Control of sympathetic and phrenic nerve activity by cholinergic mechanisms in the nucleus of the solitary tract (NTS)

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.

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Evaluation of a New Valveless all Purpose Ventilator: Effect of Ventilating Frequency PEEP, PACO2 and PAO2 on Phrenic Nerve Activity

Perspectives in High Frequency Ventilation - Developments in Critical Care Medicine and Anesthesiology ◽

10.1007/978-94-009-6711-3_15 ◽

1983 ◽

pp. 140-145 ◽

Cited By ~ 2

Author(s):

M. K. Chakrabarti ◽

J. G. Whitwam

Keyword(s):

Phrenic Nerve ◽

Nerve Activity ◽

Phrenic Nerve Activity

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

Journal of Applied Physiology ◽

10.1152/jappl.1981.51.3.732 ◽

1981 ◽

Vol 51 (3) ◽

pp. 732-738 ◽

Cited By ~ 18

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.

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