scholarly journals Effect of inactivation of carotid sinus nerve by cold block on phrenic nerve activity in cats.

1985 ◽  
Vol 35 (5) ◽  
pp. 803-815 ◽  
Author(s):  
Shun-ichi KUWANA ◽  
Teijiro NATSUI
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Phrenic Nerve Activity

Chronic hypoxia enhances the phrenic nerve response to arterial chemoreceptor stimulation in anesthetized rats

1999 ◽  
Vol 87 (2) ◽  
pp. 817-823 ◽  
Author(s):  
M. R. Dwinell ◽  
F. L. Powell
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Phrenic Nerve ◽  
Chronic Hypoxia ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Hypoxic Group ◽  
Arterial Chemoreceptor

Chronic exposure to hypoxia results in a time-dependent increase in ventilation called ventilatory acclimatization to hypoxia. Increased O2 sensitivity of arterial chemoreceptors contributes to ventilatory acclimatization to hypoxia, but other mechanisms have also been hypothesized. We designed this experiment to determine whether central nervous system processing of peripheral chemoreceptor input is affected by chronic hypoxic exposure. The carotid sinus nerve was stimulated supramaximally at different frequencies (0.5–20 Hz, 0.2-ms duration) during recording of phrenic nerve activity in two groups of anesthetized, ventilated, vagotomized rats. In the chronically hypoxic group (7 days at 80 Torr inspired [Formula: see text]), phrenic burst frequency (fR, bursts/min) was significantly higher than in the normoxic control group with carotid sinus nerve stimulation frequencies >5 Hz. In the chronically hypoxic group, peak amplitude of integrated phrenic nerve activity ( ∫ Phr, percent baseline) or change in ∫ Phr was significantly greater at stimulation frequencies between 5 and 17 Hz, and minute phrenic activity ( ∫ Phr × fR) was significantly greater at stimulation frequencies >5 Hz. These experiments show that chronic hypoxia facilitates the translation of arterial chemoreceptor afferent input to ventilatory efferent output through a mechanism in the central nervous system.

Time-dependent phrenic nerve responses to carotid afferent activation: intact vs. decerebellate rats

1993 ◽  
Vol 265 (4) ◽  
pp. R811-R819 ◽  
Author(s):  
F. Hayashi ◽  
S. K. Coles ◽  
K. B. Bach ◽  
G. S. Mitchell ◽  
D. R. McCrimmon
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Short Term ◽  
Nerve Activity ◽  
A Value ◽  
Afferent Activation ◽  
Term Potentiation ◽  
Long Term Facilitation

The objectives were to determine 1) respiratory responses to carotid chemoreceptor inputs in anesthetized rats and 2) whether the cerebellar vermis plays a role in these responses. A carotid sinus nerve was stimulated (20 Hz) with five 2-min trains, each separated by approximately 3 min. During stimulation, respiratory frequency (f), peak amplitude of integrated phrenic nerve activity (integral of Phr), and their product (f x integral of Phr) immediately increased. As stimulation continued, integral of Phr progressively increased to a plateau [short-term potentiation (STP)], but f and f x integral of Phr decreased [short-term depression (STD)] to a value still above control. Upon stimulus termination, integral of Phr progressively decreased but remained above control; f and f x integral of Phr transiently decreased below baseline. After the final stimulation, integral of Phr remained above control for at least 30 min [long-term facilitation (LTF)]. Repeated 5-min episodes of isocapnic hypoxia also elicited STP, STD, and LTF. Vermalectomy lowered the CO2-apneic threshold and eliminated LTF. In conclusion, carotid chemoreceptor activation in rats elicits STP and LTF similar to that in cats; the vermis may play a role in LTF. A new response, STD, was observed.

Effects of hypercapnia and hypoxia on phrenic nerve activity and respiratory timing

1981 ◽  
Vol 51 (3) ◽  
pp. 732-738 ◽  
Author(s):  
J. F. Ledlie ◽  
S. G. Kelsen ◽  
N. S. Cherniack ◽  
A. P. Fishman
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Peak Height ◽  
Inspiratory Time ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Chemical Stimuli ◽  
Proprioceptive Inputs ◽  
Spontaneously Breathing ◽  
Respiratory Responses

In the spontaneously breathing animal, respiratory responses to chemical stimuli are influenced by phasic proprioceptive inputs from the thorax. We have compared the effects of hypercapnia and hypoxia on the level and timing of phrenic nerve activity while these phasic afferent signals were absent. Progressive hyperoxic hypercapnia and isocapnic hypoxia were produced in anesthetized paralyzed dogs by allowing 3–5 min of apnea to follow mechanical ventilation with 100% O2 or 35% O2 in N2, respectively; during hypoxia, isocapnia was maintained by intravenous infusion of tris(hydroxymethyl)aminomethane buffer. The peak height (P) of nerve bursts, inspiratory time (TI), and expiratory time (TE) were measured from the phrenic neurogram. With the vagi intact or severed, hypoxia decreased TI, whereas hypercapnia did not; both stimuli decreased TE. At the same minute phrenic activity (P x frequency), P, TI, and TE were all less during hypoxia than during hypercapnia. The decreases in TI and TE with hypoxia were significantly less after carotid sinus denervation. The results indicate that the patterns of phrenic nerve activity in response to hypoxia and hypercapnia are different: hypoxia has a greater effect on respiratory timing, whereas hypercapnia has a greater effect on peak phrenic nerve activity. The effect of hypoxia on respiratory timing is largely mediated by the peripheral chemoreceptors.

Hypoglossal and phrenic nerve responses to carotid baroreceptor stimulation

1993 ◽  
Vol 75 (3) ◽  
pp. 1395-1403 ◽  
Author(s):  
M. J. Wasicko ◽  
R. W. Giering ◽  
S. L. Knuth ◽  
J. C. Leiter
Keyword(s):  
Phrenic Nerve ◽  
Hypoglossal Nerve ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation ◽  
Sinus Pressure ◽  
Carotid Baroreceptor Stimulation

We examined the relationship between hypoglossal and phrenic nerve activities and carotid sinus pressure. In 12 adult cats that were decerebrate, vagotomized, paralyzed, and mechanically ventilated, we isolated the left carotid sinus for perfusion and denervated the right carotid sinus. Mean arterial blood pressure was maintained at 90–100 mmHg using a low resistance-reservoir containing saline and connected to the abdominal aorta. Constant pressure was applied to the carotid sinus region. We found that increased carotid sinus pressure immediately inhibited inspiratory-synchronous (phasic) hypoglossal nerve activity and that there was a direct inverse relationship between phasic hypoglossal activity and carotid sinus pressure up to a carotid pressure of 285 mmHg. Increased carotid sinus pressure had no effect on tonic hypoglossal nerve activity and only slightly inhibited phrenic nerve activity. Cutting the left carotid sinus nerve abolished this response. We also applied pressure pulses to the carotid sinus at discrete times during the phrenic cycle. We found that baroreceptor inhibition of phasic hypoglossal nerve activity was gated during the phrenic cycle: maximum inhibition occurred when the pulse was applied in late expiration. We conclude that carotid baroreceptor stimulation preferentially inhibits inspiratory synchronous hypoglossal nerve activity and that this afferent information traveling in the carotid sinus nerve is gated by the respiratory control center.

Daily acute intermittent hypoxia enhances phrenic motor output and stimulus-evoked phrenic responses in rats

2021 ◽  
Author(s):  
Raphael Rodrigues Perim ◽  
Michael D. Sunshine ◽  
Joseph F. Welch ◽  
Juliet Santiago ◽  
Ashley Holland ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Phrenic Nerve ◽  
Intermittent Hypoxia ◽  
Neural Control ◽  
Respiratory Cycle ◽  
Evoked Responses ◽  
Nerve Activity ◽  
Synaptic Inputs ◽  
Phrenic Nerve Activity ◽  
The Impact

Plasticity is a hallmark of the respiratory neural control system. Phrenic long-term facilitation (pLTF) is one form of respiratory plasticity characterized by persistent increases in phrenic nerve activity following acute intermittent hypoxia (AIH). Although there is evidence that key steps in the cellular pathway giving rise to pLTF are localized within phrenic motor neurons (PMNs), the impact of AIH on the strength of breathing-related synaptic inputs to PMNs remains unclear. Further, the functional impact of AIH is enhanced by repeated/daily exposure to AIH (dAIH). Here, we explored the effects of AIH vs. 2 weeks of dAIH preconditioning on spontaneous and evoked responses recorded in anesthetized, paralyzed (with pancuronium bromide) and mechanically ventilated rats. Evoked phrenic potentials were elicited by respiratory cycle-triggered lateral funiculus stimulation at C2 delivered prior to- and 60 min post-AIH (or an equivalent time in controls). Charge-balanced biphasic pulses (100 µs/phase) of progressively increasing intensity (100 to 700 µA) were delivered during the inspiratory and expiratory phases of the respiratory cycle. Although robust pLTF (~60% from baseline) was observed after a single exposure to moderate AIH (3 x 5 min; 5 min intervals), there was no effect on evoked phrenic responses, contrary to our initial hypothesis. However, in rats preconditioned with dAIH, baseline phrenic nerve activity and evoked responses were increased, suggesting that repeated exposure to AIH enhances functional synaptic strength when assessed using this technique. The impact of daily AIH preconditioning on synaptic inputs to PMNs raises interesting questions that require further exploration.

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku
Keyword(s):  
Electrical Stimulation ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Chemical Stimulation ◽  
Respiratory Drive ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Respiratory Reflexes ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

scholarly journals Suppression of phrenic nerve activity as a potential predictor of imminent sudden unexpected death in epilepsy (SUDEP)

2021 ◽  
Vol 184 ◽  
pp. 108405
Author(s):  
Omar Ashraf ◽  
Trong Huynh ◽  
Benton S. Purnell ◽  
Madhuvika Murugan ◽  
Denise E. Fedele ◽  
...  
Keyword(s):  
Phrenic Nerve ◽  
Sudden Unexpected Death ◽  
Unexpected Death ◽  
Nerve Activity ◽  
Potential Predictor ◽  
Phrenic Nerve Activity
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