Carotid body denervation alters ventilatory responses to ibotenic acid injections or focal acidosis in the medullary raphe

2005 ◽  
Vol 98 (4) ◽  
pp. 1234-1242 ◽  
Author(s):  
M. R. Hodges ◽  
C. Opansky ◽  
B. Qian ◽  
S. Davis ◽  
J. M. Bonis ◽  
...  
Keyword(s):  
Heart Rate ◽  
Carotid Body ◽  
Respiratory Control ◽  
Ibotenic Acid ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Medullary Raphe ◽  
Strong Stimulation ◽  
Stimulation Of ◽  
Carotid Body Denervation

Our aim was to determine the effects of carotid body denervation (CBD) on the ventilatory responses to focal acidosis and ibotenic acid (IA) injections into the medullary raphe area of awake, adult goats. Multiple microtubules were chronically implanted into the midline raphe area nuclei either before or after CBD. For up to 15 days after bilateral CBD, arterial Pco2 (PaCO2) (13.3 ± 1.9 Torr) was increased ( P < 0.001), and CO2 sensitivity (−53.0 ± 6.4%) was decreased ( P < 0.001). Thereafter, resting PaCO2 and CO2 sensitivity returned ( P < 0.01) toward control, but PaCO2 remained elevated (4.8 ± 1.9 Torr) and CO2 sensitivity reduced (−24.7 ± 6.0%) ≥40 days after CBD. Focal acidosis (FA) at multiple medullary raphe area sites 23–44 days post-CBD with 50 or 80% CO2 increased inspiratory flow (V̇i), tidal volume (Vt), metabolic rate (V̇o2), and heart rate (HR) ( P < 0.05). The effects of FA with 50% CO2 after CBD did not differ from intact goats. However, CBD attenuated ( P < 0.05) the increase in V̇i, Vt, and HR with 80% CO2, but it had no effect on the increase in V̇o2. Rostral but not caudal raphe area IA injections increased V̇i, BP, and HR ( P < 0.05), and these responses were accentuated ( P < 0.001) after CBD. CO2 sensitivity was attenuated (−20%; P < 0.05) <7 days after IA injection, but thereafter it returned to prelesion values in CBD goats. We conclude the following: 1) the attenuated response to FA after CBD provides further evidence that the carotid bodies provide a tonic facilitory input into respiratory control centers, 2) the plasticity after CBD is not due to increased raphe chemoreceptor sensitivity, and 3) the “error-sensing” function of the carotid body blunts the effect of strong stimulation of the raphe.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

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.

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.

Effect of carotid body denervation on arousal response to hypoxia in sleeping dogs

1981 ◽  
Vol 51 (1) ◽  
pp. 40-45 ◽  
Author(s):  
G. Bowes ◽  
E. R. Townsend ◽  
L. F. Kozar ◽  
S. M. Bromley ◽  
E. A. Phillipson
Keyword(s):  
Carotid Body ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Critical Role ◽  
Ventilatory Responses ◽  
Progressive Hypoxia ◽  
Arousal Response ◽  
Arterial O2 Saturation ◽  
Carotid Body Denervation

We studied the arousal and ventilatory responses to hypoxia during sleep in three trained dogs, before and 1–4 wk after carotid body denervation (CBD). During the studies the dogs breathed through a cuffed endotracheal tube inserted via a chronic tracheostomy. Eucapnic progressive hypoxia was induced by a rebreathing technique, and arterial O2 saturation (Sao2) was measured with an ear oximeter. Sleep stage was determined by electroencephalographic and behavioral criteria. Following CBD, all dogs exhibited hypoventilation under resting conditions; hypoxic ventilatory responses during wakefulness, slow-wave sleep (SWS), and rapid-eye-movement (REM) sleep were less than 10% of control. Prior to CBD, hypoxic arousal occurred at Sao2 of 83.2 +/- 4.6% (mean +/- Se) during SWS and 70.6 +/-2.2% in REM sleep. Following CBD, arousal failed to occur during progressive desaturation to 60% in SWS and 50% in REM sleep, at which levels hypoxia was arbitrarily terminated. In a few studies following CBD where rebreathing was allowed to continue, the dogs occasionally failed to arouse at all and require active resuscitation. The results indicate a critical role for the carotid chemoreceptors in mediating the arousal response to hypoxia.

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.

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.

Cardiorespiratory responses following isoproterenol injection in rabbits

1979 ◽  
Vol 47 (2) ◽  
pp. 352-359 ◽  
Author(s):  
R. Winn ◽  
J. R. Hildebrandt ◽  
J. Hildebrandt
Keyword(s):  
Heart Rate ◽  
Carotid Artery ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Vena Cava ◽  
Direct Stimulation ◽  
Carotid Bodies ◽  
Receptor Sites ◽  
The Common ◽  
Stimulation Of

Receptor sites for the ventilatory response to isoproterenol were investigated in anesthetized rabbits with bolus injections in the common carotid artery (ia) and in the vena cava (iv). The delay from injection to the increase in ventilation (TVE) was significantly shorter following ia (1.5 s) compared to iv injections (about 5 s). The delay to the increase in heart rate (THR) was significantly shorter after iv (about 4.5 s) than after ia injections (12.5 s). When isoproterenol and NaCN injections were compared, there was no difference in TVE. Following carotid body resection, the VE response to isoproterenol was greatly reduced after iv and ia injections; however, THR was unaffected. In intact animals breathing 100% O2 the VE response to isoproterenol was significantly reduced with no change in TVE or in the heart rate response. We conclude that the ventilatory increase following the injection of isoproterenol is due primarily to direct stimulation of the carotid bodies.

Ultrastructural Abnormalities of the Carotid Body in Sudden Infant Death Syndrome

PEDIATRICS ◽  
1979 ◽  
Vol 63 (1) ◽  
pp. 13-17
Author(s):  
Solon Cole ◽  
Leslie B. Lindenberg ◽  
Frank M. Galioto ◽  
Peter E. Howe ◽  
Arthur C. DeGraff ◽  
...  
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Carotid Body ◽  
Infant Death ◽  
Respiratory Control ◽  
Sudden Infant Death ◽  
Cell Number ◽  
Sudden Infant ◽  
Electron Microscopic ◽  
Carotid Bodies ◽  
High Risk Infants

The carotid bodies of four infants who died of sudden infant death syndrome (SIDS) were compared, using electron microscopic techniques, with the carotid bodies of various control subjects. In the SIDS patients, there was a marked reduction or absence of the dense cytoplasmic granules of the carotid chemoreceptor cells, as well as a reduction in cell number and size. These ultrastructural abnormalities may be pathophysiologically related to SIDS. A defect in this respiratory control organ could block normal stimulation of respiration during the periods of hypoxia that occur during episodes of sleep apnea in infancy. Further studies by electron microscopy are required to confirm degranulation of the carotid body as a pathognomonic sign of SIDS. Screening of high-risk infants should be directed at studying the carotid body and its mediated responses to hypoxia.

Effect of carotid body denervation on breathing in neonatal goats

1999 ◽  
Vol 87 (3) ◽  
pp. 1026-1034 ◽  
Author(s):  
T. F. Lowry ◽  
H. V. Forster ◽  
L. G. Pan ◽  
M. A. Korducki ◽  
J. Probst ◽  
...  
Keyword(s):  
Control Animal ◽  
Carotid Body ◽  
Respiratory Control ◽  
Unoperated Control ◽  
Intravenous Injections ◽  
Exercise Hyperpnea ◽  
Irregular Breathing ◽  
Carotid Body Denervation

The objective of the present study was to determine in goats whether carotid body denervation (CBD) at 1–3 days of age causes permanent changes in breathing greater than those that occur after CBD in adult goats. Goats underwent CBD ( n = 6) or sham CBD ( n = 3) surgery at 1–3 days of age. In addition, one unoperated control animal was studied. Bolus intravenous injections of NaCN 2 days postsurgery verified successful CBD surgery. However, at 3, 11, and 18 mo of age, the CBD goats had regained a NaCN response that did not differ ( P > 0.10) from that of intact goats. Intracarotid NaCN injections elicited a hyperpnea in the sham CBD but not the CBD goats. Only one animal exhibited highly irregular breathing [characterized by prolonged (>9-s) apneas] after CBD, and the irregularity disappeared by 3 mo of age. One CBD goat died at 35 days of age, and autopsy revealed that death was associated with pneumonia. After 3 mo of age, there were no statistically significant differences ( P > 0.10) between sham and CBD goats in eupneic breathing, hypoxia and CO2 sensitivity, and the exercise hyperpnea. It is, therefore, concluded that CBD at 1–3 days of age in goats does not appear to affect selected aspects of respiratory control after 3 mo of age, conceivably because of the emergence of other functional chemoreceptors that compensate for the loss of the carotid chemoreceptor.

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