Naloxone attenuates poststimulatory respiratory depression of laryngeal origin in the adult cat

1995 ◽  
Vol 269 (1) ◽  
pp. R113-R123 ◽  
Author(s):  
D. Mutolo ◽  
F. Bongianni ◽  
M. Corda ◽  
G. A. Fontana ◽  
T. Pantaleo
Keyword(s):  
Respiratory Depression ◽  
Time Course ◽  
Superior Laryngeal Nerve ◽  
Endogenous Opioids ◽  
Respiratory Frequency ◽  
Inspiratory Activity ◽  
Stimulation Period ◽  
Adult Cat ◽  
Adult Cats ◽  
Alpha Chloralose

Poststimulatory depression in respiratory activity induced by superior laryngeal nerve (SLN) stimulation was quantitatively investigated in 20 adult cats. The role played in this phenomenon by endogenous opioids was studied using the opiate antagonist naloxone. The effects of hypercapnia on the same phenomenon were also investigated for comparison. Experiments were performed on cats anesthetized with pentobarbitone or alpha-chloralose, vagotomized, paralyzed, and artificially ventilated with 100% O2. Some animals were also carotid sinus denervated. Respiratory output was monitored as integrated phrenic nerve activity. SLN stimulation produced apnea, which outlasted the stimulation period; when respiration resumed, it was markedly depressed as revealed mainly by a decrease in phrenic minute output, respiratory frequency, and rate of rise of inspiratory activity. Phrenic output recovered gradually to control levels following an exponential time course. These effects varied as a function of the duration of SLN stimulation. Naloxone administration (0.8 mg/kg iv) significantly reduced the duration of poststimulatory apnea and attenuated the depression of phrenic minute output of the first recovery breath as a result of changes in peak phrenic activity; it also accelerated the time course of recovery. Hypercapnia did not affect the duration of poststimulatory apnea, but attenuated the initial poststimulatory depression because of changes in respiratory frequency; the rate of recovery was reduced. The results provide characterization of poststimulatory respiratory depression of laryngeal origin in the adult cat and suggest a role of endogenous opioids in its genesis or modulation.

Respiratory neuronal activity during apnea and poststimulatory effects of laryngeal origin in the cat

2000 ◽  
Vol 89 (3) ◽  
pp. 917-925 ◽  
Author(s):  
Fulvia Bongianni ◽  
Donatella Mutolo ◽  
Marco Carfì ◽  
Giovanni A. Fontana ◽  
Tito Pantaleo
Keyword(s):  
Respiratory Depression ◽  
Superior Laryngeal Nerve ◽  
Respiratory Neurons ◽  
Inhibitory Input ◽  
Phase Theory ◽  
Inspiratory Neurons ◽  
Three Phase ◽  
Expiratory Neurons ◽  
Inspiratory Activity ◽  
Respiratory Reflexes

We investigated the behavior of medullary respiratory neurons in cats under pentobarbitone anesthesia, vagotomized, paralysed, and artificially ventilated to elucidate neural mechanisms underlying apnea and poststimulatory respiratory depression induced by superior laryngeal nerve (SLN) stimulation. Inspiratory neurons were completely inhibited during SLN stimulation and poststimulatory apnea. During recovery of inspiratory activity, augmenting inspiratory neurons were depressed, decrementing inspiratory neurons were excited, and late inspiratory neurons displayed unchanged bursts closely locked to the end of the inspiratory phase. Augmenting expiratory neurons were either silenced or displayed different levels of tonic activity during SLN stimulation; some of them were clearly activated. These expiratory neurons displayed activity during poststimulatory apnea, before the onset of the first recovery phrenic burst. Postinspiratory or decrementing expiratory neurons were activated during SLN stimulation; their discharge continued with a decreasing trend during poststimulatory apnea. The results support the three-phase theory of rhythm generation and the view that SLN stimulation provokes a postinspiratory apnea that could represent the inhibitory component of respiratory reflexes of laryngeal origin, such as swallowing. In addition, because a subpopulation of augmenting expiratory neurons displays activation during SLN stimulation, the hypothesis can be advanced that not only postinspiratory, or decrementing expiratory neurons, but also augmenting expiratory neurons may be involved in the genesis of apnea and poststimulatory phenomena. Finally, the increase in the activity of decrementing inspiratory neurons after the end of SLN stimulation may contribute to the generation of poststimulatory respiratory depression by providing an inhibitory input to bulbospinal augmenting inspiratory neurons.

Intracerebroventricular injection of prostaglandin E2 increases splenic sympathetic nerve activity in rats

1995 ◽  
Vol 269 (3) ◽  
pp. R662-R668 ◽  
Author(s):  
T. Ando ◽  
T. Ichijo ◽  
T. Katafuchi ◽  
T. Hori
Keyword(s):  
Prostaglandin E2 ◽  
Sympathetic Nerve ◽  
Time Course ◽  
Sympathetic Nerve Activity ◽  
Dependent Manner ◽  
Central Administration ◽  
Nerve Activity ◽  
High Doses ◽  
Alpha Chloralose ◽  
Dose Dependent

The effects of central administration of prostaglandin E2 (PGE2) and its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (13V) injection of PGE2 (0.1-10 nmol/kg) increased splenic SNA in a dose-dependent manner. An I3V injection of an EP1 agonist, 17-phenyl-omega-trinor PGE2 (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a time course similar to that of PGE2-induced responses. In contrast, EP2 agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE1 (10-100 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP3/EP1 agonist, EP3 >> EP1) increased splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP1 antagonist, SC-19220 (200 and 500 nmol/kg), completely blocked the responses of splenic SNA to PGE2 (0.1 nmol/kg) and M & B-28767 (10 nmol/kg), respectively. These findings indicate that brain PGE2 increases splenic SNA through its action on EP1 receptors.

A model for the relation between respiratory neural and mechanical outputs. III. Validation

1981 ◽  
Vol 51 (4) ◽  
pp. 990-1001 ◽  
Author(s):  
M. Younes ◽  
W. Riddle ◽  
J. Polacheck
Keyword(s):  
Respiratory System ◽  
Pressure Wave ◽  
Time Course ◽  
Present Report ◽  
Occlusion Pressure ◽  
Single Breath ◽  
Wave Forms ◽  
Inspiratory Activity ◽  
Good Agreement

In the preceding two communications we described a model for the relation between respiratory neural and mechanical outputs. In the present report we test the accuracy of the model in predicting volume and flow from occlusion pressure wave forms, and vice versa. We performed single-breath airway occlusions in 21 unconscious subjects and determined the time course of occlusion pressure. We also measured the passive properties of the respiratory system. The time course of volume and flow was predicted from the occlusion pressure wave forms, and the results were compared with the spontaneous breaths immediately preceding occlusion. Inspiratory duration, shape and amplitude of occlusion-pressure wave forms, and the passive properties of the respiratory system varied widely among subjects. There was good agreement between predicted and observed values in all cases. Except for some prolongation of inspiration (Hering-Breuer reflex), diaphragmatic activity did not change during occlusion. Since occlusion pressure is proportional to inspiratory activity, we conclude that the model described provides a good approximation of the relation between inspiratory activity and spirometric output.

Diaphragmatic activity during REM sleep in the adult cat

1996 ◽  
Vol 81 (2) ◽  
pp. 751-760 ◽  
Author(s):  
J. Orem ◽  
C. A. Anderson
Keyword(s):  
Rem Sleep ◽  
Area Under The Curve ◽  
Motor Units ◽  
Nrem Sleep ◽  
Respiratory Drive ◽  
Upper Airways ◽  
Central Respiratory Activity ◽  
Time Average ◽  
Adult Cat ◽  
Adult Cats

Diaphragmatic electromyograms from five adult cats were studied to determine whether diaphragmatic activity, like central respiratory activity, increases in rapid-eye-movement (REM) sleep. Breaths with inspiratory durations between 250 and 2,000 ms were analyzed. 1) There was a greater slope of the moving time average of diaphragmatic activity in REM than in non-REM (NREM) sleep. These greater slopes occurred whether the route of breathing was through the upper airways or through an endotracheal tube and may have resulted from early recruitment of motor units. 2) Mean diaphragmatic activity was also greater, but other variables (peak activity, the area under the curve of diaphragmatic activity, mean intratracheal pressures, inspiratory airflow rates, and tidal volumes) were not greater in REM than in NREM sleep. 3) Diaphragmatic activity was similar in REM sleep and active wakefulness. 4) Across states, slope of the moving time average varied with the duration of inspiration: greater slopes were associated with shorter breaths. These results are consistent with an increase in central respiratory drive in REM sleep that increases the rate of rise of diaphragmatic activity.

Nucleus tractus solitarius and excitatory amino acids in afferent-evoked inspiratory termination

1994 ◽  
Vol 76 (3) ◽  
pp. 1293-1301 ◽  
Author(s):  
D. R. Karius ◽  
L. Ling ◽  
D. F. Speck
Keyword(s):  
Nmda Receptors ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Amino Acid ◽  
Superior Laryngeal Nerve ◽  
Nmda Antagonist ◽  
Intercostal Nerve ◽  
Laryngeal Nerve ◽  
Receptor Antagonists ◽  
Adult Cats ◽  
Stimulation Of

This study tested the hypothesis that excitatory amino acid (EAA) neurotransmission at non-N-methyl-D-aspartate (non-NMDA), but not NMDA, receptors within medial regions of the nucleus tractus solitarius (NTS) is required in the inspiratory termination elicited by vagal or intercostal nerve (ICN) stimulation. Adult cats were anesthetized, decerebrated, vagotomized, and ventilated. After control responses to stimulation of the superior laryngeal nerve (SLN), vagus, and ICN were obtained, EAA receptor antagonists were injected into the medial aspects of the NTS. Injections of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 6,7-dinitro-quinoxaline-2,3-dione (DNQX), EAA receptor antagonists; (+/-)-2-amino-5-phosphonopentanoic acid (AP5), an NMDA antagonist; or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), a non-NMDA antagonist, ipsilateral to the vagus abolished the termination response. The SLN-elicited response persisted after AP5 injection but was abolished by NBQX injections. The ICN-elicited response persisted after bilateral injections of CNQX/DNQX or procaine. We conclude that the inspiratory termination elicited by ICN stimulation is independent of the regions medial to the NTS. Inspiratory termination elicited by vagal or SLN stimulation requires non-NMDA-mediated EAA neurotransmission within medial aspects of the NTS, but the vagally elicited response also requires NMDA receptors.

An Electromyographic Analysis of Forelimb Muscles during Overground Stepping in the Cat

1978 ◽  
Vol 76 (1) ◽  
pp. 105-122 ◽  
Author(s):  
ARTHUR W.M. ENGLISH
Keyword(s):  
Energy Absorption ◽  
Time Course ◽  
The Other ◽  
Biphasic Pattern ◽  
The Third ◽  
Shoulder Region ◽  
Forelimb Muscles ◽  
Electromyographic Analysis ◽  
Adult Cats ◽  
Intramuscular Electromyography

The patterns of activity of 33 forelimb muscles during unrestrained overground stepping in eight adult cats were analysed using intramuscular electromyography. Three general patterns were found. Some muscles began activity during the first extension epoch (E1) and ceased near the end of the third extension epoch (E3) and were considered extensors. Others, considered flexors, began activity just prior to the flexion (F) epoch and ceased at or just after the onset of E1. Other muscles showed a biphasic pattern of activation; one period of activity occurring during F, the other during the extension epochs. In all regions of the limb, individual muscles displayed variation in the onset and time course of activity. The results are interpreted in terms of a model of locomotor generation which proposes specific neural output to individual muscles. Muscles of the shoulder region are proposed to act mainly to produce translatory and rotatory movements of the scapula associated with lengthening the step. Muscles of the elbow region and antebrachium are interpreted as playing roles both in producing flexionextension movements and in the absorption of energy. The latter group are considered especially suitable to energy absorption because of their pennate arrangement of muscle fasciculi and their long tendons.

Influences of superior laryngeal afferent stimulation on expiratory activity in cats

1988 ◽  
Vol 65 (1) ◽  
pp. 385-392 ◽  
Author(s):  
F. Bongianni ◽  
M. Corda ◽  
G. Fontana ◽  
T. Pantaleo
Keyword(s):  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Tetanic Stimulation ◽  
Bötzinger Complex ◽  
Dependent Activity ◽  
Inspiratory Activity ◽  
Polysynaptic Reflex ◽  
Expiratory Muscles ◽  
Excitatory Responses ◽  
Stimulation Of

The effects of superior laryngeal nerve (SLN) stimulation on the activity of the expiratory muscles and medullary expiration-related (ER) neurons were investigated in 24 pentobarbital-anesthetized cats. In some experiments the animals were also paralyzed and artificially ventilated. Sustained tetanic stimulation of SLN consistently caused an apneic response associated with the appearance of tonic CO2-dependent activity in the expiratory muscles and in ER neurons located in the caudal ventral respiratory group (VRG) and the Botzinger complex. Single shocks or brief tetani at the same stimulation intensities failed to evoke excitatory responses in the expiratory muscles and in the vast majority of ER neurons tested. At higher stimulation strengths, single shocks or short tetani elicited excitatory responses in the expiratory muscles (20- to 35-ms latency) and in the majority of ER neurons of the caudal VRG (7.5- to 15.5-ms latency). These responses were obtained only during the expiratory phase and proved to be CO2 independent. On the contrary, only inhibitory responses were evoked in the activity of Botzinger complex neurons. The observed tonic expiratory activity most likely represents a disinhibition phenomenon due to the suppression of inspiratory activity; activation of expiratory muscles at higher stimulation intensities appears to be a polysynaptic reflex mediated by ER neurons of the caudal VRG but not by Botzinger complex neurons.

Effects of almitrine on genioglossal and diaphragmatic electromyograms

1986 ◽  
Vol 61 (6) ◽  
pp. 2122-2128 ◽  
Author(s):  
D. E. Weese-Mayer ◽  
R. T. Brouillette ◽  
L. M. Klemka ◽  
C. E. Hunt
Keyword(s):  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Respiratory Drive ◽  
Peripheral Chemoreceptor ◽  
Obstructive Sleep ◽  
Adult Cats ◽  
Alpha Chloralose ◽  
Spontaneously Breathing ◽  
Dose Dependent

We previously demonstrated dose-dependent increases in both hypoglossal and phrenic electroneurograms after almitrine in anesthetized, paralyzed, and vagotomized cats. We have now investigated the effect of this peripheral chemoreceptor stimulant on diaphragmatic and genioglossal (GG, an upper airway-maintaining muscle) electromyograms in five unanesthetized, chronically instrumented, spontaneously breathing adult cats during slow-wave sleep. In 12 studies almitrine doses of 1.0–6.0 mg/kg increased inspired minute ventilation (VI), frequency (f), and tidal volume (VT) and decreased expiratory time (TE). However, almitrine doses as high as 6.0 mg/kg failed to augment phasic inspiratory GG activity. To determine why almitrine induced phasic inspiratory upper airway activity in anesthetized, vagotomized cats but not in sleeping cats, additional studies were performed. In four dose-response studies in three pentobarbital-anesthetized cats, almitrine, 1.0–6.0 mg/kg, did not produce phasic inspiratory GG activity. Almitrine did induce phasic inspiratory GG activity in two of three studies in three vagotomized, tracheostomized, alpha-chloralose-urethan-anesthetized cats. These results suggest that almitrine would not be useful in obstructive sleep apnea, yet because almitrine markedly increased VI, f, and VT and decreased TE in unanesthetized sleeping cats the drug may be effective in patients who lack normal central neural respiratory drive, such as the preterm infant.

Gap Junctions and Inhibitory Synapses Modulate Inspiratory Motoneuron Synchronization

2001 ◽  
Vol 85 (4) ◽  
pp. 1543-1551 ◽  
Author(s):  
Céline Bou-Flores ◽  
Albert J. Berger
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Time Scale ◽  
Respiratory Rhythm ◽  
Respiratory Frequency ◽  
Glycyrrhetinic Acid ◽  
Inhibitory Synapses ◽  
Short Time Scale ◽  
Inspiratory Activity ◽  
Short Time

Interneuronal electrical coupling via gap junctions and chemical synaptic inhibitory transmission are known to have roles in the generation and synchronization of activity in neuronal networks. Uncertainty exists regarding the roles of these two modes of interneuronal communication in the central respiratory rhythm-generating system. To assess their roles, we performed studies on both the neonatal mouse medullary slice and en bloc brain stem-spinal cord preparations where rhythmic inspiratory motor activity can readily be recorded from both hypoglossal and phrenic nerve roots. The rhythmic inspiratory activity observed had two temporal characteristics: the basic respiratory frequency occurring on a long time scale and the synchronous neuronal discharge within the inspiratory burst occurring on a short time scale. In both preparations, we observed that bath application of gap-junction blockers, including 18α-glycyrrhetinic acid, 18β-glycyrrhetinic acid, and carbenoxolone, all caused a reduction in respiratory frequency. In contrast, peak integrated phrenic and hypoglossal inspiratory activity was not significantly changed by gap-junction blockade. On a short-time-scale, gap-junction blockade increased the degree of synchronization within an inspiratory burst observed in both nerves. In contrast, opposite results were observed with blockade of GABAA and glycine receptors. We found that respiratory frequency increased with receptor blockade, and simultaneous blockade of both receptors consistently resulted in a reduction in short-time-scale synchronized activity observed in phrenic and hypoglossal inspiratory bursts. These results support the concept that the central respiratory system has two components: a rhythm generator responsible for the production of respiratory cycle timing and an inspiratory pattern generator that is involved in short-time-scale synchronization. In the neonatal rodent, properties of both components can be regulated by interneuronal communication via gap junctions and inhibitory synaptic transmission.

Phase resetting and dysrhythmic responses of the respiratory oscillator

1987 ◽  
Vol 252 (1) ◽  
pp. R55-R62 ◽  
Author(s):  
D. Paydarfar ◽  
F. L. Eldridge
Keyword(s):  
Respiratory Rhythm ◽  
S Phase ◽  
Phase Resetting ◽  
Periaqueductal Gray Matter ◽  
Nerve Activity ◽  
Midbrain Reticular Formation ◽  
Inspiratory Activity ◽  
Adult Cats ◽  
The Times ◽  
End Tidal

This study explores resetting of respiratory rhythm by facilitatory perturbations. The midbrain reticular formation and periaqueductal gray matter were electrically stimulated to evoke facilitation of phrenic nerve activity in nine anesthetized, vagotomized, and glomectomized adult cats. The animals were paralyzed and servo-ventilated to keep end-tidal PCO2 constant. Brief midbrain stimuli were given at various times in the respiratory cycle and the times of onset of rescheduled breaths after stimulation were measured. A plot of phase resetting as a function of stimulus strength and time of delivery defined a helicoid surface. The axis of this helicoid identified a unique stimulus which, when given at the inspiratory-expiratory transition, resulted in unpredictable resetting of respiratory rhythm. This stimulus had a strength that was intermediate to that which identified types 1 and 0 resetting. In one experiment, the singular stimulus often initiated a breath having prolonged inspiratory activity; resumption of the normal rhythm was delayed significantly (P less than 0.01). We conclude that the dysrhythmias observed in this study represent the respiratory oscillator''s phase singularity.

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