Naloxone enhances respiratory output in cats

1979 ◽  
Vol 47 (5) ◽  
pp. 1105-1111 ◽  
Author(s):  
E. E. Lawson ◽  
T. G. Waldrop ◽  
F. L. Eldridge
Keyword(s):  
Phrenic Nerve ◽  
Opiate Receptors ◽  
Physiological Role ◽  
Opiate Antagonist ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
Decerebrate Cats ◽  
End Tidal Co2

To investigate the physiological role of opiate receptors and opiatelike neurotransmitters, which are present in brain-stem respiratory centers, we administered naloxone to 10 cats by intravenous injection. These animals were vagotomized, paralyzed, and servo-ventilated to maintain constant end-tidal CO2; in addition, their carotid sinus nerves were sectioned bilaterally. Respiratory output was assessed by integration of phrenic nerve activity. Control saline infusions had no effect on respiratory output. However, administration of naloxone (0.4 mg/kg) caused phrenic minute output to increase significantly in each of five anesthetized cerebrate cats (control 7,272 +/- 1,615 U/min; 30 min postnaloxone 12,920 +/- 3,857 U/min; P less than 0.05) and five unanesthetized decerebrate cats (control 10,368 +/- 1,222 U/min; naloxone 14,648 +/- 3,225 U/min; P less than 0.05). In addition to the effect on phrenic minute output, naloxone infusion resulted in an increase of the inspiratory rate of rise of phrenic nerve activity in each cat. There was no change in the ratio of inspiratory duration to total respiratory period (TI/Ttot). Because naloxone is a specific opiate antagonist, we suggest that endogenous opiatelike neurotransmitters (endorphins) may modulate central inspiratory drive.

Inspiratory rhythm in airway smooth muscle tone

1985 ◽  
Vol 58 (3) ◽  
pp. 911-920 ◽  
Author(s):  
R. A. Mitchell ◽  
D. A. Herbert ◽  
D. G. Baker
Keyword(s):  
Smooth Muscle ◽  
Vagus Nerve ◽  
Airway Smooth Muscle ◽  
Phrenic Nerve ◽  
Nerve Activity ◽  
Lung Inflation ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Stimulation Of

In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.

Unique spectral peak in phrenic nerve activity characterizes gasps in decerebrate cats

1986 ◽  
Vol 60 (3) ◽  
pp. 782-790 ◽  
Author(s):  
C. A. Richardson
Keyword(s):  
Central Pattern Generator ◽  
Phrenic Nerve ◽  
Central Pattern Generators ◽  
Power Spectra ◽  
Pattern Generator ◽  
Respiratory Pattern ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Spectral Peaks ◽  
Decerebrate Cats

The respiratory pattern of gasping has been characterized on the phrenic nerve as rapidonset, rapid-rise, large-amplitude bursts of neural activity. Furthermore, medullary sites critical for the neurogenesis of gasping have been identified and are not the sites of identified respiratory neurons, such as the dorsal and ventral respiratory groups. I classified envelopes of phrenic nerve activity as eupneic breaths, or gasps based on the time-domain features of duration, shape, and amplitude. Gasps were elicited by hypoxia and low blood pressure in 9 of 12 decerebrate cats. Inspiratory times were 1.15 +/- 0.43 (SD) for eupneic breaths and 0.55 +/- 0.18s for gasps. The high-frequency peaks in the power spectra of phrenic nerve activity were at 80 +/- 13 Hz for eupneic breaths and at 120 +/- 21 Hz for gasps. Three of the 12 cats developed a breathing pattern that began as a normal breath and terminated in a gasp. Power spectra of the normal portion had eupneic spectral peaks (75 +/- 24 Hz); power spectra of the gasp portion had the high peaks at 110 +/- 23 Hz, a value 1.5 times higher than that for the normal peaks. Although this analysis of peripheral nerve activity cannot distinguish between two central pattern generators at two distinct anatomical sites or one pattern generator operating in two distinct modes, the fact that gasps were much shorter in duration and had markedly higher spectral peaks than control breaths supports the idea that the central pattern generator for gasping is not the central pattern generator for eupnea.

Medullary lateral tegmental field neurons influence the timing and pattern of phrenic nerve activity in cats

2006 ◽  
Vol 101 (2) ◽  
pp. 521-530 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Susan M. Barman
Keyword(s):  
Nmda Receptors ◽  
Respiratory Rate ◽  
Phrenic Nerve ◽  
Normal Pattern ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Selective Blockade ◽  
Burst Amplitude ◽  
Proper Balance

In an effort to characterize the role of the medullary lateral tegmental field (LTF) in regulating respiration, we tested the effects of selective blockade of excitatory (EAA) and inhibitory amino acid (IAA) receptors in this region on phrenic nerve activity (PNA) of vagus-intact and vagotomized cats anesthetized with dial-urethane. We found distinct patterns of changes in central respiratory rate, duration of inspiratory and expiratory phases of PNA (Ti and Te, respectively), and I-burst amplitude after selective blockade of EAA and IAA receptors in the LTF. First, blockade of N-methyl-d-aspartate (NMDA) receptors significantly ( P < 0.05) decreased central respiratory rate primarily by increasing Ti but did not alter I-burst amplitude. Second, blockade of non-NMDA receptors significantly reduced I-burst amplitude without affecting central respiratory rate. Third, blockade of GABAA receptors significantly decreased central respiratory rate by increasing Te and significantly reduced I-burst amplitude. Fourth, blockade of glycine receptors significantly decreased central respiratory rate by causing proportional increases in Ti and Te and significantly reduced I-burst amplitude. These changes in PNA were markedly different from those produced by blockade of EAA or IAA receptors in the pre-Bötzinger complex. We propose that a proper balance of excitatory and inhibitory inputs to several functionally distinct pools of LTF neurons is essential for maintaining the normal pattern of PNA in anesthetized cats.

Cervical sympathetic and phrenic nerve responses to progressive brain hypoxia

1990 ◽  
Vol 68 (1) ◽  
pp. 53-58 ◽  
Author(s):  
M. J. Wasicko ◽  
J. E. Melton ◽  
J. A. Neubauer ◽  
N. Krawciw ◽  
N. H. Edelman
Keyword(s):  
Blood Pressure ◽  
Phrenic Nerve ◽  
Progressive Reduction ◽  
Nerve Activity ◽  
Brain Hypoxia ◽  
Activity Peak ◽  
Inspiratory Activity ◽  
Cervical Sympathetic ◽  
End Tidal ◽  
End Tidal Co2

To determine if depression of central respiratory output during progressive brain hypoxia (PBH) can be generalized to other brain stem outputs, we examined the effect of PBH on the tonic (tSCS) and inspiratory-synchronous (iSCS) components of preganglionic superior cervical sympathetic (SCS) nerve activity. Peak phrenic and SCS activity were measured in nine anesthetized, paralyzed, peripherally chemodenervated, vagotomized cats. PBH was produced by inhalation of 0.5% CO in 40% O2 while blood pressure and end-tidal CO2 were maintained constant. A progressive reduction in arterial O2 content from 14.3 +/- 0.6 to 4.5 +/- 0.3 vol% caused a 79 +/- 7% depression of peak phrenic activity and an 84 +/- 10% reduction of iSCS activity, but tSCS activity increased 42 +/- 21%. During CO2 rebreathing, iSCS activity increased in parallel with peak phrenic activity while tSCS activity was unchanged. The slopes of the CO2 responses of both phrenic (6.3 +/- 1.2%max/mmHg) and iSCS (4.6 +/- 0.8%max/mmHg) activity were unaffected by PBH. In four of nine hypocapnic and three of nine hypoxic studies, inspiratory activity in the SCS nerve was observed even after completely silencing the phrenic neurogram.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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