Intercostal Activity Research Articles

Relative impact of respiratory muscle activity on tidal flow and end expiratory volume in healthy neonates

It has been suggested that infants dynamically regulate their tidal flow and end-expiratory volume level. The interaction between muscle activity, flow and lung volume in spontaneously sleeping neonates is poorly studied, since it requires the assessment of transcutaneous electromyography of respiratory muscles (rEMG) in matched comparison to lung function measurements. After determining feasibility and repeatability of rEMG in 20 spontaneously sleeping healthy neonates, we measured the relative impact of intercostal and diaphragmatic EMG activity in direct comparison to the resulting tidal flow and FRC. We found good feasibility, repeatability and correlation of timing indices between rEMG activity and flow. The rEMG amplitude was significantly dependent on the resistive load of the face mask. Diaphragm and intercostal muscle activity commenced prior to the onset of flow and remained active during the expiratory cycle. The relative contribution of intercostal and diaphragmatic activity to flow was variable and changed dynamically. Using matched rEMG, air flow and lung volume measurements, we have found good feasibility and repeatability of intercostal and diaphragm rEMG measurements and provide the first quantitative measures of the temporal relationship between muscle activity and flow in spontaneously sleeping healthy neonates. Lung mechanical function is dynamically regulated and adapts on a breath to breath basis. So, non-invasive rEMG measurements alone or in combination with lung function might provide a more comprehensive picture of pulmonary mechanics in future studies. The data describing the timing of EMG and flow may be important for future studies of EMG triggered mechanical ventilation.

Aminophylline increases parasternal intercostal muscle activity during hypoxia in humans

To clarify the mechanism of action of aminophylline on the hypoxic ventilatory response in humans, we analyzed the effects of aminophylline on respiratory neural output. To evaluate the respiratory neural output, we analyzed the electromyogram (EMG) of the parasternal intercostal muscle, one of the major inspiratory muscles, in eight healthy subjects. Both before and during aminophylline administration, measurements of ventilatory parameters with EMG recordings were conducted in room air, mild hypoxia (F(I)(o)(2) 0.15), and severe hypoxia (F(I)(o)(2) 0.11). Before administering aminophylline, hypoxic stimulation elicited ventilatory augmentation in a hypoxia-intensity dependent manner. Administration of aminophylline caused significant increases in ventilation (V (I)), tidal volume (V(T)), respiratory frequency (f(R)), and the respiration-related phasic moving averaged EMG amplitude (tidal EMG), at corresponding levels of hypoxia compared to before aminophylline. Augmentation patterns of hypoxia-induced increases in V(T) and tidal EMG showed close similarity. These results indicate that augmentation of hypoxic ventilatory response by aminophylline is mainly mediated by an increase in the respiratory neural drive in healthy humans.

External intercostal muscles and external anal sphincter electromyographic activity during coughing

Few studies focused on concomitant electromyographic recordings of pelvic floor muscles and muscles involved in cough initiation. The objective of this study was to investigate the temporal course of external anal sphincter activation during coughing. Informed consent was obtained from ten healthy volunteers and ten women presenting with stress urinary incontinence (SUI). Simultaneously, recordings of electromyographic activity of external intercostal muscles (EIC EMGi) and external anal sphincter (EAS EMGi) during coughing have been performed. It was chosen to study intercostals muscles because they are synchronous to diaphragmatic muscle during cough initiation. Median (interquartile range) latency between the onset of the EAS EMGi and the onset of the EIC EMGi was -210 ms (-398; -135) and 0 ms (-30; +111.7) in volunteers' group and in SUI group, respectively (p = 0.0009). Abnormal temporal course of external anal sphincter activation is observed during coughing in women presenting with SUI compared to healthy volunteers.

Abnormal pelvic response to cough in women with stress urinary incontinence

To assess how muscular fatigue deteriorates the modulation of pelvic contraction during increasing cough efforts. Furthermore, we investigated the correlation between the temporal course of pelvic floor activation during cough. Informed consent was obtained from 20 women presenting with SUI and 6 continent women (overactive bladder syndrome [OAB]). Bladder pressure (BP) and external anal sphincter electromyographic activity (EAS EMGi) were recorded concomitantly during increasing cough efforts. Modulation of pelvic contraction was assessed before and after two types of intense pelvic exercise (Exercise #1: 10 successive strong cough efforts; Exercise #2: 10 pelvic contractions followed by a maximal pelvic contraction) at 0, 200, and 400 ml of bladder filling. We have also recorded electromyographic activity of external intercostal (EIC) muscles. Whereas the Exercise 1 had no effect on modulation, the Exercise 2 altered significantly the modulation of pelvic contraction during increasing cough efforts (P = 0.043) only in women presenting with SUI. The bladder filling volume seems to not significantly modify this modulation (P = 0.12). Median latency between the onset of the EAS EMGi and the onset of the EIC EMGi was -470 and -60 msec in OAB group and in SUI group, respectively (P = 0.012). There was a good correlation between mean latency (default of EAS EMGi pre-activation) and an altered modulation of pelvic contraction during increasing cough efforts (P = 0.040). Some women with SUI exhibit an altered pattern of the PFM response during increasing coughing efforts. The lack of this modulation of PFM response to stress may be one of the pathophysiologic factors of SUI.

Intercostal Muscle Contraction or Rib Bone Marrow Activity?

Diffuse and uniform FDG uptake in the ribs and the intercostal muscles might appear similar on FDG-PET images and a reliable differentiation between the two is important for accurately identifying the underlying process. The former usually suggests excessive contraction of intercostal muscles mostly due to chronic obstructive pulmonary disease, whereas the latter signifies either bone marrow stimulation or involvement by a pathologic process. At times, images may appear confusing and may be misinterpreted. However, in both clinical settings, there are additional ancillary signs, which are helpful in making a correct diagnosis. We herein present 2 case vignettes from each category in which other ancillary signs helped to distinguish FDG rib uptake from intercostal muscle uptake.

Role of pleural pressure in the coupling between the intercostal muscles and the ribs

The inspiratory intercostal muscles elevate the ribs and thereby elicit a fall in pleural pressure (DeltaPpl) when they contract. In the present study, we initially tested the hypothesis that this DeltaPpl does, in turn, oppose the rib elevation. The cranial rib displacement (Xr) produced by selective activation of the parasternal intercostal muscle in the fourth interspace was measured in dogs, first with the rib cage intact and then after DeltaPpl was eliminated by bilateral pneumothorax. For a given parasternal contraction, Xr was greater after pneumothorax; the increase in Xr per unit decrease in DeltaPpl was 0.98+/-0.11 mm/cmH2O. Because this relation was similar to that obtained during isolated diaphragmatic contraction, we subsequently tested the hypothesis that the increase in Xr observed during breathing after diaphragmatic paralysis was, in part, the result of the decrease in DeltaPpl, and the contribution of the difference in DeltaPpl to the difference in Xr was determined by using the relation between Xr and DeltaPpl during passive inflation. With diaphragmatic paralysis, Xr during inspiration increased approximately threefold, and 47+/-8% of this increase was accounted for by the decrease in DeltaPpl. These observations indicate that 1) DeltaPpl is a primary determinant of rib motion during intercostal muscle contraction and 2) the decrease in DeltaPpl and the increase in intercostal muscle activity contribute equally to the increase in inspiratory cranial displacement of the ribs after diaphragm paralysis.

Effects of single‐lung inflation on inspiratory muscle function in dogs

After single-lung transplantation (SLT) for emphysema, a hyperinflated (native) lung operates in parallel with a normal (transplanted) lung. The interpulmonary distribution of the changes in pleural pressure (DeltaP(pl)) during breathing, however, is unknown. To approach the problem, two endotracheal tubes were inserted in the right and left main stem bronchi of anaesthetized dogs, one lung was passively inflated, and the values of inspiratory DeltaP(pl) over the two lungs were assessed by measuring the changes in airway opening pressure (DeltaP(ao)) in the two tubes during occluded breaths. With single-lung inflation, DeltaP(ao) decreased in both lungs, but the decrease in the inflated lung was invariably larger than in the non-inflated lung; when transrespiratory pressure in the inflated lung was set at 30 cmH(2)O, DeltaP(ao) in this lung was 27.7 +/- 2.0% of the value of functional residual capacity (FRC), whereas DeltaP(ao) in the non-inflated lung was 74.4 +/- 4.5% (P < 0.001). This difference was abolished after the ventral mediastinal pleura was severed. The ribs in both hemithoraces were displaced cranially with inflation, such that the displacement in the contralateral hemithorax was 75% of that in the ipsilateral hemithorax, and parasternal intercostal activity remained unchanged. These observations suggest that in patients with SLT for emphysema (1) the inspiratory DeltaP(pl) over the transplanted lung are greater than those over the native lung and (2) this difference results primarily from the greater pressure-generating ability of the inspiratory muscles, in particular the diaphragm, on the transplanted side.

Respiratory muscle activity and respiratory obstruction after abdominal surgery

Respiratory movements in patients after abdominal surgery are frequently abnormal, with associated disturbances in the pattern of inspiratory pressure generation. The reasons for these abnormalities are not clear and have been attributed to impaired action of the diaphragm. However, an alternative is that partial airway obstruction could trigger reflex activation of the inspiratory ribcage muscles, which would cause a similar pattern of inspiratory pressure change. Direct measurement of electrical activity can indicate if reflex activation of inspiratory muscles occurs when partial airway obstruction is present. In an open study, we implanted electrodes to measure the EMG of scalene, intercostal and external oblique abdominal muscles in patients after lower abdominal surgery. Analgesia was with morphine i.v. by patient control. We used nasal cannulae to measure nasal airflow and compared EMG activity when airway obstruction was present with activity when breathing was not obstructed. The pattern of activity of the different muscles was distinct. Intercostal activity reached a maximum during inspiration, before the scalene muscles, whereas scalene activity increased in phase with increasing lung volume. Abdominal muscle activity commenced when expiratory flow had ceased and continued until the next inspiration. In all three muscle groups, partial airway obstruction did not alter muscle activity. Partial airway obstruction does not activate inspiratory ribcage muscles, in patients receiving morphine for postoperative analgesia after lower abdominal surgery. Changes in respiratory pressures and abnormalities of chest wall movement described in previous studies cannot be attributed to reflex responses and probably result from increased airway resistance and abdominal muscle action.

External anal sphincter contraction during cough: Not a simple spinal reflex

To assess whether the anal contraction during voluntary coughing is a simple spinal reflex-mediated activity or not. To address this question we studied the external intercostal (EIC) muscle activity and external anal sphincter (EAS) response to cough. Electromyographic recordings were made from pre-gelled disposable surface electrodes. EAS electromyographic recordings were made from the EAS of the pelvic floor in 15 continent women all suffering from urgency and/or frequency without urge or stress urinary incontinence, and referred for urodynamic investigation. Electromyographic signal was immediately integrated (EMGi). The abdominal pressure was recorded with bladder and rectal pressure. EAS EMGi was recorded during successive voluntary cough. In three women, we have also recorded EIC EMGi activity since it is synchronous with diaphragmatic EMG activity during cough initiation. In all subjects, EAS EMGi activity precedes the onset of the abdominal pressure increase. The mean latency of EAS EMGi was 615 msec (+/-278). In the three subjects whose EMGi activity was recorded both on EAS and EIC, the onset of EAS EMGi activity occurred before the EIC EMGi activity (latency ranging from 40 to 780 msec) and before the increase in the abdominal pressure. The present study suggests that during coughing, EAS EMG activity increases before external intercostal muscle EMGi activity. The contraction of the EAS preceding the activation of muscles involved in coughing indicates that this response is not a result of a simple spinal reflex, but more likely the result of a more intricate reflex involving complex integrative centers.

Gas exchange during separate diaphragm and intercostal muscle breathing.

In patients with diaphragm paralysis, ventilation to the basal lung zones is reduced, whereas in patients with paralysis of the rib cage muscles, ventilation to the upper lung zones in reduced. Inspiration produced by either rib cage muscle or diaphragm contraction alone, therefore, may result in mismatching of ventilation and perfusion and in gas-exchange impairment. To test this hypothesis, we assessed gas exchange in 11 anesthetized dogs during ventilation produced by either diaphragm or intercostal muscle contraction alone. Diaphragm activation was achieved by phrenic nerve stimulation. Intercostal muscle activation was accomplished by electrical stimulation by using electrodes positioned epidurally at the T(2) spinal cord level. Stimulation parameters were adjusted to provide a constant tidal volume and inspiratory flow rate. During diaphragm (D) and intercostal muscle breathing (IC), mean arterial Po(2) was 97.1 +/- 2.1 and 88.1 +/- 2.7 Torr, respectively (P < 0.01). Arterial Pco(2) was lower during D than during IC (32.6 +/- 1.4 and 36.6 +/- 1.8 Torr, respectively; P < 0.05). During IC, oxygen consumption was also higher than that during D (0.13 +/- 0.01 and 0.09 +/- 0.01 l/min, respectively; P < 0.05). The alveolar-arterial oxygen difference was 11.3 +/- 1.9 and 7.7 +/- 1.0 Torr (P < 0.01) during IC and D, respectively. These results indicate that diaphragm breathing is significantly more efficient than intercostal muscle breathing. However, despite marked differences in the pattern of inspiratory muscle contraction, the distribution of ventilation remains well matched to pulmonary perfusion resulting in preservation of normal gas exchange.

Mechanical effect of muscle spindles in the canine external intercostal muscles.

High-frequency mechanical vibration of the ribcage increases afferent activity from external intercostal muscle spindles, but the effect of this procedure on the mechanical behaviour of the respiratory system is unknown. In the present study, we have measured the changes in external intercostal muscle length and the craniocaudal displacement of the ribs during ribcage vibration (40 Hz) in anaesthetized dogs. With vibration, external intercostal inspiratory activity increased by approximately 50 %, but the respiratory changes in muscle length and rib displacement were unaltered. A similar response was obtained after the muscles in the caudal segments of the ribcage were sectioned and the caudally oriented force exerted by these muscles on the rib was removed, thus suggesting that activation of external intercostal muscle spindles by vibration generates little tension. Prompted by this observation, we also examined the role played by the external intercostal muscle spindles in determining the respiratory displacement of the ribs during breathing against high inspiratory airflow resistances. Although resistances consistently elicited prominent reflex increases in external intercostal inspiratory activity, the normal inspiratory cranial displacement of the ribs was reversed into an inspiratory caudal displacement. Also, this caudal rib displacement was essentially unchanged after section of the external intercostal muscles, whereas it was clearly enhanced after denervation of the parasternal intercostals. These findings indicate that stretch reflexes in external intercostal muscles confer insufficient tension on the muscles to significantly modify the mechanical behaviour of the respiratory system.

Contribution of spindle reflexes to post‐inspiratory activity in the canine external intercostal muscles

1. The external intercostal muscles have greater post-inspiratory activity than the parasternal intercostal muscles and are more abundantly supplied with muscle spindles. In the present study, the hypothesis was tested that spindle afferent inputs play a major role in determining this activity. 2. The electrical activity of the external and parasternal intercostal muscles in the rostral interspaces was recorded in anaesthetized spontaneously breathing dogs, and the ribs were manipulated so as to alter their normal caudal displacement and the normal lengthening of the muscles in early expiration. 3. Post-inspiratory activity in the external intercostal muscles showed a reflex decrease when the caudal motion of the ribs and the lengthening of the muscles was impeded, and it showed a reflex increase when the rate of caudal rib motion and muscle lengthening was increased. In contrast, the small post-inspiratory activity in the parasternal intercostal muscles remained unchanged. 4. When the two ribs making up the interspace investigated were locked to keep muscle length constant, post-inspiratory activity in the external intercostal muscles was reduced and no longer responded to cranial rib manipulation. 5. These observations confirm that afferent inputs from muscle receptors, presumably muscle spindles, are a primary determinant of post-inspiratory activity in the canine external intercostal muscles. In anaesthetized animals, the contribution of central control mechanisms to this activity is small.

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.

Pitfalls of intramuscular electromyographic recordings from the human costal diaphragm

Objective: Techniques for intramuscular recordings from the costal diaphragm have been described. This report describes procedures to assist with precise placement of these electrodes using ultrasound imaging and describes several sources of error that must be excluded when interpreting recordings made with intramuscular electrodes.Methods: Fine-wire electrodes were inserted into the left costal diaphragm under the guidance of ultrasound imaging in 17 healthy volunteers. Various respiratory maneuvers were performed to confirm the accuracy of the electromyographic (EMG) recordings and the electrode placement was confirmed with intercostal nerve blocks in one subject.Results: EMG recordings can be made from the costal diaphragm. However, despite precise electrode placement and use of intramuscular electrodes with small receptive areas, the EMG recording could be contaminated by cross-talk (discrete motor unit activity) from the adjacent internal intercostal muscle and from movement of the electrode relative to the muscle fibers during breathing. Furthermore, it is necessary to distinguish between expiratory intercostal muscle activity and units in the diaphragm that discharge tonically throughout expiration.Conclusions: While ultrasound guidance of intramuscular electrode insertion can assist with accurate electrode placement in the diaphragm, confirmation of the stability of the recording and absence of cross-talk is critical to avoid misinterpretation of diaphragm function.

Rnx deficiency results in congenital central hypoventilation.

The genes Tlx1 (Hox11), Enx (Hox11L2, Tlx-2) and Rnx (Hox11L2, Tlx-3) constitute a family of orphan homeobox genes. In situ hybridization has revealed considerable overlap in their expression within the nervous system, but Rnx is singularly expressed in the developing dorsal and ventral region of the medulla oblongata. Tlx1-deficient and Enx-deficient mice display phenotypes in tissues where the mutated gene is singularly expressed, resulting in asplenogenesis and hyperganglionic megacolon, respectively. To determine the developmental role of Rnx, we disrupted the locus in mouse embryonic stem (ES) cells. Rnx deficient mice developed to term, but all died within 24 hours after birth from a central respiratory failure. The electromyographic activity of intercostal muscles coupled with the C4 ventral root activity assessed in a medulla-spinal cord preparation revealed a high respiratory rate with short inspiratory duration and frequent apnea. Furthermore, a coordinate pattern existed between the abnormal activity of inspiratory neurons in the ventrolateral medulla and C4 motorneuron output, indicating a central respiratory defect in Rnx mice. Thus, Rnx is critical for the development of the ventral medullary respiratory centre and its deficiency results in a syndrome resembling congenital central hypoventilation.

Response of the canine inspiratory intercostal muscles to chest wall vibration.

High-frequency mechanical vibration of the rib cage reduces dyspnea, but the effect of this procedure on the respiratory muscles is largely unknown. In the present studies, we have initially assessed the electrical and mechanical response to vibration (40 Hz) of the canine parasternal and external intercostal muscles (third interspace) during hyperventilation-induced apnea. When the vibrator was applied to the segment investigated, prominent external intercostal activity was recorded in the seven animals studied, whereas low-amplitude parasternal intercostal activity was recorded in only four animals. Similarly, when the vibrator was applied to more rostral and more caudal interspaces, activity was recorded commonly from the external intercostal but only occasionally from the parasternal. The two muscles, however, showed similar changes in length. We next examined the response to vibration of the muscles in seven spontaneously breathing animals. Vibrating the rib cage during inspiration (in-phase) had no effect on parasternal intercostal inspiratory activity but induced a marked increase in neural drive to the external intercostals. For the animal group, peak external intercostal activity during the control, nonvibrated breaths averaged (mean +/- SE) 43.1 +/- 3.7% of the activity recorded during the vibrated breaths (p < 0.001). External intercostal activity during vibration also occurred earlier at the onset of inspiration and commonly carried on after the cessation of parasternal intercostal activity. Yet tidal volume was unchanged. Vibrating the rib cage during expiration (out-of-phase) did not elicit any parasternal or external intercostal activity in six animals. These observations thus indicate that the external intercostals, with their larger spindle density, are much more sensitive to chest wall vibration than the parasternal intercostals. They also suggest that the impact of this procedure on the mechanical behavior of the respiratory system is relatively small.

Postinspiratory activity of the parasternal and external intercostal muscles in awake canines.

Previous studies have shown in awake dogs that activity in the crural diaphragm, but not in the costal diaphragm, usually persists after the end of inspiratory airflow. It has been suggested that this difference in postinspiratory activity results from greater muscle spindle content in the crural diaphragm. To evaluate the relationship between muscle spindles and postinspiratory activity, we have studied the pattern of activation of the parasternal and external intercostal muscles in the second to fourth interspaces in eight chronically implanted animals. Recordings were made on 2 or 3 successive days with the animals breathing quietly in the lateral decubitus position. The two muscles discharged in phase with inspiration, but parasternal intercostal activity usually terminated with the cessation of inspiratory flow, whereas external intercostal activity persisted for 24.7 +/- 12.3% of inspiratory time (P < 0.05). Forelimb elevation in six animals did not affect postinspiratory activity in the parasternal but prolonged postinspiratory activity in the external intercostal to 45.4 +/- 16.3% of inspiratory time (P < 0.05); in two animals, activity was still present at the onset of the next inspiratory burst. These observations support the concept that muscle spindles are an important determinant of postinspiratory activity. The absence of such activity in the parasternal intercostals and costal diaphragm also suggests that the mechanical impact of postinspiratory activity on the respiratory system is smaller than conventionally thought.

Response of respiratory muscles to intravenous nicotine challenge in anaesthetized cats

The effects of an intravenous nicotine challenge on the ventilation and activity of rib cage muscles were studied in 33 pentobarbitone-chloralose anaesthetized cats. Bolus injection of nicotine (200 μg) into the right femoral vein evoked in 19 of the intact animals prompt, short-lived apnoea, or prolongation of the first expiration after the drug, the occurrence of which was significantly reduced by midcervical vagotomy ( P<0.001). In breaths that followed the apnoea, peak activity of the parasternal intercostal muscles increased from a baseline of 3.1±0.8 to 9.2±1.8 arbitrary units ( P<0.001). Nicotine produced a similar increase in peak phrenic ENG (7.0±0.5 to 14.5±1.2 arbitrary units; P<0.001). Peak triangularis sterni muscle EMG was reduced from 8.9±1.2 to 6±1.7 arbitrary units ( P<0.05) and the onset of response was delayed to 30 s after the challenge. The changes of respiratory effectors induced by nicotine were independent of vagal integrity. The results show that post-nicotine apnoea is to large extent vagally dependent though the response of the respiratory muscles is mediated by non-vagal influences.

Spatial distribution of external and internal intercostal activity in dogs.

1. The observation that the external and internal interosseous intercostal muscles in the dog show marked regional differences in mechanical advantage has prompted us to re-examine the topographic distribution of electrical activity among these muscles during spontaneous breathing. 2. Inspiratory activity was recorded only from the areas of the external intercostals with an inspiratory mechanical advantage, and expiratory activity was recorded only from the areas of the internal intercostals with an expiratory mechanical advantage. The expiratory discharges previously recorded from the caudal external intercostals and the inspiratory discharges recorded from the rostral internal intercostals were probably due to cross-contamination. 3. Activity in each muscle area was also quantified relative to the activity measured during tetanic, supramaximal nerve stimulation (maximal activity). External intercostal inspiratory activity was consistently greater in the areas with a greater inspiratory advantage (i.e. the dorsal aspect of the rostral segments) than in the areas with a smaller inspiratory advantage, and internal intercostal expiratory activity was invariably greatest in the areas with the greatest expiratory advantage (i.e. the dorsal aspect of the caudal segments). 4. This topographic distribution of neural drive confers to the external intercostal muscles an inspiratory action on the lung during breathing and to the internal interosseous intercostals an expiratory action.

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.