Central and peripheral chemoreceptor inputs to phrenic and hypoglossal motoneurons

1982 ◽  
Vol 53 (6) ◽  
pp. 1504-1511 ◽  
Author(s):  
E. N. Bruce ◽  
J. Mitra ◽  
N. S. Cherniack
Keyword(s):  
Opposite Effect ◽  
Carotid Sinus ◽  
Ventral Surface ◽  
Carotid Sinus Nerve ◽  
Peripheral Chemoreceptor ◽  
Hypoglossal Motoneurons ◽  
Nerve Response ◽  
Bilateral Carotid ◽  
Hypoglossal Motoneuron ◽  
Before And After

We tested the hypothesis that phrenic and hypoglossal responses to progressive hypercapnia differ qualitatively because the CO2-related drive inputs to their respective motoneuron pools are different. The relative contributions of carotid sinus and central chemoreceptor inputs to hypoglossal and phrenic responses during hyperoxic hypercapnia were determined by comparing the two nerve activities during rebreathing runs done either before and after bilateral carotid sinus nerve (CSN) section, or without and with cooling of the intermediate, I(s), area on the ventral surface of the medulla. The studies were performed on chloralose-anesthetized, vagotomized, paralyzed cats. Cooling of the I(s) area impaired phrenic responsiveness to hypercapnia more than hypoglossal responsiveness, whereas CSN section had the opposite effect. Thus phrenic nerve response was more dependent on central chemoreceptor input than was the hypoglossal response, but hypoglossal response was more dependent on carotid sinus chemoreceptor input. We conclude that the phrenic and hypoglossal motoneuron pools each receive a different functional input from both the medullary and the carotid sinus chemoreceptors.

scholarly journals Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

2010 ◽  
Vol 299 (1) ◽  
pp. R192-R205 ◽  
Author(s):  
Cécile A. Julien ◽  
Lalah Niane ◽  
Richard Kinkead ◽  
Aida Bairam ◽  
Vincent Joseph
Keyword(s):  
Blood Pressure ◽  
Intermittent Hypoxia ◽  
Carotid Sinus ◽  
Splanchnic Nerve ◽  
Carotid Sinus Nerve ◽  
Peripheral Chemoreceptor ◽  
Arterial Blood ◽  
Nerve Response ◽  
Carotid Sinus Nerve Stimulation

We tested the hypothesis that exposure to neonatal intermittent hypoxia (n-IH) in rat pups alters central integrative processes following acute and intermittent peripheral chemoreceptor activation in adults. Newborn male rats were exposed to n-IH or normoxia for 10 consecutive days after birth. We then used both awake and anesthetized 3- to 4-mo-old rats to record ventilation, blood pressure, and phrenic and splanchnic nerve activities to assess responses to peripheral chemoreflex activation (acute hypoxic response) and long-term facilitation (LTF, long-term response after intermittent hypoxia). In anesthetized rats, phrenic and splanchnic nerve activities and hypoxic responses were also recorded with or without intact carotid body afferent signal (bilateral chemodenervation) or in response to electrical stimulations of the carotid sinus nerve. In awake rats, n-IH alters the respiratory pattern (higher frequency and lower tidal volume) and increased arterial blood pressure in normoxia, but the ventilatory response to repeated hypoxic cycles was not altered. In anesthetized rats, phrenic nerve responses to repeated hypoxic cycles or carotid sinus nerve stimulation were not altered by n-IH; however, the splanchnic nerve response was suppressed by n-IH compared with control. In control rats, respiratory LTF was apparent in anesthetized but not in awake animals. In n-IH rats, respiratory LTF was not apparent in awake and anesthetized animals. Following intermittent electrical stimulation, however, phrenic LTF was clearly present in n-IH rats, being similar in magnitude to controls. We conclude that, in adult n-IH rats: 1) arterial blood pressure is elevated, 2) peripheral chemoreceptor responses to hypoxia and its central integration are not altered, but splanchnic nerve response is suppressed, 3) LTF is suppressed, and 4) the mechanisms involved in the generation of LTF are still present but are masked most probably as the result of an augmented inhibitory response to hypoxia in the central nervous system.

Baroreceptor and chemoreceptor contributions to the hypertensive response to bilateral carotid occlusion in conscious mice

2010 ◽  
Vol 299 (6) ◽  
pp. H1990-H1995 ◽  
Author(s):  
R. M. Lataro ◽  
J. A. Castania ◽  
M. W. Chapleau ◽  
H. C. Salgado ◽  
R. Fazan
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Peripheral Chemoreceptor ◽  
Femoral Catheter ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
C57bl Mice ◽  
Common Carotid Arteries ◽  
Sustained Increase

This study aimed to characterize the role played by baroreceptors and chemoreceptors in the hypertensive response to bilateral carotid occlusion (BCO) in conscious C57BL mice. On the day before the experiments the animals were implanted with pneumatic cuffs around their common carotid arteries and a femoral catheter for measurement of arterial pressure. Under the same surgical approach, groups of mice were submitted to aortic or carotid sinus denervation or sham surgery. BCO was performed for 30 or 60 s, promoting prompt and sustained increase in mean arterial pressure and fall in heart rate. Compared with intact mice, the hypertensive response to 30 s of BCO was enhanced in aortic-denervated mice (52 ± 4 vs. 41 ± 4 mmHg; P < 0.05) but attenuated in carotid sinus-denervated mice (15 ± 3 vs. 41 ± 4 mmHg; P < 0.05). Suppression of peripheral chemoreceptor activity by hyperoxia [arterial partial pressure of oxygen (PaO2) > 500 mmHg] attenuated the hypertensive response to BCO in intact mice (30 ± 6 vs. 51 ± 5 mmHg in normoxia; P < 0.05) and abolished the bradycardia. It did not affect the hypertensive response in carotid sinus-denervated mice (20 ± 4 vs. 18 ± 3 mmHg in normoxia; P < 0.05). The attenuation of the hypertensive response to BCO by carotid sinus denervation or hyperoxia indicates that the hypertensive response in conscious mice is mediated by both baro- and chemoreceptors. In addition, aortic denervation potentiates the hypertensive response elicited by BCO in conscious mice.

Carotid sinus nerve is involved in cardiorespiratory responses to intracarotid injection of capsaicin in the rat

2006 ◽  
Vol 100 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Rurong Wang ◽  
Fadi Xu ◽  
Jianguo Zhuang ◽  
Cancan Zhang
Keyword(s):  
Carotid Sinus ◽  
Minute Ventilation ◽  
Right Atrial ◽  
Carotid Sinus Nerve ◽  
Cardiorespiratory Responses ◽  
C Fibers ◽  
Before And After ◽  
High Doses ◽  
The Right ◽  
Spontaneously Breathing

The carotid sinus nerve (CSN), important in cardiorespiratory modulation, mainly contains C fibers (CSCFs). Previous studies have demonstrated that selective stimulation of bronchopulmonary C fibers (PCFs) via right atrial injection of capsaicin (Cap; ∼0.25 μg) results in an apnea (∼3 s) associated with hypotension and bradycardia. The present study was undertaken to determine the effects of activating CSCFs on cardiorespiratory activities. Intracarotid injection of Cap was performed before and after bilateral transection of the CSN in anesthetized and spontaneously breathing rats. Our results showed that 1) low doses of Cap (up to 2 ng) produced an increase in minute ventilation by elevating both tidal volume and respiratory frequency with the threshold dosage at 1.0 ng ( P < 0.05); 2) high doses (4–64 ng) generated an apnea (prolongation of expiratory duration by ∼8-fold) and hypertension ( P < 0.05); 3) bilateral transection of the CSN reduced excitatory and inhibitory respiratory responses by 30 and 81%, respectively, and increased the hypertension by 88% ( P < 0.05); and 4) the same doses of Cap delivered into the right atrium to stimulate PCFs failed to evoke detectable cardiorespiratory responses. Our results suggest that compared with PCFs, CSCFs are more sensitive to Cap stimulation and that activation of these fibers significantly modulates cardiorespiratory activity in anesthetized rats.

Effects of calcium channel blockers on isolated carotid baroreceptors and baroreflex

1983 ◽  
Vol 245 (4) ◽  
pp. H653-H661 ◽  
Author(s):  
C. M. Heesch ◽  
B. M. Miller ◽  
M. D. Thames ◽  
F. M. Abboud
Keyword(s):  
Carotid Sinus ◽  
Physiological Solution ◽  
Physiological Salt Solution ◽  
Channel Blockers ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Carotid Baroreceptors ◽  
Carotid Baroreflex ◽  
Bilateral Carotid

Our study determined the effects of the calcium antagonists, nifedipine and verapamil, on the carotid sinus baroreceptors and baroreflex. The left carotid sinus region in dogs was vascularly isolated and filled with oxygenated physiological salt solution. Steady-state multiunit activity was recorded from the carotid sinus nerve for sinus pressures of 50-200 mmHg after bathing the carotid sinus region in a solution containing no drug, 10 micrograms/ml nifedipine (n = 6), or 5 micrograms/ml verapamil (n = 5). The slopes of the curves relating carotid sinus nerve activity (% of maximum control) to carotid sinus pressure were control, 0.81 +/- 0.06; nifedipine, 1.29 +/- 0.14; and verapamil, 0.48 +/- 0.06%/mmHg, indicating that nifedipine increased and verapamil decreased the sensitivity of the carotid sinus baroreceptors. Additional studies with bilateral carotid sinus isolation (carotid sinus nerves intact) indicated that nifedipine enhanced and verapamil attenuated carotid baroreflex control of renal sympathetic nerve activity. Pressure-volume curves generated in the isolated carotid sinus showed that effects on smooth muscle do not account for the opposing effects of the two Ca2+ antagonists. Omitting Ca2+ from the physiological solution resulted in increased carotid sinus nerve activity, an effect blocked by verapamil but not nifedipine. Verapamil, but not nifedipine, inhibited veratrine-induced (Na+-dependent) excitation of carotid baroreceptors. Thus the excitatory effects of nifedipine on the carotid sinus baroreceptors are dependent on Ca2+ mechanisms, whereas the inhibitory effects of verapamil may be due mainly to interference with the inward Na+ current.

Dose-dependent Effects of Halothane on the Phrenic Nerve Responses to Acute Hypoxia in Vagotomized Dogs 

1997 ◽  
Vol 87 (6) ◽  
pp. 1428-1439 ◽  
Author(s):  
Eckehard A. E. Stuth ◽  
Zoran Dogas ◽  
Mirko Krolo ◽  
John P. Kampine ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Carotid Body ◽  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Hypoxic Response ◽  
Nerve Response ◽  
Bilateral Carotid ◽  
Dose Dependent

Background Previous studies in dogs and humans suggest that the carotid body chemoreceptor response to hypoxia is selectively impaired by halothane. The present studies in an open-loop canine preparation were performed to better delineate the effects of anesthetic concentrations of halothane on the carotid body chemoreceptor-mediated phrenic nerve response to an acute hypoxic stimulus. Methods Three protocols were performed to study the effects of halothane anesthesia on the phrenic nerve response to 1 min of isocapnic hypoxia (partial pressure of oxygen [PaO2] at peak hypoxia, 35-38 mmHg) in unpremedicated, anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. In protocol 1, the dose-dependent effects of halothane from 0.5-2.0 minimum alveolar concentration (MAC) on the hypoxic response during moderate hypercapnia (partial pressure of carbon dioxide [PaCO2], 60-65 mmHg) were studied in 10 animals. In protocol 2, the hypoxic responses at 1 MAC halothane near normocapnia (PaCO2, 40-45 mmHg) and during moderate hypercapnia were compared in an additional four animals. In protocol 3, the hypoxic response of 4 of 10 dogs from protocol 1 was also studied under sodium thiopental (STP) anesthesia after they completed protocol 1. Results Protocol 1: Peak phrenic nerve activity (PPA) increased significantly during the hypoxic runs compared with the isocapnic hyperoxic controls at all halothane doses. The phrenic nerve response to the hypoxic stimulus was present even at the 2 MAC dose. Protocol 2: The net hypoxic responses for the two carbon dioxide background levels at 1 MAC were not significantly different. Protocol 3: The net hypoxic response of PPA for the STP anesthetic was not significantly different from the 1 MAC halothane dose. Bilateral carotid sinus denervation abolished the PPA response to hypoxia. Conclusions The phrenic nerve response to an acute, moderately severe isocapnic hypoxic stimulus is dose-dependently depressed but not abolished by surgical doses of halothane. This analysis does not suggest a selective depression of the carotid body chemoreceptor response by halothane. The observed hypoxic phrenic response was mediated by the carotid body chemoreceptors in vagotomized dogs because bilateral carotid sinus denervation abolished all increases in PPA.

scholarly journals Bilateral carotid sinus nerve transection exacerbates morphine-induced respiratory depression

2018 ◽  
Vol 834 ◽  
pp. 17-29 ◽  
Author(s):  
Santhosh M. Baby ◽  
Ryan B. Gruber ◽  
Alex P. Young ◽  
Peter M. MacFarlane ◽  
Luc J. Teppema ◽  
...  
Keyword(s):  
Respiratory Depression ◽  
Carotid Sinus ◽  
Nerve Transection ◽  
Carotid Sinus Nerve ◽  
Bilateral Carotid

Reversible vascular isolation of carotid sinuses in conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H809-H814 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Response Curves ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Before And After ◽  
Surgical Preparation ◽  
Sinus Pressure

A surgical technique has been developed that permits reversible vascular isolation of both carotid sinuses in the conscious dog. Seven dogs so prepared were studied over periods of 4-12 wk. Repeatable stimulus-response curves relating arterial blood pressure to carotid sinus pressure were obtained for sinus pressures of 40-240 mmHg. Two studies gave evidence that the ability of the carotid baroreceptors to influence arterial pressure was not or was minimally affected by the surgical dissection. In 10 dogs one sinus was surgically prepared; 3 wk later the dogs were anesthetized and vagotomized. The steady-state stimulus-response curves for the chronically prepared sinuses showed no consistent differences from the curves for the opposite, acutely prepared sinuses. In 8 other dogs the hypertensive responses to bilateral carotid occlusion were compared before and after surgical preparation of both sinuses. The responses to carotid occlusion tended to be decreased after surgery but the differences were small and were significant only in 3 dogs.

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