemoreceptors ◽  
Carotid Bodies ◽  
Carotid Body Chemoreceptors ◽  
Relative Gains ◽  
Ventilatory Response To Co2

We assessed the speed of the ventilatory response to square-wave changes in alveolar Pco2 and the relative gains of the steady-state ventilatory response to CO2 of the central chemoreceptors vs. the carotid body chemoreceptors in intact, unanesthetized dogs. We used extracorporeal perfusion of the reversibly isolated carotid sinus to maintain normal tonic activity of the carotid body chemoreceptor while preventing it from sensing systemic changes in CO2, thereby allowing us to determine the response of the central chemoreceptors alone. We found the following. 1) The ventilatory response of the central chemoreceptors alone is 11.2 (SD = 3.6) s slower than when carotid bodies are allowed to sense CO2 changes. 2) On average, the central chemoreceptors contribute ∼63% of the gain to steady-state increases in CO2. There was wide dog-to-dog variability in the relative contributions of central vs. carotid body chemoreceptors; the central exceeded the carotid body gain in four of six dogs, but in two dogs carotid body gain exceeded central CO2 gain. If humans respond similarly to dogs, we propose that the slower response of the central chemoreceptors vs. the carotid chemoreceptors prevents the central chemoreceptors from contributing significantly to ventilatory responses to rapid, transient changes in arterial Pco2 such as those after periods of hypoventilation or hyperventilation (“ventilatory undershoots or overshoots”) observed during sleep-disordered breathing. However, the greater average responsiveness of the central chemoreceptors to brain hypercapnia in the steady-state suggests that these receptors may contribute significantly to ventilatory overshoots once unstable/periodic breathing is fully established.

Increased propensity for apnea via dopamine-induced carotid body inhibition in sleeping dogs

2005 ◽  
Vol 98 (5) ◽  
pp. 1732-1739 ◽  
Author(s):  
Bruno J. Chenuel ◽  
Curtis A. Smith ◽  
Kathleen S. Henderson ◽  
Jerome A. Dempsey
Keyword(s):  
Steady State ◽  
Carotid Body ◽  
Pressure Support Ventilation ◽  
Pressure Support ◽  
Ventilatory Response ◽  
Rapid Eye Movement Sleep ◽  
The Difference ◽  
End Tidal ◽  
Carotid Body Chemoreceptors

We determined the effects of specific carotid body chemoreceptor inhibition on the propensity for apnea during sleep. We reduced the responsiveness of the carotid body chemoreceptors using intravenous dopamine infusions during non-rapid eye movement sleep in six dogs. Then we quantified the difference in end-tidal Pco2 (PetCO2) between eupnea and the apneic threshold, the “CO2 reserve,” by gradually reducing PetCO2 transiently with pressure support ventilation at progressively increased tidal volume until apnea occurred. Dopamine infusions decreased steady-state eupneic ventilation by 15 ± 6%, causing a mean CO2 retention of 3.9 ± 1.9 mmHg and a brief period of ventilatory instability. The apneic threshold PetCO2 rose 5.1 ± 1.9 Torr; thus the CO2 reserve was narrowed from −3.9 ± 0.62 Torr in control to −2.7 ± 0.78 Torr with dopamine. This decrease in the CO2 reserve with dopamine resulted solely from the 20.5 ± 11.3% increase in plant gain; the slope of the ventilatory response to CO2 below eupnea was unchanged from normal. We conclude that specific carotid chemoreceptor inhibition with dopamine increases the propensity for apnea during sleep by narrowing the CO2 reserve below eupnea. This narrowing is due solely to an increase in plant gain as the slope of the ventilatory response to CO2 below eupnea was unchanged from normal control. These findings have implications for the role of chemoreceptor inhibition/stimulation in the genesis of apnea and breathing periodicity during sleep.

Effects of Halothane on the Phrenic Nerve Responses to Carbon Dioxide Mediated by Carotid Body Chemoreceptors in Vagotomized Dogs 

1997 ◽  
Vol 87 (6) ◽  
pp. 1440-1449 ◽  
Author(s):  
Eckehard A. E. Stuth ◽  
Zoran Dogas ◽  
Mirko Krolo ◽  
John P. Kampine ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Carotid Body ◽  
Phrenic Nerve ◽  
Halothane Anesthesia ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Background Levels ◽  
Nerve Response ◽  
Carotid Body Chemoreceptors ◽  
Dose Dependent

Background Previous studies in dogs showed that the phrenic nerve response to an acute hypoxic stimulus was dose dependently depressed by 0.5-2.0 minimum alveolar concentration (MAC) of halothane but not abolished. Because a carbon dioxide stimulus is transduced by a different mechanism in the carotid body chemoreceptors (CBCRs) than is a hypoxic stimulus, inhalational anesthetics may preferentially depress one of these transduction processes, the central neuronal processing, or both, of the integrated responses to these two types of inputs. Methods Carotid body chemoreceptor stimulation was produced by short (1-1.5 s), bilateral, 100% carbon dioxide in saline infusions into the carotid arteries during neural inspiration in unpremedicated, halothane-anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. The phrenic neurogram quantified the neural inspiratory response. Four protocols were performed in the study: (1) the dose-dependent effects of halothane anesthesia (0.5-2.0 MAC) during hyperoxic hypercapnia on phrenic nerve activity, (2) the effects of three background levels of the partial pressure of carbon dioxide (PaCO2) on the magnitude of the carbon dioxide infusion responses at 1 MAC halothane, (3) the effects of anesthetic type on the magnitude of the carbon dioxide infusion response, and (4) the effects of CBCR denervation. Results Peak phrenic nerve activity (PPA) increased significantly during the carbon dioxide-stimulated phrenic burst in protocols 1-3; after denervation there was no response (protocol 4). Halothane produced a dose-dependent reduction in the PPA of control and carbon dioxide infusion-stimulated phrenic bursts and in the net carbon dioxide response. The net PPA responses for the different PaCO2 background levels were not different but were somewhat larger for sodium thiopental anesthesia than for 1.0 MAC halothane. Conclusions The phrenic nerve response to an acute, severe carbon dioxide stimulus was dose dependently depressed by surgical doses of halothane. The observed responses to carbon dioxide infusion were mediated by the CBCRs because they were eliminated by CBCR denervation. These results suggest that the CBCR transduction and central transmission of the carbon dioxide signal in terms of inspiratory excitatory drive are not abolished at surgical levels of halothane anesthesia.

Separation of carotid body chemoreceptor responses to O2 and CO2 by oligomycin and by antimycin A

1982 ◽  
Vol 242 (3) ◽  
pp. C200-C206 ◽  
Author(s):  
E. Mulligan ◽  
S. Lahiri
Keyword(s):  
Steady State ◽  
Carbonic Anhydrase ◽  
Partial Pressure ◽  
Carotid Body ◽  
Body Tissue ◽  
Antimycin A ◽  
Tissue Ph ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Metabolic Hypothesis

The cat carotid chemoreceptor O2 and CO2 responses can be separated by oligomycin and by antimycin A. Both of these agents greatly diminish or abolish the chemoreceptor O2 response but not the nicotine or CO2 responses. After either oligomycin or antimycin, the responses to increases and decreases in arterial CO2 partial pressure (PaCO2) consisted of increases and decreases in activity characterized respectively by exaggerated overshoots and undershoots. These were eliminated by the carbonic anhydrase inhibitor, acetazolamide, suggesting that they resulted from changes in carotid body tissue pH. The steady-state PaCO2 response remaining after oligomycin was no longer dependent on arterial O2 partial pressure (PaO2). All effects of antimycin were readily reversible in about 20 min. The separation of the responses to O2 and CO2 indicates that there may be at least partially separate pathways of chemoreception for these two stimuli. The similarity of the oligomycin and antimycin results supports the metabolic hypothesis of chemoreception.

Excitatory amino acid receptors in commissural nucleus of the NTS mediate carotid chemoreceptor responses

1993 ◽  
Vol 264 (1) ◽  
pp. R41-R50 ◽  
Author(s):  
A. Vardhan ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Amino Acid ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Minute Ventilation ◽  
Neuronal Cell ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Neuronal Cell Bodies ◽  
Carotid Body Chemoreceptors ◽  
Stimulation Of

Stimulation of carotid body chemoreceptors by saline saturated with 100% CO2 elicited an increase in mean arterial pressure, respiratory rate, tidal volume, and minute ventilation (VE). Microinjections of L-glutamate into a midline area 0.5-0.75 mm caudal and 0.3-0.5 mm deep with respect to the calamus scriptorius increased VE. Histological examination showed that the site was located in the commissural nucleus of the nucleus tractus solitarii (NTS). The presence of excitatory amino acid receptors [N-methyl-D-aspartic acid (NMDA); kainate, quisqualate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and trans 1-amino-cyclopentane-trans-1,3-dicarboxylic acid (ACPD)] in this area was demonstrated by microinjections of appropriate agonists. Simultaneous blockade of NMDA and non-NMDA receptors by combined injections of DL-2-aminophosphonoheptanoate (AP-7; 1 nmol) and 6,7-dinitro-quinoxaline-2,3-dione (DNQX; 1 nmol) abolished the responses to stimulation of carotid body on either side. Combined injections of AP-7 and DNQX did not produce a nonspecific depression of neurons because the responses to another agonist, carbachol, remained unaltered. Inhibition of the neurons in the aforementioned area with microinjections of muscimol (which hyperpolarizes neuronal cell bodies but not fibers of passage) also abolished the responses to subsequent carotid body stimulation on either side.(ABSTRACT TRUNCATED AT 250 WORDS)

Excitatory amino acid receptors within NTS mediate arterial chemoreceptor reflexes in rats

1993 ◽  
Vol 265 (2) ◽  
pp. H770-H773 ◽  
Author(s):  
W. Zhang ◽  
S. W. Mifflin
Keyword(s):  
Electrical Stimulation ◽  
Amino Acid ◽  
Receptor Antagonist ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Pressor Responses ◽  
Carotid Body Chemoreceptors ◽  
Arterial Chemoreceptor ◽  
Stimulation Of ◽  
Arterial Baroreceptor

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.

Respiration in man during metabolic alkalosis

1962 ◽  
Vol 17 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Daniel J. Stone
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Lung Function ◽  
Gas Exchange ◽  
Metabolic Alkalosis ◽  
Time Lag ◽  
Respiratory Compensation ◽  
Arterial Ph ◽  
Oral Sodium ◽  
Ventilation Response

A steady state metabolic alkalosis was induced in two subjects over a period of several days utilizing oral sodium bicarbonate in dosages of 50 g/day. The purpose of inducing steady state metabolic alkalosis was to study the effects of such a state on the respiratory center responses to inspired gas mixtures, containing carbon dioxide, and to contrast these results with the control studies. The experiment was so designed that the arterial pH in both subjects tended to return toward normal in the presence of significant increases in blood bicarbonate. Repeated study of ventilation responses with room air and 4% and 6% carbon dioxide in inspired air revealed a definite and significant decrease in ventilation response to carbon dioxide during the periods of steady state alkalosis as compared to the control periods. Normal responses returned after some time lag. A consistent rise in paCOCO2 occurred with alkalosis, thus demonstrating respiratory compensation. In neither subject was total lung function or gas exchange affected by the alkalosis. The experiment was confirmed on several occasions with reproducible results. Note: (With the Research Assistance of Mary Di Lieto) Submitted on May 22, 1961

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