Worth the risk? Effects of prolonged hypoxia and hypercapnia on ventilatory responses in patients with bilateral resection of the carotid bodies

2021 ◽  
Author(s):  
Steven Spector ◽  
Ryan Debi
Keyword(s):  
Risk Effects ◽  
Ventilatory Responses ◽  
Carotid Bodies

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.

Ventilatory response to drug-induced hypermetabolism

1975 ◽  
Vol 38 (5) ◽  
pp. 827-833 ◽  
Author(s):  
S. Levine ◽  
W. E. Huckabee
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Minute Ventilation ◽  
The Body ◽  
Low Oxygen ◽  
Drug Induced ◽  
Afferent Pathways ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Carotid Bodies

Previous workers have demonstrated that an increase in minute ventilation accompanies tissue hypermetabolism induced by uncouplers of oxidative phosphorylation. The mechanism of this increase in minute ventilation has not been established. Accordingly, 2.5 mg/kg of 2,4-dinitrophenol (DNP) or 8–15 mg/kg of ethyl methylene blue (EMB) were infused into chloralose-anesthetized mongrel dogs; Vo2 increased 105 plus or minus 3% and VE INCREASED 107 PLUS OR MINUS 14%. Heads of vagotomized dogs were then perfused entirely with normal unchanging blood. Spinal cord remained intact. (The carotid bodies lay within the region of the perfused head.) Ventilatory responses of these head-perfused animals to breathing low oxygen and to breathing high CO2 gas mixtures were greatly attenuated. However, when DNP or EMB was infused into the body, VO2 increased 114 plus or minus 23% and VE increased 123 plus or minus 22%. When similar doses of DNP or emb were selectively administered to the head, increases in VE were limited to 21 plus or minus 6%. It is concluded that a major portion of the stimulus to ventilation, which accompanies infusion of DNP or of EMB, arises in tissues other than arterial chemoreceptors and brain. Presumably, this ventilatory stimulus is transmitted to the respiratory center via afferent pathways of the cervical spinal cord.

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.

Dopamine and ventilatory effects of hypoxia and almitrine in chronically hypoxic rats

1989 ◽  
Vol 67 (1) ◽  
pp. 186-192 ◽  
Author(s):  
R. A. Wach ◽  
D. Bee ◽  
G. R. Barer
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Response Curves ◽  
Enhancing Effect ◽  
Stimulus Response ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Ventilatory Effects ◽  
Ventilatory Response To Hypoxia

We hypothesized that the temporary blunted ventilatory response to hypoxia seen in chronically hypoxic rats could be related to the increased amount of dopamine found in their carotid bodies. Rats, kept 2–3 wk in 10% O2, showed reduced nonisocapnic ventilatory responses to 21–12% inspiratory O2 fraction compared with control rats. Stimulus-response curves to almitrine, which simulates the action of hypoxia on the carotid body, were also depressed in chronically hypoxic rats. Responses to hypoxia and almitrine were significantly correlated in the two groups of rats. Dopamine depressed ventilation during normoxia, hypoxia, and almitrine stimulation in both groups, an action abolished by the dopamine-2 antagonist domperidone. Domperidone slightly increased responses to hypoxia and almitrine in control rats but had a greater enhancing effect in chronically hypoxic rats, such that there was no longer a difference between the responses of the two groups.

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.

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.

Influence of ischemia and hypoxia on breathing in ducks

1983 ◽  
Vol 55 (2) ◽  
pp. 400-408 ◽  
Author(s):  
R. S. Lillo ◽  
D. R. Jones
Keyword(s):  
Carotid Body ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Lower Body ◽  
Ventilatory Responses ◽  
Pekin Ducks ◽  
Carotid Bodies ◽  
Thoracic Spinal ◽  
Spinal Section ◽  
The Brain

We examined the influence of whole and lower body hypoxia and lower body ischemia on breathing in White Pekin ducks, Anas platyrhynchos, excluding pathways involving the carotid bodies. Carotid body denervated birds breathing 10 or 5% O2 developed a tachypnea after a latency of 30-100 s. The tachypnea was more pronounced with the more severe hypoxia, resulting in almost a doubling of minute ventilation (VE). Occlusion of the abdominal aorta in unanesthetized ducks produced immediate development of hypertension. Ventilation was unaffected for the 1st min; a tachypnea then developed rapidly and persisted for the duration of the occlusion resulting in a 25% increase in VE. After thoracic spinal section, all ventilatory responses to occlusion were eliminated. Experimental perfusion of the brain and single intact carotid body in unanesthetized ducks with hyperoxic blood during low O2 breathing (6-9% O2) resulted in tachypnea, also after a considerable latency. These results suggest that severe hypoxia can affect breathing in birds via pathways other than those involving the carotid bodies.

Effect of carotid body resection on ventilatory and acid-base control during exercise

1975 ◽  
Vol 39 (3) ◽  
pp. 354-358 ◽  
Author(s):  
K. Wasserman ◽  
B. J. Whipp ◽  
S. N. Koyal ◽  
M. G. Cleary
Keyword(s):  
Steady State ◽  
Metabolic Acidosis ◽  
Carotid Body ◽  
Constant Load ◽  
Incremental Exercise ◽  
Acid Base ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Significant Difference ◽  
Exercise Hyperpnea

To investigate the role of the carotid bodies in exercise hyperpnea and acid-base control, normal and carotid body-resected subjects (CBR) were studied during constant-load and incremental exercise. There was no significant difference in the first-breath ventilatory responses to exercise between the groups; some subjects in each reproducibly exhibited abrupt responses. The subsequent change in Ve toward steady state was slower in the CBR group. The steady-state ventilatory responses were the same in both groups at work rates below the anaerobic threshold (AT). However, above the AT, the hyperpnea was less marked in the CBR group. Ve and acid-base measurements revealed that the CBR group failed to hyperventilate in response to the metabolic acidosis of either constant-load or incremental exercise. We conclude that the carotid bodies 1) are not responsible for the initial exercise hyperpnea, 2) do affect the time course of Ve to its steady state, and 3) are responsible for the respiratory compensation for the metabolic acidosis of exercise.

Ventilatory responses to lung inflation and arterial CO2 in halothane-anesthetized dogs

1988 ◽  
Vol 64 (4) ◽  
pp. 1433-1438 ◽  
Author(s):  
G. S. Mitchell ◽  
B. D. Selby
Keyword(s):  
Left Lung ◽  
Surgical Removal ◽  
Halothane Anesthesia ◽  
Burst Frequency ◽  
Lung Inflation ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Anesthetized Dogs ◽  
The Right

Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration (TE) in chloralose-urethan-anesthetized dogs. Surgical removal of the carotid bodies abolishes this interaction. Since halothane anesthesia in hyperoxia greatly impairs peripheral chemoreflexes, experiments were conducted to determine whether hypercapnia would attenuate the effects of Paw on f and TE in halothane-anesthetized dogs (approximately 1.5 minimum alveolar concentration). Integrated activity of the phrenic nerve was monitored as a function of Paw (2-12 cmH2O) in a vascularly isolated left lung at varied levels of arterial PCO2 (PaCO2; 38-80 Torr) controlled by inspired gas concentrations ventilating the denervated but perfused right lung. Halothane was administered only to the right lung. The results were as follows: 1) integrated phrenic amplitude increased with PaCO2 but was unaffected by Paw; 2) f decreased as Paw increased but was not affected by PaCO2; 3) the inspiratory duration (TI) increased as PaCO2 increased but was unaffected by Paw; 4) TE increased as Paw increased but was unaffected by PaCO2; and 5) there was no phrenic response to intravenous sodium cyanide (50-100 micrograms/kg). Thus, unlike chloralose-urethan-anesthetized dogs, hypercapnia does not attenuate the effect of lung inflation on f or TE in halothane-anesthetized dogs. Furthermore, hypercapnia increases TI during halothane anesthesia, an effect found after carotid denervation but not found in intact chloralose-urethan-anesthetized dogs. It is suggested that these differences between chloralose-urethan- and halothane-anesthetized dogs may be due to functional carotid chemoreceptor denervation by halothane.

Ventilatory reflexes originated from carotid and extracarotid chemoreceptors in rats

1983 ◽  
Vol 244 (1) ◽  
pp. R119-R125 ◽  
Author(s):  
H. Cardenas ◽  
P. Zapata
Keyword(s):  
Tidal Volume ◽  
Respiratory Frequency ◽  
Intravenous Injections ◽  
Ventilatory Responses ◽  
Laryngeal Nerves ◽  
Carotid Bodies ◽  
Nodose Ganglia ◽  
Bilateral Carotid ◽  
Ventilatory Depression ◽  
Thoracic And Abdominal

Ventilatory responses to transient stimulation and inhibition of arterial chemoreceptors--by hypoxia and hyperoxia, respectively--were studied in 10 pentobarbitone-anesthetized rats. N2 tests and intravenous injections of NaCN provoked transient increases in tidal volume and respiratory frequency, while O2 tests elicited decreases of these parameters. After bilateral carotid neurotomy, ventilatory responses to N2 and NaCN were still present although reduced in all rats, while ventilatory depression in response to O2 tests was observed in 60% of these rats. Further bilateral sectioning of main vagus, aortic, and superior laryngeal nerves immediately below the nodose ganglia abolished the ventilatory responses to NaCN in only one of the five rats subjected to this procedure, the remaining animals showing moderate hyperventilation in response to large doses of this drug. Mild ventilatory depression in response to hyperoxia, indicative of a persistent peripheral chemosensory drive, was still present in two of these rats. It is concluded that, although the carotid bodies constitute the main source of ventilatory chemoreflexes in rats, other vagally and nonvagally innervated chemoreceptors (presumably thoracic and abdominal) may elicit ventilatory reflexes in this species.

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