Central vs. peripheral chemoreceptors in ventilatory stimulation by Hacetate

1987 ◽  
Vol 62 (6) ◽  
pp. 2154-2159 ◽  
Author(s):  
E. E. Nattie
Keyword(s):  
Cerebrospinal Fluid ◽  
Partial Pressure ◽  
Carotid Body ◽  
Intravenous Infusion ◽  
Co2 Partial Pressure ◽  
Central Chemoreceptors ◽  
Per Se ◽  
Conscious Rabbits ◽  
Csf Production

Intravenous infusion of Hacetate in conscious rabbits induces a greater decrease in cerebrospinal fluid (CSF) [HCO3-] and arterial CO2 partial pressure (PaCO2) than does HCl, HNO3, or Hacetate. To test whether acetate per se can stimulate central chemoreceptors, HCl- or Hacetate-acidified mock CSF was infused via the cisterna magna in conscious rabbits with catheters preimplanted under anesthesia. HCl infusion induced a greater decrease in PaCO2 refuting this hypothesis. To evaluate the role of the carotid body HCl and Hacetate were infused intravenously in an intact (CB+) and a chemodenervated group (CB-). In CB+ rabbits Hacetate infusion produced a greater decrease in PaCO2. In CB- rabbits, the fractional decrease in arterial PaCO2 was less for both acids compared with that of the CB+ rabbits, but it was significantly greater for Hacetate infusion (21.2 +/- 2.5%, mean +/- SE) than for HCl infusion (14.5 +/- 1.8%). Thus the carotid body is not necessary for the greater Hacetate ventilatory stimulation. The working hypothesis is that nonionic diffusion of Hacetate into brain or acetate replacement of HCO3- in CSF production lowers [HCO3-] near central chemoreceptors.

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.

Role of central and peripheral chemoreceptors in diving responses of ducks

1982 ◽  
Vol 243 (5) ◽  
pp. R537-R545 ◽  
Author(s):  
D. R. Jones ◽  
W. K. Milsom ◽  
G. R. Gabbott
Keyword(s):  
Carotid Body ◽  
Significant Contribution ◽  
Cardiovascular Responses ◽  
Peripheral Circulation ◽  
Blood Gas ◽  
Peripheral Chemoreceptors ◽  
Central Chemoreceptors ◽  
The Right ◽  
Stimulation Of

Using techniques of vascular isolation and subsequent perfusion we have investigated the effects of altering blood gas tensions, in the cerebral and carotid body circulations, on some cardiovascular responses to diving in unanesthetized ducks. After denervating the right carotid body, perfusion of the innervated left carotid body with hyperoxic blood significantly reduced diving bradycardia and reduced the increase in hindlimb vascular resistance (HLVR) in 1-min dives compared with dives in which the innervated carotid body was autoperfused. Denervation of systemic arterial baroreceptors reduced the fall in heart rate (HR) and increased the rise in HLVR in all dives. Cross-perfusion of the head, from a donor with blood of normal blood gas tensions, did not significantly affect HR or HLVR in 2-min dives compared with dives in which the head was autoperfused. however, cross-perfusing the cerebral circulation with blood of elevated PaCO2 caused significantly greater increases in HLVR than when high PaCO2 only affected the peripheral circulation. We conclude that peripheral chemoreceptors cause virtually all the bradycardia in the later stages of a dive but only about one-half the increase in HLVR, a significant contribution comes from the stimulation of central chemoreceptors with blood of high PaCO2.

Effect of hypoxia and hypercapnia on catecholamine content in cat carotid body

1983 ◽  
Vol 54 (5) ◽  
pp. 1408-1413 ◽  
Author(s):  
R. S. Fitzgerald ◽  
P. Garger ◽  
M. C. Hauer ◽  
H. Raff ◽  
L. Fechter
Keyword(s):  
Methyl Ester ◽  
Partial Pressure ◽  
Analysis Of Variance ◽  
Carotid Body ◽  
Co2 Partial Pressure ◽  
Catecholamine Content ◽  
O2 Partial Pressure ◽  
Before And After

The purpose of this study was to determine the content of catecholamines (CA) in the cat carotid body before and after 0.5 h exposures to normoxic normocapnia [arterial O2 partial pressure (Pao2) 126 +/- 28 Torr, arterial CO2 partial pressure (Paco2) 36.4 +/- 1.5 Torr], hypoxic normocapnia (Pao2 25 +/- 3 Torr, Paco2 36.7 +/- 3.3 Torr), and normoxic hypercapnia (Pao2 132 +/- 13 Torr, Paco2 = 98.2 +/- 7.6 Torr). CA synthesis was blocked using alpha-methylparatyrosine methyl ester (AMPT) prior to alterations in the inspired air. There was a significant decrease in carotid body content of dopamine (DA), norepinephrine (NE), and epinephrine (E) 1 h after AMPT administration. Analysis of variance and Duncan new multiple range procedures revealed that during the subsequent 0.5-h exposures to normoxia, hypoxia, or hypercapnia, only the decrease in DA during hypoxia was significantly greater than that during normoxia; the loss during hypercapnia was not. The decreases in NE during the three exposures were indistinguishable among themselves as were the decreases in E. The decrease in CA content is probably attributable to increased release. The data reveal that the release of CAs during the chemoreception of hypoxia is different from that during the chemoreception of hypercapnia and support the concept of different mechanisms for the chemoreception of hypoxia and hypercapnia.

CSF acid-base regulation and ventilation in iso- and hypocapnic Hacetate acidosis

1986 ◽  
Vol 61 (3) ◽  
pp. 851-858 ◽  
Author(s):  
E. E. Nattie ◽  
P. Moore
Keyword(s):  
Ventilatory Response ◽  
Specific Effect ◽  
Conscious State ◽  
Production Mechanism ◽  
Central Venous ◽  
Acid Base ◽  
Co2 Partial Pressure ◽  
Per Se ◽  
Csf Production ◽  
Do So

Intravenous infusion in conscious rabbits of Hacetate decreases both arterial CO2 partial pressure PaCO2 and cerebrospinal fluid (CSF) HCO3- more than observed with HCl or HNO3 infusion. These acids did not affect CSF HCO3- in isocapnic conditions, and this study asks whether Hacetate infusion will do so. Arterial, central venous, and cisterna magna catheters were implanted in pentobarbital-anesthetized rabbits and all subsequent measurements were performed in the conscious state. Hacetate was infused intravenously over 6 h to decrease plasma HCO3- the same amount in a group allowed to decrease its PaCO2 in response to the acid (hypocapnic) and one in which PaCO2 was maintained at control levels (isocapnic). CSF HCO3- decreased significantly in isocapnia, although the change was less than in hypocapnia. Stoichiometrically by 6 h the measured CSF HCO3- change was balanced by an increase in acetate in hypocapnia and the sum of an increase in acetate and a decrease in chloride in isocapnia. Mechanistically, net acetate entry into CSF appears to involve an exchange for chloride as proposed for NO3-/Cl- and a process that lowers CSF HCO3-. This process could be competitive replacement of HCO3- by acetate in the CSF production mechanism or nonionic diffusive entry of Hacetate into CSF with subsequent titration of HCO3-. The decreases in CSF HCO3- result from the acetate mechanism and the hypocapnic effect on Cl- and HCO3-. The greater ventilatory response results from the greater CSF acidification or a specific effect of acetate per se.

scholarly journals Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO2: role of carotid body CO2

2015 ◽  
Vol 593 (18) ◽  
pp. 4225-4243 ◽  
Author(s):  
Curtis. A. Smith ◽  
Grégory M. Blain ◽  
Kathleen S. Henderson ◽  
Jerome A. Dempsey
Keyword(s):  
Carotid Body ◽  
Peripheral Chemoreceptors ◽  
Central Chemoreceptors ◽  
Respiratory Sensitivity

Role of NaCl cotransport in cerebrospinal fluid production: effects of loop diuretics

1991 ◽  
Vol 71 (3) ◽  
pp. 795-800 ◽  
Author(s):  
S. Javaheri
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Ionic Composition ◽  
Reasonable Assumption ◽  
Cerebral Ventricles ◽  
Fluid Production ◽  
Production Effects ◽  
Nacl Cotransport ◽  
Csf Production

Cerebrospinal fluid (CSF) is secreted primarily by the choroid plexus (CP) located in the cerebral ventricles. Although much is known about ionic composition of cisternal CSF, the mechanisms involved in secretion of CSF in mammals are still not understood. The main aim of this report is to critically review the role of NaCl cotransport carrier in CSF production. On the basis of the studies in the literature, a model for CSF production by the CP is proposed. In this model, CP cells are assumed to be equipped with an NaCl cotransport carrier located on the basolateral (blood-facing) membrane. Because Na+ and Cl- are the two principal ions in CSF, their continued secretions into cerebral ventricles by CP cells require an adequate intracellular supply, which may be guaranteed by the NaCl cotransport carrier. Although this appears to be a reasonable assumption, making the processes involved in CSF production similar to those of other secretory epithelial cells, the presence of such a carrier in mammalian CP remains controversial. The reasons for this controversy are critically reviewed, and some suggestions for further studies are made.

Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation

1984 ◽  
Vol 247 (3) ◽  
pp. R412-R417 ◽  
Author(s):  
H. Raff ◽  
J. Shinsako ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Partial Pressure ◽  
Carotid Body ◽  
Plasma Renin ◽  
Angiotensin I ◽  
Co2 Partial Pressure ◽  
O2 Partial Pressure ◽  
Bilateral Carotid ◽  
Hypercapnic Hypoxia ◽  
Carotid Body Denervation

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.

Ventilatory response to inspired CO2 in normal and carotid body-denervated ponies

1982 ◽  
Vol 52 (6) ◽  
pp. 1614-1622 ◽  
Author(s):  
J. P. Klein ◽  
H. V. Forster ◽  
G. E. Bisgard ◽  
R. P. Kaminski ◽  
L. G. Pan ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Control Period ◽  
Experimental Period ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Insight Into

The purpose of these studies was to gain insight into mechanisms regulating pulmonary ventilation (VE), arterial CO2 partial pressure (PaCO2), and arterial pH (pHa) in ponies when inspired CO2 partial pressure (PICO2) is above normal. Ponies were studied four times daily each weekday for 2 wk in an environmental chamber. Each study consisted of a 15-min control period (PICO2 = 0.7 Torr) followed by a 15- to 30-min experimental period during which PICO2 in the chamber was 0.7, 7, 14, 21, 28, or 42 Torr (PIO2 = 147 Torr throughout). Between 11 and 15 min of each period, four 3-ml samples of arterial blood were drawn, each over 45 s. In 12 normal ponies, elevation of PICO2 to 7 Torr caused PaCO2 to increase approximately 0.4 Torr (P less than 0.01) and pHa to decrease approximately 0.003 (P less than 0.02) relative to control. The hypercapnia and acidosis increased progressively as PICO2 was increased in 7- to 14-Torr increments to 42 Torr (P less than 0.02). Accordingly, the hyperpnea in these ponies during CO2 inhalation could have been mediated by carotid and intracranial chemoreceptors. One month after carotid body denervation (CBD) in nine ponies, PaCO2 during control conditions was 6 Torr above normal, but during CO2 inhalation, PaCO2 changed less from control than during CO2 inhalation before CBD (P less than 0.01). The delta VE/ delta PaCO2 near eupneic PaCO2 appeared to be above normal 1 mo after CBD (P less than 0.01). The mechanism of this increase was not discernible from our data. Finally, our data indicated that the magnitude of the hypercapnia and acidosis during CO2 inhalation was inversely related to PaCO2 and breathing frequency during control conditions.

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