Respiratory Muscle Activity Research Articles

Role of the medial medullary reticular formation in relaying vestibular signals to the diaphragm and abdominal muscles

Changes in posture can affect the resting length of respiratory muscles, requiring alterations in the activity of these muscles if ventilation is to be unaffected. Recent studies have shown that the vestibular system contributes to altering respiratory muscle activity during movement and changes in posture. Furthermore, anatomical studies have demonstrated that many bulbospinal neurons in the medial medullary reticular formation (MRF) provide inputs to phrenic and abdominal motoneurons; because this region of the reticular formation receives substantial vestibular and other movement-related input, it seems likely that medial medullary reticulospinal neurons could adjust the activity of respiratory motoneurons during postural alterations. The objective of the present study was to determine whether functional lesions of the MRF affect inspiratory and expiratory muscle responses to activation of the vestibular system. Lidocaine or muscimol injections into the MRF produced a large increase in diaphragm and abdominal muscle responses to vestibular stimulation. These vestibulo–respiratory responses were eliminated following subsequent chemical blockade of descending pathways in the lateral medulla. However, inactivation of pathways coursing through the lateral medulla eliminated excitatory, but not inhibitory, components of vestibulo–respiratory responses. The simplest explanation for these data is that MRF neurons that receive input from the vestibular nuclei make inhibitory connections with diaphragm and abdominal motoneurons, whereas a pathway that courses laterally in the caudal medulla provides excitatory vestibular inputs to these motoneurons.

Effect of pulmonary stretch receptor feedback and CO(2) on upper airway and respiratory pump muscle activity in the rat.

1. Our purpose was to examine the effects of chemoreceptor stimulation and lung inflation on neural drive to tongue protrudor and retractor muscles in the rat. 2. Inspiratory flow, tidal volume, transpulmonary pressure, compliance and electromyographic (EMG) activity of genioglossus (GG), hyoglossus (HG) and inspiratory intercostal (IIC) muscles were studied in 11 anaesthetized, tracheotomized and spontaneously breathing rats. Mean EMG activity during inspiration was compared with mean EMG activity during an occluded inspiration, at each of five levels of inspired CO(2) (0, 3, 6, 9 and 12 %). 3. Lung inflation suppressed EMG activity in all muscles, with the effect on both tongue muscles exceeding that of the intercostal muscles. Static elevations of end-expiratory lung volume evoked by 2 cmH(2)O positive end-expiratory pressure (PEEP) had no effect on tongue muscle activity. 4. Despite increasing inspiratory flow, tidal volume and transpulmonary pressure, the inhibition of tongue muscle activity by lung inflation diminished as arterial PCO2 (P(a),CO(2)) increased. 5. The onset of tongue muscle activity relative to the onset of IIC muscle activity advanced with increases in P(a),CO(2) but was unaffected by lung inflation. This suggests that hypoglossal and external intercostal motoneuron pools are controlled by different circuits or have different sensitivities to CO(2), lung inflation and/or anaesthetic agents. 6. We conclude that hypoglossal motoneuronal activity is more strongly influenced by chemoreceptor-mediated facilitation than by lung volume-mediated inhibition. Hypoglossal motoneurons driving tongue protrudor and retractor muscles respond identically to these stimuli.

Patient-ventilator interaction during noninvasive pressure supported spontaneous respiration in patients with hypercapnic COPD

Noninvasive pressure support ventilation (NPSV) demands triggering with each breath. This study investigates the effects of NPSV via face mask on breathing pattern, ventilation and respiratory muscle loading in patients with hypercapnic stable COPD. 7 patients (age 66 +/- 9 years; FEV1 43 +/- 13% predicted; PaO2 52 +/- 19 mmHg; PaCO2 58 +/- 12 mmHg) were included. The physiologic variables were evaluated during spontaneous breathing and at the end of a 60 minutes period with NPSV. Inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) were adjusted to 12-14 cm H2O and 3 cm H2O, respectively. Respiratory muscle activity was measured as esophageal and transdiaphragmatic pressure time product (PTPes and PTPdi). Non-triggering was observed only occasionally. Compared to unsupported spontaneous breathing NPSV improved ventilation: PaCO2 was reduced from 58 +/- 11 mmHg to 50 +/- 14 mmHg (p +/- 0.05). Respiratory muscles were unloaded by 30% (p +/- 0.05). Breathing frequency and breathing pattern did not change. In patients with hypercapnic stable COPD NPSV effectively recognizes and supports breathing efforts. As a result ventilation is improved and respiratory muscles are unloaded.

Respiratory Muscle Activity Measured with a Noninvasive EMG Technique: Technical Aspects and Reproducibility.

Respiratory Muscle Activity Measured with a Noninvasive EMG Technique: Technical Aspects and Reproducibility.

Modulations in respiratory and laryngeal activity associated with changes in vocal intensity during speech.

We tested the hypothesis that different strategies are used to alter tracheal pressure (Pt) during sustained and transient increases in intensity. It has been suggested that the respiratory system plays the primary role in Pt changes associated with alteration in overall intensity, whereas laryngeal adjustment is primary for transient change in Pt related to emphasis. Tracheal pressure, obtained via tracheal puncture, airflow (U), and laryngeal electromyography from the thyroarytenoid muscle (TA EMG) were collected from 6 subjects during sentence production at different intensity levels and with various stress patterns. Using a technique described in a previous study, we computed lower airway resistance (Rlaw) from measures of Pt and U obtained during a sudden change in upper airway resistance. We used this resistance value, together with direct measures of Pt and U during speech, to derive a time-varying measure of alveolar pressure (Pa), the pressure created by respiratory muscle activity and elastic recoil of the lungs. Pa provided a measure of respiratory drive that was unaffected by laryngeal activity. Laryngeal airway resistance (Rlx) and TA EMG provided measures of laryngeal activity. The results of this study indicated that, contrary to the outcome predicted by the hypothesis, there was no difference in the strategies used to alter Pt during sustained and transient increases in intensity. Although changes in both Pa and Rlx contributed to increase in Pt, the contribution of Pa was substantially greater. On average, Pa contributed to 94% and Rlx to 6% of the increase in Pt associated with vocal intensity. A secondary purpose of the study was to determine the extent to which laryngeal muscle activity was related to Rlx during speech. We found TA EMG activity increased with intensity but was not well correlated with Rlx, suggesting that when it contracts, the TA muscle may affect intensity by loosening the cover, which allows for greater amplitude of vocal fold vibration, without necessarily increasing laryngeal airway resistance.

Respiratory muscle activity measured with a noninvasive EMG technique: technical aspects and reproducibility.

A new method is being developed to investigate airway obstruction in young children by means of noninvasive electromyography (EMG) of diaphragmatic and intercostal muscles. The purpose of this study was to evaluate the reproducibility of the EMG measurements. Eleven adults, 39 school children (20 healthy, 19 asthmatic), and 16 preschool children were studied during tidal breathing on separate occasions: two for adults with a time interval of 3 wk and three for children with time intervals of 1 and 24 h. Single electrodes were placed on the second intercostal space left and right of the sternum and at the height of the frontal and the dorsal diaphragm. Bipolar electrode pairs were placed on the rectus abdominis muscle. A newly designed digital physiological amplifier without any analog filtering was used to measure the EMG signals. Except for the average dorsal diaphragm EMG derivation in healthy school children on the second occasion, a significant correlation between the mean peak-to-peak inspiratory activity of average diaphragmatic and intercostal EMG was found in the different age groups on the different measurement occasions (P < 0.05). To assess the repeatability, we described the agreement between the repeated measurements within the same subjects. No significant differences were found between the measurements on the separate occasions. Our observations indicate that the EMG signals derived from the diaphragm and intercostal muscles are, in different age groups with and without asthma, reproducible during tidal breathing.

The contribution of the cerebellum to speech processing

Lesions to or diseases of the cerebellum may disrupt the motor components of speech production both at the segmental and suprasegmental level giving rise to “ataxic dysarthria”, a syndrome characterized, among others, by slowed speaking rate, distorted consonant and vowel productions and impaired prosodic modulation of sentence utterances. The concept of ataxic dysarthria has been further refined by measurements at the acoustic speech signal, tracking of articulatory movements and preliminary functional imaging studies. In summary, the available parametric data indicate the cerebellum to support several aspects of speech processing: acceleration of orofacial gestures, timing (coordination) of complex articulatory sequences, presumably, in cooperation with the anterior perisylvian language zone and control of brainstem reflexes monitoring respiratory and laryngeal muscle activity. Lesion studies and functional imaging indicate superior aspects of the cerebellum to mediate the speech motor functions referred to. Laterality and extent of the respective representation area, presumably, depend upon task demands. Besides speech motor deficits, recent investigations found disrupted speech perception in cerebellar subjects in terms of impaired categorization of specific durational minimal pairs.

Study of myographic signals from sternomastoid muscle in patients with chronic obstructive pulmonary disease.

Analysis of the respiratory muscle activity is a promising technique for diagnosis of respiratory diseases, such as chronic obstructive pulmonary disease (COPD). The sternomastoid muscle (SMM) was selected to study the activity of respiratory muscles due to its accessibility in order to define a noninvasive analysis. The aims of this work are two: analyze the relationship between the SMM function and pulmonary obstruction, and study the influence of spectral estimator on frequency parameters related with the muscle activity. For the first goal, we propose the analysis of vibromyographic and electromyographic signals from the SMM to study the muscle function during two ventilatory tests. Activity of SMM was found by means of several indexes: root-mean-square (rms) values, mean and median frequencies, and ratio between high and low-frequency components. For the second goal, spectral analysis was performed by means of nonparametric methods: Correlogram and Welch periodogram, and parametric methods: autoregressive (AR), moving average (MA), and ARMA models. It is deduced that these indexes show muscle activity and certain fatigue of the SMM, whose muscle function depends on the level of pulmonary obstruction, and they depend a lot of spectral estimator being the more suitable an AR model with high order.

Impact of brainstem sleep mechanisms on pharyngeal motor control

Suppression of respiratory muscle activity in sleep, particularly evident in the pharyngeal muscles, is pivotal to the pathogenesis of common sleep-related breathing disorders such as obstructive sleep apnea. Obstructive apneas are caused by sleep-related decrements in pharyngeal muscle activity that leads to snoring and airway obstruction in individuals with underlying structural narrowing of the upper airway. Since obstructive apneas occur exclusively during sleep, this disorder by definition is state-dependent and ultimately caused by the influences of brainstem sleep mechanisms on pharyngeal motoneurons in individuals with compromised upper airway anatomy. This paper reviews the central neuronal mechanisms by which sleep reduces the output to the pharyngeal muscles and the neurotransmitters implicated in this alteration. The experimental approaches used to address this problem are also mentioned and their relative advantages and disadvantages discussed. In particular, the information derived from reduced animal preparations is reviewed and the need for studies in natural sleep is emphasised. Identifying the central neuronal mechanisms and neurotransmitters involved in sleep-related suppression of pharyngeal muscle activity not only has important basic relevance to understanding state-dependent respiratory control, it also has immediate clinical relevance to understanding common sleep-related breathing disorders at the central neuronal level. Determining these basic mechanisms also has immediate clinical relevance to understanding the pathogenesis of airway occlusions, and guiding neuro-pharmacological approaches aimed at preventing the sleep-related decrements in pharyngeal muscle tone that are ultimately the root cause of obstructive sleep apnea.

Sound-induced laryngeal and respiratory reflexes originate from vestibular afferents.

To determine whether the auditory or vestibular system causes the sound-induced laryngeal reflex, which has been considered to participate in the auditory feedback control of vocalization, click-induced laryngeal responses were compared before and after sectioning of the cochlear and/or vestibular nerves in cats. The sound-induced reflex modulation of respiratory muscle activity was also investigated, because respiratory movement is important for vocal control. Sectioning of the cochlear nerves had little influence on these responses. In contrast, sectioning of the vestibular nerves abolished these responses. It was concluded that the sound-induced laryngeal and respiratory reflexes are attributed to the vestibular system.

Energy expenditure during physiotherapist-assisted and self-treatment in cystic fibrosis

Cystic fibrosis (CF) results in increased energy requirements at rest. However, the energy expended during physiotherapy management is unknown. The aim of this study, therefore, is to examine the energy expended during two commonly used forms of chest physiotherapy in CF subjects. Twenty-six CF subjects completed a randomised crossover trial with 48 hours between treatments. Two regimens of treatment were conducted: therapist-assisted treatment (active cycle of breathing, ACBT, with percussion, vibration), and independent treatment (ACBT alone, under the supervision of a physiotherapist). Subjects completed pulmonary function tests before and after either treatment. Indirect calorimetry and oximetry parameters were recorded at rest, during, and following treatment. Treatment groups were compared using ANOVA and two-sample crossover t-tests. When compared to resting values, physiotherapy treatment resulted in significant increases in VO2, VCO2 and respiratory exchange ratio. No difference was evident between treatment regimens for the change in VO2 between baseline and treatment. The increase in ventilation (baseline to treatment) was significantly greater for the therapist-assisted treatment. The therapist-assisted ACBT was associated with a significant carryover effect for forced expiratory flow at 50% of vital capacity (FEF50). Oxygen requirements for the two treatments were similar. However, the assisted regimen resulted in greater changes in minute ventilation during treatment and improved 48-hour post-treatment pulmonary function after only one treatment session. These findings suggest that the inclusion of percussion and vibration within the ACBT may influence respiratory muscle activity during treatment and result in improved pulmonary function.

Breathing pattern in patients with Parkinson’s disease

The improvement in motor performance resulting from levodopa administration in patients with Parkinson’s disease (PD) provides the opportunity to investigate ventilatory changes brought about by the disease. The aim of this study has been to investigate these changes in order to specify the mechanisms of the impairment in breathing in PD. Breathing patterns at rest were investigated in 11 patients with idiopathic PD both before (Off) and after (On) administration of levodopa at a dose improving their motor performance by at least 30%. Airflow (Fleisch head mounted on a mask), rib cage and abdomen movements (inductance plethysmography) were recorded in the Off condition 1 h after subjects woke up. Subjects then received levodopa and a new set of recordings was obtained 1 h later, in the On condition. Breath-by-breath processing of recordings was carried out and tidal volume (Vt), inspiratory (Ti) and expiratory (Te) durations were measured. The main finding was a lengthening of Ti resulting in a decrease in ventilation and in Vt/Ti, and an increase in Ti/Ttot in the On compared to the Off condition. In the On condition abnormal rib cage–abdomen plots patterns were found in four out of six subjects. A hypothesis on the effect of PD on breathing is proposed on grounds of normal diaphragmatic activity but impaired activity of the other respiratory muscles and more specifically the intercostal muscles.

Estimation of alveolar pressure during speech using direct measures of tracheal pressure.

The pressure in the alveoli of the lungs, created by the elastic recoil of the lungs and respiratory muscle activity, is referred to as alveolar pressure (Pa). The extent to which tracheal pressure (Pt) approximates Pa depends on the resistance to airflow offered by structures above and below the point at which tracheal pressure is measured. An understanding of the relationship among Pa, Pt, and upper and lower airway resistance, and how these values fluctuate during speech, could aid in interpretation and modeling of speech aerodynamics. The purpose of this study was to (a) obtain values for lower airway resistance (Rlow), (b) use these Rlow values to estimate Pa during speech, and (c) quantify the degree to which Pt approximates Pa during production of voiced and voiceless sounds, in comparison to inhalation. In addition, the results were discussed in terms of the degree to which the respiratory system functions as a pressure source. Tracheal pressure (obtained with tracheal puncture) and airflow were measured during sentence production in 6 subjects. Using a technique introduced in this paper, Rlow was determined from measures of tracheal pressure and flow obtained during a sudden change in upper airway resistance because of release of a voiceless plosive. Mean Rlow values ranged from 0.14 to 0.32 kPa/(l/s). Each subject's mean Rlow was used to derive a time-varying measure of Pa during speech from continuous measures of tracheal pressure and airflow. Pt was approximately 95% of Pa during phonation (i.e., when the vocal folds were adducted), 75% of Pa during release of the voiceless stop consonant /p/, and 55% of Pa during inhalation (i.e., when the vocal folds were abducted). Therefore, the degree to which the respiratory system functioned as an ideal pressure source varied during speech. The ability to estimate Pa provides a measure of the pressure produced by the respiratory system that is not influenced by laryngeal activity.

Fuerza y resistencia de los músculos respiratorios en pacientes con SAHS. Efecto de la aplicación nocturna de CPAP

During nighttime episodes of obstructive apnea in patients with sleep apnea-hypopnea syndrome (SAHS), repeated and progressive inspiratory efforts are made. Such intense nighttime activity can have a deleterious effect on daytime function of respiratory muscles. The objective of this study was to evaluate daytime respiratory muscle function in a group of SAHS patients before and after two months of treatment with nighttime continuous positive airway pressure (CPAP). We enrolled 12 patients with SAHS and 10 normal subjects (control group). To evaluate respiratory muscle strength we measured maximum esophageal pressure (Pesmax), transdiaphragmatic pressure (Pdimax) and inspiratory pressure in the mouth (PM). Respiratory muscle resistance was assessed using peak pressure in the mouth (PMPeak), time of tolerance (Tlim) and maximum inspiratory pressure-time index (PTimax). We also analyzed the nighttime function of respiratory muscles during apneic episodes in 10 of the 12 SAHS patients. We propose and define an index of nighttime respiratory muscle activity (RMian) as the product of the tension-time index for the diaphragm observed at the end of nighttime apneic episodes (TTdiapnea) and the apnea-hypopnea index (AHI). Respiratory muscle strength was similar in the two groups and no changes were observed in SAHS patients after treatment with nighttime CPAP. However, tolerance was lower in SAHS patients (PMpeak--30%, Tlim--31% and PTimax--49%). Two months of nighttime CPAP normalized all three variables in these patients. MRian was related to percent improvement in PMpeak after treatment with nighttime CPAP in SAHS patients (r = 0.66, p < 0.04). SAHS has an adverse effect on the daytime endurance of respiratory muscles that is proportional to the increase of nighttime mechanical muscle activity. The application of nighttime CPAP is restorative, probably because it allows respiratory muscles to rest.

Model of functional restriction in chronic obstructive pulmonary disease, transplantation, and lung reduction surgery.

Mechanical interactions between lung and chest wall are important determinants of respiratory function. When chest wall expansion during maximal inhalation generates insufficiently negative pleural pressures, the lungs remain functionally underinflated; this may be termed functional restriction. To explore mechanisms and effects of functional restriction in patients with emphysema, and to predict effects of single lung transplantation and lung volume reduction surgery (LVRS), we used a computational model based on standard physiology and measurements from individual patients. The model's lungs, separated by a compliant mediastinum, exhibit flow limitation according to the equal pressure point approach of Mead and coworkers. Pulmonary elastic recoil pressure is characterized by an exponential equation modified to reflect airway closure. Simulated respiratory maneuvers can be specified by variations in flow or pressure at the airway opening or in respiratory muscle activation. Model simulations successfully mimic recordings from individual patients. Input parameter values may then be altered to predict effects of surgical interventions in these same patients. The model simulations show the following. Single lung transplantation in emphysema can cause functional restriction of the normal transplanted lungs, and larger transplanted lungs may perform less well than smaller ones. LVRS improves lung and chest wall function in emphysema, but not in normal states. Surgical reduction of the native emphysematous lung after single lung transplantation can reduce functional restriction of the transplant and thereby improve its function.

Sleep-related changes in the human ‘neuromuscular’ ventilatory response to hypoxia

The ventilatory responses to hypercapnia and hypoxia are reduced during sleep compared to wakefulness. However, sleep-related increases in upper airways’ resistance could reduce these ventilatory responses independently of any change in the neural output to the respiratory pump muscles. It is therefore possible that respiratory chemosensitivity, per se, is unchanged by sleep. To investigate this, four healthy male subjects were mechanically ventilated to abolish spontaneous respiratory muscle activity. The response to transient isocapnic hypoxia was quantified from the magnitude of the electromyographic activity induced in the diaphragm and from the associated reduction in peak inspiratory pressure; these indicies of respiratory motor output will not be affected by any sleep-related changes in upper airways’ resistance. In all individuals, the responses to hypoxia were markedly attenuated during sleep compared to wakefulness. These observations, assessing the ‘neuromuscular’ ventilatory response, are consistent with a sleep-related reduction in respiratory chemosensitivity that is independent of any changes that may be due to increases in upper airways’ resistance.

Modified Campbell diagram to assess respiratory muscle action in speech.

Ten normal and four moderate to severe stutterers participated in the study. Pleural (Ppl) and abdominal (Pab) pressure was studied using oesophageal and gastric balloon catheter systems and VL (VL) was studied using magnetometry. The classical Campbell diagram was modified by plotting Pab versus VL. In a preliminary study we determined whether a surrogate curve could be substituted for the true curve in the Campbell diagram. We obtained true relaxation curves in six subjects. We obtained surrogate chest wall relaxation curves by joining the Pab value at functional residual capacity (FRC) to a point on the dynamic expiratory Pab, VL curve where Pab had decreased to half its maximum inspiratory excursion. In order to obtain the mirror image of the elastic recoil curve of the lung subjects breathed slowly from FRC to total lung capacity. Dynamic Pab, VL and Ppl, VL measurements during quiet breathing and speech were superimposed on static lung and chest wall curves. The simultaneous plot of Ppl and Pab provided a continuous measure of transdiaphragmatic pressure as a function of VL. We inferred non-diaphragmatic muscle recruitment vis-à-vis the diaphragm by the relationship of Pab to Ppl and Pab to the relaxation curve. We compared dynamic Ppl during phonation with that during breath-holding with the glottis open at the same VL, as an estimate of subglottic pressure (Psg). Analysis of variance testing showed that the true, surrogate and predicted relaxation slopes were not significantly different. The strategies that stutterers used to speak were either higher or lower VL than normal subjects and they had a different pattern of respiratory muscle recruitment. Stutterers were unable to achieve the appropriate degree of recruitment to develop and maintain a normal Psg for conversational speech and this contributed to dysfluency. We conclude that the quiet breathing loops can provide a reasonable approximation to the relaxation curve in normal healthy subjects and that modifications to the Campbell diagram provide useful means of measuring Psg and assessing respiratory muscle recruitment patterns.

Pontine carbachol elicits multiple rapid eye movementsleep-like neural events in urethane-anaesthetized rats

Microinjection of a cholinergic agonist, carbachol, into the pontine reticular formation of chronically instrumented intact or acutely decerebrate rats and cats has been used extensively to study rapid eye movement sleep mechanisms. In this study, we sought to develop a reduced carbachol model of rapid eye movement sleep-like neural events exhibiting multiple physiological markers of this state, and allowing for the use of invasive electrophysiological techniques. Accordingly, we investigated whether pontine carbachol could produce rapid eye movement sleep-like motor atonia and electrocortical changes in urethane-anaesthetized rats. We recorded cortical and hippocampal electroencephalograms and genioglossus and inspiratory intercostal muscle activities in 13 urethane-anaesthetized, spontaneously breathing, tracheotomized and vagotomized rats. In steady-state periods with high-voltage/low-frequency electroencephalogram activity, carbachol microinjections (15–40 nl, 10 mM) were placed in the medial pontine reticular formation. In 12 rats, carbachol elicited episodes of stereotyped hypotonia of genioglossus but not intercostal muscle activity, typical of rapid eye movement sleep, with a latency and duration of 2.2±0.3 min (mean±S.E.M.) and 11.0±2.9 min, respectively. In four of these rats, also similar to rapid eye movement sleep, the major suppression of genioglossus activity (−74±9%) was accompanied by electroencephalogram desynchronization, appearance of hippocampal theta rhythm, and a respiratory rate increase (+14±3%). In the remaining eight rats, the stereotyped suppression of genioglossus activity (−48±3%) occurred without electroencephalogram desynchronization and hippocampal theta, and was accompanied by a respiratory rate decrease (−6±2%); a pattern of response typical of decerebrate animals. Within a rat, similar patterns of response to repeated carbachol injections at the same anatomical site were obtained. Pontine atropine prevented responses to subsequent carbachol injections. Thus, in urethane-anaesthetized rats, pontine carbachol consistently produced a differential suppression of pharyngeal versus respiratory pump muscle activity, and in a subset of animals, this was also accompanied by cortical and hippocampal electrographic changes typical of rapid eye movement sleep. This shows that complex and stereotyped neuronal events underlying both ascending and descending signs of rapid eye movement sleep can be pharmacologically activated under general anaesthesia. Such a reduced preparation may be useful for studies into the central neuronal mechanisms underlying generation of rapid eye movement sleep; particularly for studies requiring techniques that are difficult to implement in intact, naturally sleeping animals. The acceleration of the respiratory rate observed only when carbachol induced electroencephalogram desynchronization suggests that neural events associated with electrocortical changes contribute to the respiratory rate increases observed in natural rapid eye movement sleep.

Characterization of pontine neurons which respond to hypoxia in fetal sheep

Hypoxia causes apnea and postural muscle hypotonia in fetal sheep, a response thought to arise by descending inhibition from a group of lateral pontine neurons that express FOS protein after hypoxia. To determine the neurochemical phenotype, and whether these neurons project to the cervical spinal cord, the retrograde tracer CTB-gold was injected into the C5-C8 ventral horn of four fetal sheep at 110 days gestation. Then, at 135 days each fetus was made hypoxic for 2 h by allowing the mother to breathe 7–8% O 2. Immunocytochemistry showed that FOS-positive neurons in the subcoeruleus and Kolliker–Fuse regions of the pons were catecholaminergic, but not cholinergic or GABAergic, and a proportion of them contained CTB-gold particles, indicating direct connection with the cervical spinal cord. We suggest that these pontine neurons inhibit respiratory and postural muscle activities during hypoxia in fetal sheep.

Résisteur de starling et stabilité du couple sommeil-ventilation

The upper airway can be described as a collapsible segment (the pharynx) interposed between two rigid bony (the cavum) or cartilaginous (the trachea) segments. Due to this structure, the pharynx behaves as a collapsible tube, in which airflow does not depend on the downstream pressure, but is limited to a maximum value which depends only on the upstream pressure and on the pressure surrounding the collapsible segment; this behavior, known as a Starling resistor can be modeled by the waterfall effect. Thus, the upper airways can be in three different conditions: an occluded condition, in which no flow is possible, a patent condition, in which flow depends on the difference between upstream and downstream pressures (according to Poiseuille's law), and a situation in which flow is limited. The behavior of the upper airway is largely dependent on its anatomic structure, but functional factors play a critical role. Among these sleep state is both a determinant of the collapsibility of the pharynx, and determined by the simulation of upper airway mechanoreceptors whose activity depends on the activity of respiratory muscles. Thus the interplay of three factors: ventilatory drive, upper airway collapsibility, and arousal threshold can predict most of the situations of stable and unstable ventilatory behavior during sleep. The level of the arousal threshold governs the stability of the ventilatory pattern, as it determines whether a combination of slow, respiratory effort, and blood gases can be maintained or is interrupted by an arousal.