Respiration in awake cats: sympathectomy and deafferentation of carotid bifurcations

1987 ◽  
Vol 62 (3) ◽  
pp. 932-940 ◽  
Author(s):  
P. C. Szlyk ◽  
D. B. Jennings
Keyword(s):  
Carotid Sinus ◽  
Minute Ventilation ◽  
Reflex Modulation ◽  
Carotid Sinus Nerve ◽  
Inspiratory Time ◽  
Nerve Section ◽  
Arterial Pco2 ◽  
Bilateral Carotid ◽  
Arterial Po2 ◽  
Awake Cats

Respiratory effects of sympathectomy of the carotid bifurcations and, in a subsequent experiment, bilateral carotid sinus nerve section were examined in six awake resting cats. In each intact and denervated state, sequential breaths were analyzed at 10-min intervals up to 80 min. Individual breath frequency (f), tidal volume (VT), and ventilation (V = f X VT) were determined. In individual cats, sympathectomy or deafferentation could cause significant increases or decreases in ventilation or no change. Thus the range of spontaneous variability in breath V as well as minute ventilation (VE), averaged for the group, were not consistently altered in the same direction by either sympathectomy or deafferentation of the carotid bifurcations. Interestingly, in most cats after both sympathectomy (5 of 6) and deafferentation (4 of 6), VT increased and f decreased relative to V. Despite this, after sinus nerve section in two cats arterial PO2 decreased and arterial PCO2 tended to increase relative to VE, suggesting possible effects of deafferentation on ventilation-perfusion balance. Sympathectomy also affected timing such that inspiratory time began to exceed 0.5 of the breath duration at a lower breath f; this effect of sympathectomy was reversed to intact values by subsequent sinus deafferentation. Thus, in eupneic awake cats, sympathetics normally suppress reflex modulation of central timing from carotid chemoreceptors and/or baroreceptors.

Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs

1985 ◽  
Vol 59 (3) ◽  
pp. 869-874 ◽  
Author(s):  
M. A. Bureau ◽  
J. Lamarche ◽  
P. Foulon ◽  
D. Dalle
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Occlusion Pressure ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Postnatal Maturation ◽  
Arterial Po2

The contribution of the carotid body chemoreceptor to postnatal maturation of breathing was evaluated in lambs from 7 to 70 days of age. The study was conducted by comparing the eupneic ventilation and resting pneumograms in intact conscious lambs with those of lambs that were carotid body chemodenervated (CBD) at birth. In comparison to the 1-wk-old intact lambs, the CBD lambs had significant decreases in minute ventilation (VE, 313 vs. 517 ml/kg), tidal volume (VT, 7.2 vs. 10.5 ml/kg), respiratory rate (f, 44 vs. 51 breaths/min), and occlusion pressure (P0.1, 2.8 vs. 7.2 cmH2O). Arterial PO2's were 59 vs. 75 Torr (P less than 0.05) and arterial PCO2's 47 vs. 36 Torr (P less than 0.05), respectively, in CBD and intact lambs. In intact lambs from 7 to 70 days, resting VE decreased progressively from 517 to 274 ml/kg (P less than 0.01) due to a fall in VT, mean inspiratory flow (VT/TI), and f, whereas the ratio of inspiratory time to total breath duration remained constant. P0.1 decreased from 7.2 to 3.9 cmH2O from 7 to 42 days. In contrast the CBD lambs experienced only minimal changes in VE, VT, VT/TI, and f during the same period. VE only decreased from 313 to 218 and P0.1 from 2.8 to 2.4 cmH2O. In contrast to that of intact lambs the resting pneumogram of CBD lambs remained relatively fixed from 7 to 70 days. Three CBD lambs died unexpectedly, without apparent cause, in the 4th and 5th wk of life.

Ventilatory afterdischarge in the awake goat

1991 ◽  
Vol 71 (4) ◽  
pp. 1511-1517 ◽  
Author(s):  
M. J. Engwall ◽  
L. Daristotle ◽  
W. Z. Niu ◽  
J. A. Dempsey ◽  
G. E. Bisgard
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Minute Ventilation ◽  
Critical Factor ◽  
Carotid Sinus Nerve ◽  
Arterial Pco2 ◽  
The Mean ◽  
Mean Time ◽  
Stimulation Of ◽  
Anesthetized Cat

Ventilatory afterdischarge (VAD) has been defined as a persistent gradually diminishing elevation of ventilatory activity that occurs after withdrawal of a variety of respiratory stimuli. The phenomenon has been well documented in the anesthetized cat, piglet, and lamb in response to electrical stimulation of the carotid sinus nerve. We sought to determine whether VAD could be demonstrated in the standing awake goat (n = 7) by use of an extracorporeal circuit to provide square-wave physiological stimulation of the carotid chemoreceptor (carotid body PO2 40 Torr). After 5 min of isolated carotid body stimulation, the mean time constants for diminishing inspired minute ventilation, tidal volume, and respiratory frequency were 27.7, 34.5, and 25.5 s, respectively. These results indicate that VAD does exist in the awake goat model. A critical factor for the demonstration of VAD is the maintenance of systemic arterial PCO2 (isocapnia) during the period of increased ventilatory activity. If arterial PCO2 is allowed to decrease even slightly during the hyperventilation, the magnitude and duration of VAD are greatly attenuated.

scholarly journals Carotid sinus nerve transection abolishes the facilitation of breathing that occurs upon cessation of a hypercapnic gas challenge in male mice

2021 ◽  
Author(s):  
Paulina M. Getsy ◽  
Sripriya Sundararajan ◽  
Stephen John Lewis
Keyword(s):  
Carotid Sinus ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nerve Transection ◽  
Carotid Sinus Nerve ◽  
Ventilatory Responses ◽  
Bilateral Carotid ◽  
Baseline Values ◽  
Freely Moving

Arterial pCO2 elevations increase minute ventilation via activation of chemosensors within the carotid body (CB) and brainstem. Although the roles of CB chemoafferents in the hypercapnic (HC) ventilatory response have been investigated, there are no studies reporting the role of these chemoafferents in the ventilatory responses to a HC challenge or the responses that occur upon return to room-air, in freely-moving mice. This study found that a HC challenge (5%CO2, 21% O2, 74% N2 for 15 min) elicited an array of responses, including increases in frequency of breathing (accompanied by decreases in inspiratory and expiratory times), and increases in tidal volume, minute ventilation, peak inspiratory and expiratory flows, and inspiratory and expiratory drives in sham-operated (SHAM) adult male C57BL6 mice, and that return to room-air elicited a brief excitatory phase followed by gradual recovery of all parameters toward baseline values over a 15 min period. The array of ventilatory responses to the HC challenge in mice with bilateral carotid sinus nerve transection (CSNX) performed 7 days previously, occurred more slowly but reached similar maxima as SHAM mice. A major finding was responses upon return to room-air were dramatically lower in CSNX mice than SHAM mice, and the parameters returned to baseline values within 1-2 min in CSNX mice, whereas it took much longer in SHAM mice. These findings are the first evidence that CB chemoafferents play a key role in initiating the ventilatory responses to HC challenge in C57BL6 mice and are essential for the expression of post-HC ventilatory responses.

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.

Carotid bifurcation sympathectomy and deafferentation: respiration during hypercapnia

1988 ◽  
Vol 255 (2) ◽  
pp. R252-R258
Author(s):  
D. B. Jennings ◽  
P. C. Szlyk
Keyword(s):  
Carotid Sinus ◽  
Carotid Bifurcation ◽  
The Other ◽  
Afferent Activity ◽  
Nerve Section ◽  
Absolute Level ◽  
Respiratory Effects ◽  
Percent Change ◽  
Fractional Concentration ◽  
Awake Cats

The respiratory effects of hypercapnia were studied in six awake cats 1) after bilateral sympathectomy of the carotid bifurcations and 2) after bilateral section of the carotid sinus nerves. When cats breathed either 2 or 4% CO2 in air, neither denervation affected the absolute level of ventilation, the percent change in ventilation, or the range of breath-to-breath variability in ventilation (V). However, in all six cats tidal volume (VT) increased for some levels of breath V after sympathectomy of the carotid bifurcations during inhalation of 4% CO2 in air. Moreover, after the subsequent carotid deafferentation, increased VT during fractional concentration of inspired CO2 (FICO2) of 4% persisted in four of six cats. Thus increased VT after sympathectomy could not be attributed to increased carotid chemoreceptor afferent activity but may have been due to reduced baroreceptor activity. On the other hand, sympathectomy-induced differences in breath timing, present during inhalation of 2% CO2, were reversed to intact values after sinus nerve section. In contrast to 2% CO2, changes in respiratory timing in intact cats associated with 4% CO2 were not altered significantly by sympathectomy or deafferentation of the carotid bifurcations. The latter indicates that above a critical FICO2 central mechanisms, unrelated to the carotid bifurcation, dominated respiratory timing in the hypercapnic awake cats.

Reflex limb dilatation following norepinephrine and angiotensin II in conscious dogs

1976 ◽  
Vol 230 (3) ◽  
pp. 557-563 ◽  
Author(s):  
SF Vatner ◽  
RJ McRitchie
Keyword(s):  
Angiotensin Ii ◽  
Iliac Artery ◽  
Carotid Sinus ◽  
Conscious Dogs ◽  
Beta Blockade ◽  
Prostaglandin Synthetase ◽  
Nerve Section ◽  
Iliac Arteries ◽  
Bilateral Carotid ◽  
Bilateral Vagotomy

Effects of intravenous and intra-arterial norepinephrine (NE) and angiotensin II (AN) were compared in 18 conscious dogs instrumented with Doppler or electromagnetic flow probes on the iliac, mesenteric, and renal arteries, and catheters in the aorta and iliac arteries. NE and AN administered intravenously constricted the mesenteric and renal beds, and constricted the iliac bed when administered directly into the iliac artery. In contrast, intravenous NE and AN caused striking reflex increases in iliac flow and reductions in iliac resistance, respectively, in 12 of 18 dogs studied. The reflex iliac dilatation was not prevented by beta blockade with propranolol, cholinergic blockade with atropine, or prostaglandin synthetase inhibition with indomethacin. However, the responses were abolished by either phentolamine, 1 mg/kv iv, or after local blockade of the limb with either phentolamine, 0.5 mg/kg, or with tripelennamine, 2 mg/kg. The dilatation was not prevented by either bilateral carotid sinus and aortic nerve section or by bilateral vagotomy alone, but was prevented by a combination of these procedures. Thus, intravenous NE and AN cause striking reflex iliac dilatation in the limb in the conscious dog; the afferent arc of this reflex involves both arterial baroreceptor and vagal pathways, while the efferent mechanism involves an interaction of alpha-adrenergic and histaminergic receptors.

scholarly journals The Role of Carotid Sinus Nerve Input in the Hypoxic-Hypercapnic Ventilatory Response in Juvenile Rats

2020 ◽  
Vol 11 ◽  
Author(s):  
Paulina M. Getsy ◽  
Gregory A. Coffee ◽  
Stephen J. Lewis
Keyword(s):  
Carotid Sinus ◽  
Nucleus Tractus Solitarius ◽  
Minute Ventilation ◽  
Respiratory Pattern ◽  
Whole Body ◽  
Carotid Sinus Nerve ◽  
Sprague Dawley ◽  
Juvenile Rats ◽  
Ventilatory Responses ◽  
Chemosensory Pathway

In juvenile rats, the carotid body (CB) is the primary sensor of oxygen (O2) and a secondary sensor of carbon dioxide (CO2) in the blood. The CB communicates to the respiratory pattern generator via the carotid sinus nerve, which terminates within the commissural nucleus tractus solitarius (cNTS). While this is not the only peripheral chemosensory pathway in juvenile rodents, we hypothesize that it has a unique role in determining the interaction between O2 and CO2, and consequently, the response to hypoxic-hypercapnic gas challenges. The objectives of this study were to determine (1) the ventilatory responses to a poikilocapnic hypoxic (HX) gas challenge, a hypercapnic (HC) gas challenge or a hypoxic-hypercapnic (HH) gas challenge in juvenile rats; and (2) the roles of CSN chemoafferents in the interactions between HX and HC signaling in these rats. Studies were performed on conscious, freely moving juvenile (P25) male Sprague Dawley rats that underwent sham-surgery (SHAM) or bilateral transection of the carotid sinus nerves (CSNX) 4 days previously. Rats were placed in whole-body plethysmographs to record ventilatory parameters (frequency of breathing, tidal volume and minute ventilation). After acclimatization, they were exposed to HX (10% O2, 90% N2), HC (5% CO2, 21% O2, 74% N2) or HH (5% CO2, 10% O2, 85% N2) gas challenges for 5 min, followed by 15 min of room-air. The major findings were: (1) the HX, HC and HH challenges elicited robust ventilatory responses in SHAM rats; (2) ventilatory responses elicited by HX alone and HC alone were generally additive in SHAM rats; (3) the ventilatory responses to HX, HC and HH were markedly attenuated in CSNX rats compared to SHAM rats; and (4) ventilatory responses elicited by HX alone and HC alone were not additive in CSNX rats. Although the rats responded to HX after CSNX, CB chemoafferent input was necessary for the response to HH challenge. Thus, secondary peripheral chemoreceptors do not compensate for the loss of chemoreceptor input from the CB in juvenile rats.

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.

Postnatal maturation of carotid chemoreceptor responses to O2 and CO2 in the cat

1993 ◽  
Vol 75 (6) ◽  
pp. 2383-2391 ◽  
Author(s):  
J. L. Carroll ◽  
O. S. Bamford ◽  
R. S. Fitzgerald
Keyword(s):  
Time Course ◽  
Carotid Sinus ◽  
Neonatal Period ◽  
Moving Average ◽  
Neural Responses ◽  
Arterial Pco2 ◽  
Postnatal Maturation ◽  
Steady Level ◽  
Adult Cats ◽  
Arterial Po2

This study aimed to characterize neural responses of the carotid chemoreceptors of the maturing cat to natural stimuli and to determine the time course of carotid chemoreceptor development from the neonatal period to adulthood. Carotid sinus nerve (CNS) responses to O2 and CO2 were studied in cats at 1, 4, and 8 wk of age and in adult cats (n = 6 at each age). Pentobarbital sodium-anesthetized cats were exposed to three levels of O2 (arterial PO2 = 40–45, 80–90, and > 300 Torr) at five levels of arterial PCO2 (22, 35, 48, 63, and 75 Torr) while the moving average of whole nerve output from the CSN was recorded. Ganglioglomerular nerves were sectioned. All cats at every age increased CSN activity during hypoxia. However, the CSN response to hypoxia was not sustained in some immature cats. Of the cats that sustained CSN activity during hypoxia, four of the six 1-wk-old cats showed a biphasic pattern of response, with an initial overshoot followed by a steady level of discharge. Older cats did not exhibit this pattern. CNS sensitivity to hypoxia was weakest in 1-wk-old kittens but increased to nearly adult levels by 4 wk of age. Carotid chemoreceptor responses to CO2 were also smallest in 1-wk-old kittens and increased with maturation. However, unlike hypoxia responses, CO2 sensitivity during hypoxia continued to develop between 8 wk and adulthood. O2-CO2 interaction did not become significant until after 4 wk of age. Thus, carotid chemoreceptor responses to both O2 and CO2 are weak in newborn cats and increase during postnatal development.(ABSTRACT TRUNCATED AT 250 WORDS)

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