Relative responses of aortic body and carotid body chemoreceptors to carboxyhemoglobinemia

1981 ◽  
Vol 50 (3) ◽  
pp. 580-586 ◽  
Author(s):  
S. Lahiri ◽  
E. Mulligan ◽  
T. Nishino ◽  
A. Mokashi ◽  
R. O. Davies
Keyword(s):  
Carbon Monoxide ◽  
Carotid Body ◽  
Carotid Chemoreceptors ◽  
State Response ◽  
Discharge Rates ◽  
Carotid Bodies ◽  
Tissue Po2 ◽  
Stimulus Source ◽  
Carotid Body Chemoreceptors ◽  
O2 Delivery

The effects of carbon monoxide inhalation and of consequent carboxyhemoglobinemia (HbCO) on the discharge rates of aortic body and carotid body chemoreceptor afferents were investigated in 18 anesthetized cats. In 10 experiments both aortic and carotid chemoreceptor activities were monitored simultaneously. Carbon monoxide inhalation during normoxia always stimulated aortic chemoreceptors before carotid chemoreceptors, and the steady-state response of aortic chemoreceptors to HbCO was greater than that of most carotid chemoreceptors. Only 2 of the 18 carotid chemoreceptor fibers tested showed a distinct increase in activity in response to moderate increases in HbCO%. Thus, oxyhemoglobin contributed substantially to maintain tissue PO2 of all aortic chemoreceptors and of a few carotid chemoreceptors. Hyperoxia diminished the response of both aortic and carotid chemoreceptors to HbCO, indicating a lowered tissue PO2 as the stimulus source. We hypothesize that the aortic bodies have a much lower perfusion relative to their O2 utilization compared to the carotid bodies. As a consequence, the aortic chemoreceptors are able to act as a sensitive monitor of O2 delivery and to generate a circulatory chemoreflex for O2 homeostasis. carotid chemoreceptors monitor O2 tension and initiate strong reflex effects on the level of ventilation.

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.

Chronic CO inhalation and carotid body catecholamines: testing of hypotheses

1989 ◽  
Vol 67 (1) ◽  
pp. 239-242 ◽  
Author(s):  
S. Lahiri ◽  
D. G. Penney ◽  
A. Mokashi ◽  
K. H. Albertine
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Direct Action ◽  
Systemic Effect ◽  
Hypoxic Hypoxia ◽  
Tissue Blood Flow ◽  
Catecholamine Content ◽  
Carotid Bodies ◽  
Significant Stimulation ◽  
Tissue Po2

The purpose of this study was twofold: one concerns carotid blood flow and tissue PO2 and the other the effect of chronic hypoxic hypoxia on enhanced catecholamine content. The rationale was that chronic CO inhalation would not mimic the effect of hypoxia on the carotid body if its tissue blood flow is sufficiently high to counteract the effect of CO on O2 delivery and, hence, on tissue PO2. The differential effects of CO on the carotid body and erythropoietin-producing tissue would also indicate that the effect of hypoxic hypoxia on the carotid body is the result of a direct action of a local low O2 stimulus rather than secondary to a systemic effect initiated by other O2-sensing tissues. To test these alternatives we studied the effects of chronic CO inhalation on carotid body catecholamine content and hematocrit in the rats, which were exposed to an inspired PCO of 0.4–0.5 Torr at an inspired PO2 of approximately 150 Torr for 22 days. The hematocrit of CO-exposed rats was 75 +/- 1.1% compared with 48 +/- 0.7% in controls. Dopamine and norepinephrine content of the carotid bodies (per pair) was 5.88 +/- 0.91 and 3.02 +/- 0.19 ng, respectively, in the CO-exposed rats compared with 6.20 +/- 1.0 and 3.29 +/- 0.6 ng, respectively, in the controls. Protein content of the carotid bodies (per pair) was 18.4 +/- 1.6 and 20.5 +/- 0.9 micrograms, respectively. Thus, despite a vigorous erythropoietic response, the CO-exposed rats failed to show any significant stimulation of carotid body in terms of the content of either catecholamine or protein. The results suggest that carotid body tissue PO2 is not compromised by moderate carboxyhemoglobinemia because of its high tissue blood flow and that the chronic effect of hypoxic hypoxia on carotid body is direct.

Carotid body chemoreceptor reflexes and their interactions in the seal

1977 ◽  
Vol 232 (5) ◽  
pp. H517-H525 ◽  
Author(s):  
R. Elsner ◽  
J. E. Angell-James ◽  
M. de Burgh Daly
Keyword(s):  
Carotid Body ◽  
Superior Laryngeal Nerve ◽  
Harbor Seal ◽  
Minute Volume ◽  
Respiratory Response ◽  
Carotid Bodies ◽  
The Central Nervous System ◽  
Carotid Body Chemoreceptors ◽  
Spontaneously Breathing ◽  
Stimulation Of

In the anesthetized spontaneously breathing harbor seal Phoca vitulina stimulation of the carotid body chemoreceptors by intracarotid injections of sodium cyanide or by hypoxic hypercapnic blood causes an increase in tidal volume, respiratory frequency, and respiratory minute volume. The heart rate invariably decreased. Experimental dives caused apnea and bradycardia. When the carotid bodies are stimulated within 10 s of the commencement of a dive, the chemoreceptor-respiratory response is abolished, but the chemoreceptor-cardioinhibitory response is considerably enhanced. Electrical stimulation of the central cut end of a superior laryngeal nerve also causes apnea and bradycardia; stimulation of the carotid body now fails to produce a respiratory response but the cardioinhibitory effect is enhanced. These results indicate that the carotid bodies cause reflexly hyperventilation and bradycardia, and that these responses are considerably modified by other inputs to the central nervous system.

Changes in breathing pattern mediated by intrapulmonary CO2 receptors in chickens

1982 ◽  
Vol 52 (1) ◽  
pp. 162-167 ◽  
Author(s):  
R. D. Tallman ◽  
A. L. Kunz
Keyword(s):  
Carotid Body ◽  
Breathing Pattern ◽  
Complete Removal ◽  
Whole Body ◽  
Fixed Duration ◽  
Experimental Protocol ◽  
Phase Switching ◽  
Carotid Chemoreceptors ◽  
Carotid Bodies ◽  
Body Plethysmograph

The ventilation of unanesthetized tracheostomized chickens was measured using a whole-body plethysmograph. The inspired CO2 fraction was quickly manipulated between 0.05 and 0.0 in such a way as to limit the fresh air inspired to a fixed duration pulse preceded and followed by 5% CO2. As was previously shown with this experimental protocol [Tallman et al., Am. J. Physiol. 237 (Regulatory Integrative Comp. Physiol. 6): R260–R265, 1979], the duration of inspiration and expiration (TI and TE, respectively) was dependent on the timing, relative to inspiration, that the pulse of air arrived at the lung. To study the possible involvement of arterial chemoreceptors in this reflex, a method of denervating the carotid chemoreceptors in this reflex, a method of denervating the carotid bodies was developed. After denervation, the hyperpneic response to intravenous NaCN and 2–3 breaths of N2 was eliminated, indicating the complete removal of arterial chemoreflexes. When tested with the same protocol of CO2 inhalation following carotid body denervation, TI and TE were still dependent on the delay of the fresh air pulse. These experiments support the conclusion that intrapulmonary CO2 receptors (IPC) mediate the reflexes studied and provide evidence that IPC affect the phase-switching mechanisms on a breath-to-breath basis.

Chemoreceptor involvement in cortisol responses to hypoxia in ventilated dogs

1982 ◽  
Vol 52 (4) ◽  
pp. 1092-1096 ◽  
Author(s):  
H. Raff ◽  
S. P. Tzankoff ◽  
R. S. Fitzgerald
Keyword(s):  
Carbon Monoxide ◽  
Carotid Body ◽  
Secretion Rate ◽  
Hypoxic Hypoxia ◽  
Cortisol Secretion ◽  
Carotid Bodies ◽  
Cortisol Responses

Changes in cortisol secretion rate (CSR) in response to hypoxic hypoxia (HH) and to carbon monoxide hypoxia (COH) were assessed in mongrel dogs that had intact chemoreceptors (INT); surgically deafferented carotid bodies (CBD) or aortic bodies (ABD); or both carotid and aortic chemoreceptors denervated (SAD). All dogs were anesthetized, paralyzed, ventilated, and maintained normocapnic. In the INT and ABD groups, CSR responded “maximally” to HH, whereas in CBD and SAD animals, the CSR was attenuated but not eliminated. COH, which does not stimulate the carotid body, caused a submaximal increase in CSR regardless of chemoreceptor status. It is concluded that 1) the carotid bodies are the principal chemoreceptor influence on CSR during HH and 2) there is a nonchemoreceptor-mediated increase in CSR during hypoxia.

Relative latency of responses of chemoreceptor afferents from aortic and carotid bodies

1980 ◽  
Vol 48 (2) ◽  
pp. 362-369 ◽  
Author(s):  
S. Lahiri ◽  
T. Nishino ◽  
E. Mulligan ◽  
A. Mokashi
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Carotid Body ◽  
Blood Gases ◽  
Unexpected Result ◽  
Blood Gas ◽  
Arterial Blood Gases ◽  
Carotid Chemoreceptors ◽  
Arterial Blood ◽  
Carotid Bodies

Discharges from aortic and carotid body chemoreceptor afferents were simultaneously recorded in 18 anesthetized cats to test the hypothesis that aortic chemoreceptors, because of their proximity to the heart, respond to changes in arterial blood gases before carotid chemoreceptors. We found that carotid chemoreceptor responses to the onset of hypoxia and hypercapnia, and to the intravenously administered excitatory drugs (cyanide, nicotine, and doxapram), preceded those of aortic chemoreceptors. Postulating that this unexpected result was due to differences in microcirculation and mass transport, we also investigated their relative speed of responses to changes in arterial blood pressure. The aortic chemoreceptors responded to decreases in arterial blood pressure before the carotid chemoreceptors, supporting the idea that the aortic body has microcirculatory impediments not generally present in the carotid body. These findings strengthened the concept that carotid bodies are more suited for monitoring blood gas changes due to respiration, whereas aortic bodies are for monitoring circulation.

Hypoxic arousal in intact and carotid chemodenervated sleeping cats

1981 ◽  
Vol 51 (5) ◽  
pp. 1294-1299 ◽  
Author(s):  
J. A. Neubauer ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Carotid Body ◽  
Rem Sleep ◽  
Severe Hypoxia ◽  
Rapid Eye Movement ◽  
Carotid Chemoreceptors ◽  
Carotid Bodies ◽  
Arterial O2 Saturation ◽  
Carotid Body Denervation

To determine whether the carotid chemoreceptors or hyperpnea are required for arousal from sleep by hypoxia, 14 sleep-deprived cats were studied during slow-wave (SWS) and rapid-eye-movement (REM) sleep. Rapid hypoxia was produced by inhalation of 5% O2 in N2 or 6% CO in 40% O2 by intact cats and 5% O2 in N2 after carotid body denervation. Preliminary studies identified a period of SWS unassociated with spontaneous arousals. In 69 studies during SWS unassociated with spontaneous arousals, arterial O2 saturation (SaO2) values at arousal were: 47.1 +/- 1.5% (mean +/- SE) (5% O2, intact); 48.9 +/- 1.4% (6% CO, intact); and 49.9 +/- 2.0% (5% O2, denervated). During SWS associated with spontaneous arousals, SaO2 values at arousal were 71.6 +/- 1.8% (5% O2, intact). Arousal from REM occurred at significantly lower values: 31.7 +/- 3.9% (6% CO, intact) and 43.5 +/- 2.3% (5% O2, intact). During both SWS and REM, inhalation of 5% O2 by intact animals caused a substantial increase in ventilation while 6% CO did not. We conclude that more severe hypoxia is required for arousal from SWS when studies are done in a period unassociated with spontaneous arousals than from SWS associated with spontaneous arousals. Hypoxic arousal does not appear to require activation of the carotid bodies or hyperpnea.

Cobalt stimulates carotid body chemoreceptors

1990 ◽  
Vol 68 (5) ◽  
pp. 1844-1849 ◽  
Author(s):  
C. Di Giulio ◽  
W. X. Huang ◽  
S. Lahiri ◽  
A. Mokashi ◽  
D. G. Buerk
Keyword(s):  
Direct Effect ◽  
Carotid Body ◽  
Cobalt Chloride ◽  
Blood Gases ◽  
Tissue Po2 ◽  
Before And After ◽  
Carotid Body Chemoreceptors ◽  
Dose Dependent ◽  
Saturation Dose ◽  
O2 Sensing

Because cobalt administration is known to elicit erythropoietin response, it is a reasonable hypothesis that cobalt would also stimulate the O2-sensing process in the peripheral chemoreceptors. We tested this hypothesis by measuring the effects of cobalt chloride on carotid chemosensory fibers in pentobarbital-anesthetized cats that were paralyzed and artificially ventilated. Responses of carotid chemoreceptor afferents to graded doses of cobalt given by intra-arterial injections (0.08-2.10 mumols) were measured at constant blood gases. Responses of the same chemoreceptor afferents to hypoxia, before and after a saturation dose of cobalt, were measured. In two experiments carotid body tissue PO2 was also simultaneously measured. The chemosensory fibers showed prolonged excitation after a brief period of inhibition subsequent to cobalt administration. The stimulatory effect showed a dose-dependent saturation response. Cobalt augmented rather than blocked carotid chemoreceptor response to hypoxia. The effect of cobalt was not mediated by tissue PO2. These results are consistent with the hypothesis that cobalt stimulates the O2-sensing mechanism, although a direct effect of cobalt on the excitability of the chemosensory terminal remains a possibility.

Control of diving responses by carotid bodies and baroreceptors in ducks

1982 ◽  
Vol 242 (1) ◽  
pp. R105-R108 ◽  
Author(s):  
R. S. Lillo ◽  
D. R. Jones
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Carotid Body ◽  
Cardiovascular Responses ◽  
Pekin Ducks ◽  
Cardiac Responses ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
Carotid Body Chemoreceptors

The precise role of carotid body chemoreceptors and systemic baroreceptors in cardiovascular responses during experimental diving in ducks is controversial. The diving responses of chronically baroreceptor-denervated, chemoreceptor-denervated, and combined baroreceptor- and chemoreceptor-denervated White Pekin ducks, Anas platyrhynchos, were compared with those of intact and sham-operated birds. All three types of denervation elevated predive heart rates on average by 100-150 beats/min. During submergence, the cardiac rate of the barodenervates quickly dropped and after 60 s stabilized at levels similar to those of submerged intact ducks for the remainder of a 2-min dive. However, arterial blood pressure declined drastically in the barodenervates. Ducks without functional carotid bodies showed significant bradycardia during submergence, although heart rate only fell to the predive rate of intact animals. Birds with combined baroreceptor and chemoreceptor denervation exhibited the same degree of bradycardia as chemoreceptor denervates, and arterial blood pressure rose spectacularly during a dive. It is concluded that during experimental diving in ducks 1) cardiac responses are not baroreflexive in origin, 2) the major portion of bradycardia is due to stimulation of carotid body chemoreceptors, and 3) intact system baroreceptors appear essential for maintenance of blood pressure.

Control of heart rate by carotid body chemoreceptors during diving in tufted ducks

1982 ◽  
Vol 53 (6) ◽  
pp. 1405-1410 ◽  
Author(s):  
P. J. Butler ◽  
A. J. Woakes
Keyword(s):  
Heart Rate ◽  
Carotid Body ◽  
Dominant Role ◽  
Dive Duration ◽  
Domestic Ducks ◽  
Diving Ducks ◽  
Carotid Bodies ◽  
Radio Transmitters ◽  
Carotid Body Chemoreceptors ◽  
Carotid Body Denervation

Previous work has shown that during forcible submersion of domestic ducks there is a gradual reduction in heart rate to 10–20% of its predive value after 45–60 s. Bilateral denervation of the carotid body chemoreceptors abolishes most of this bradycardia. By use of implanted radio transmitters it has been shown that in free-swimming tufted ducks, Aythya fuligula, there is an immediate reduction in heart rate, on spontaneous diving, from an elevated predive level. It then increases for a few seconds before it stabilizes at a level similar to that recorded when the duck is swimming fairly vigorously. The present study has shown that, following bilateral denervation of the carotid bodies, there is a significant increase in mean dive duration but no effect on the immediate reduction in heart rate on submersion. Heart rate is, however, significantly higher toward the end of spontaneous dives after carotid body denervation. Unlike the situation in mallards and their domesticated varieties, carotid body denervation has no effect on heart rate in tufted ducks during the first 40 s of forced dives. The carotid bodies therefore do not play the dominant role in cardiac control during submersion of diving ducks that has been suggested by work involving the forcible submersion of the mallard duck and its domesticated varieties.

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