Internal Intercostal Activity Research Articles

Effects of pulse lung inflation on chest wall expiratory motor activity

The effects of pulse lung inflation (LI) on expiratory muscle activity and phase duration (Te) were determined in anesthetized, spontaneously breathing dogs (n = 20). A volume syringe was used to inflate the lungs at various times during the expiratory phase. The magnitude of lung volume was assessed by the corresponding change in airway pressure (Paw; range 2-20 cmH(2)O). Electromyographic (EMG) activities were recorded from both thoracic and abdominal muscles. Parasternal muscle EMG was used to record inspiratory activity. Expiratory activity was assessed from the triangularis sterni (TS), internal intercostal (IIC), and transversus abdominis (TA) muscles. Lung inflations <7 cmH(2)O consistently inhibited TS activity but had variable effects on TA and IIC activity and expiratory duration. Lung inflations resulting in Paw values >7 cmH(2)O, however, inhibited expiratory EMG activity of each of the expiratory muscles and lengthened Te in all animals. The responses of expiratory EMG and Te were directly related to the magnitude of the lung inflation. The inhibition of expiratory motor activity was independent of the timing of pulse lung inflation during the expiratory phase. The inhibitory effects of lung inflation were eliminated by bilateral vagotomy and could be reproduced by electrical stimulation of the vagus nerve. We conclude that pulse lung inflation resulting in Paw between 7 and 20 cmH(2)O produces a vagally mediated inhibition of expiratory muscle activity that is directly related to the magnitude of the inflation. Lower inflation pressures produce variable effects that are muscle specific.

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.

Rapid and transient excitation of respiration mediated by central chemoreceptor.

We evaluated rapid and transient changes in phrenic nerve (PN) and internal intercostal (IIC) activities when 0.2-0.5 ml of saline saturated with 100% CO2 was injected into the vertebral artery during various respiratory phases in decerebrated spontaneously breathing cats. The injections evoked an initial transient inhibition of ongoing PN or IIC activity with a mean onset latency of 0.17 s, followed by excitation of subsequent respiratory activities with an onset latency ranging from 0.4 to 2.7 s; the average onset latency of expiratory excitation (1.49 s) was significantly longer than that of inspiratory facilitation (0.89 s). The initial inhibitory responses were analogous to reflex effects of injections of phenyl biguanide, indicating that the initial inhibition was due to activation of vascular nociceptors and the subsequent excitation was due to stimulation of the central chemoreceptors. In addition, CO2-saline injections during hypocapnic apnea developed a quick reappearance of respiratory rhythm, and the first facilitatory effect appeared in tonic IIC activity, which became more active before rhythm started. In summary, the present study, by use of a technique of vertebral arterial injections of 100% CO2-saline, revealed dynamic properties of respiratory control system mediated by central chemoreceptors and vascular nociceptors.

Effect of cisternal administration of acetazolamide on rapid excitation of central chemoreceptors.

We evaluated rapid and transient changes in phrenic (PN) and internal intercostal (IIC) activities when 0.5 ml of saline saturated with 100% CO2 was injected into the vertebral artery at the C1 level before and after cisternal administration of carbonic anhydrase inhibitor (acetazolamide) in decerebrated, spontaneously breathing cats. Before acetazolamide administration, the injections evoked an initial, transient inhibition of ongoing PN or IIC activity, followed by excitation of subsequent respiratory activities with a short onset latency of less than 3 sec. On the other hand, cisternal administration of acetazolamide abolished both the initial inhibition and the subsequent rapid excitation of respiratory activities, although there still existed a delayed, weak and prolonged excitation of respiration. These results indicated that hydration of CO2 accelerated by carbonic anhydrase within the brain would be essential for the rapid changes in respiratory activity mediated by the central chemoreceptors.

Effects of acetylcholine on internal intercostal muscle activity in the rabbit

In pentobarbitone-anesthetized rabbits, intracarotid injections of acetylcholine (ACh, 3–30 μg) during inspiration led to an inhibition of internal intercostal muscle activity (IIMA). After the section of the carotid sinus nerve (CSN), ACh-induced inhibitory responses in IIMA were abolished. In addition, changes of the rabbit carotid chemoreceptor activity were studied by ACh (3–30 μg) given into the carotid body region during inspiration. Spontaneous chemoreceptor activity was inhibited in a dose-dependent manner by ACh. These results suggest that the inhibitory responses of IIMA to ACh are probably mediated through the carotid chemoreceptor reflexes.

Effects of transient hypoxia on internal intercostal muscle activity in vagotomized rabbits.

The effects of transient hypoxia on the responses of internal intercostal (IIC) muscle activity before and after surgical denervation of the carotid sinus nerves were studied in the bilaterally vagotomized rabbits. Bilateral vagotomy caused a complete inhibition of IIC activity in 11 of 13 animals. In the vagotomized animals with no expiratory activity in the IIC muscles, lung inflations with low O2 gas mixture (6% O2 in N2) produced an increase in IIC activity, whereas these excitatory effects were remarkably reduced after sectioning the carotid sinus nerves. In addition, the effects of lung inflation with low O2 gas mixture (6% O2 in N2) on carotid chemoreceptor activity were also studied in the vagotomized rabbits. Lung inflations with hypoxic gas caused an increase in carotid chemoreceptor activity. These results indicate that in the absence of proprioceptive input from the lungs, hypoxic stimulation of the carotid chemoreceptors is capable of activating the expiratory activity in the IIC muscles.

Effects of temporal trachea-occlusion at the end of expiration on internal intercostal muscle activity in the rabbit.

The effects of temporal trachea-occlusion at the end of expiration on internal intercostal muscle activity (IIMA) and diaphragmatic activity (DMA) were studied in the vagi-intact rabbit. This tracheal occlusion caused a marked prolongation of inspiration time due to a diminution of the vagally mediated inspiratory inhibition but the significant change in the next IIMA was not observed after releasing tracheal occlusion. In addition, the effects of temporal trachea-occlusion on pulmonary stretch receptor activity (PSRA) and DMA were also studied in the unilaterally vagotomized rabbit. The procedures remarkably inhibited the respiratory modulation of PSRA from inspiration to expiration. These results indicate that the change of PSRA in response to temporal trachea-occlusion does not significantly affect the next IIMA.

Effects of bronchoconstriction on respiratory muscle activity during expiration.

The effect of methacholine-induced bronchoconstriction on the electrical activity of respiratory muscles during expiration was studied in 12 anesthetized spontaneously breathing dogs. Before and after aerosols of methacholine, diaphragm, parasternal intercostal, internal intercostal, and external oblique electromyograms were recorded during 100% O2 breathing and CO2 rebreathing. While breathing 100% O2, five dogs showed prolonged electrical activity of the diaphragm and parasternal intercostals in early expiration, postinspiratory inspiratory activity (PIIA). Aerosols of methacholine increased pulmonary resistance, decreased tidal volume, and elevated arterial PCO2. During bronchoconstriction, when PCO2 was varied by CO2 rebreathing, PIIA was shorter at low levels of PCO2, and external oblique and internal intercostal were higher at all levels of PCO2. Vagotomy shortened PIIA in dogs with prolonged PIIA. After vagotomy, methacholine had no effects on PIIA but continued to increase external oblique and internal intercostal activity at all levels of PCO2. These findings indicate that bronchoconstriction influences PIIA through a vagal reflex but augments expiratory activity, at least in part, by extravagal mechanisms.

Effects of carotid chemoreceptor stimulating and depressing agents on internal intercostal muscle activity in the rabbit.

The effects of carotid chemoreceptor stimulating and depressing agents on internal intercostal muscle activity (IIMA) were studied before and after surgical denervation of the carotid sinus nerve (CSN) in the rabbit. An intracarotid injection of 30 micrograms of sodium cyanide (NaCN) during inspiration caused an increase in both IIMA and respiratory rate (RR). In contrast, intracarotid administration of 10 micrograms of dopamine (DA) during inspiration resulted in a decrease in both IIMA and RR. The NaCN- and DA-induced characteristic responses in IIMA were abolished by the section of the CSN. The results indicate that the excitatory and inhibitory responses of IIMA to intracarotid injections of NaCN and DA are mainly mediated through carotid chemoreflexes.

Immediate changes in ventilation and respiratory pattern associated with onset and cessation of locomotion in the cat.

In high decerebrate unanaesthetized cats (pre-collicular/pre-mamillary) which developed spontaneous co-ordinated locomotor activity, ventilation, breathing pattern, phrenic nerve, external and internal intercostal electromyogram (e.m.g.) activities were examined. Locomotion was also induced by electrical stimulation of the subthalamic locomotor region and in a few cases the mesencephalic locomotor region. Quadriceps muscle e.m.g. was used to monitor locomotor activity. Spontaneous locomotor activity was associated with an immediate increase in ventilation and shift of the ventilatory CO2 response curve to the left. Tidal volume was smaller and respiratory rate larger at any given level of ventilation during spontaneous locomotion. Increases in respiratory rate were due to reductions in both inspiratory and expiratory duration. Upon cessation of locomotion, these changes abruptly returned to control values. Within the first one or two walking steps of spontaneous locomotor activity, the rate of rise of phrenic activity increased slightly while peak phrenic activity remained relatively constant; peak internal intercostal activity increased markedly while peak external intercostal activity decreased. Similar changes in ventilation, phrenic, external and internal intercostal activities were observed in association with locomotion induced by stimulation within the subthalamic or mesencephalic locomotor regions. In contrast to spontaneous locomotor activity, however, increases in both external and internal intercostal activities were often observed. Peak amplitudes of both external and internal intercostal activities increased linearly with increasing levels of end-tidal PCO2 during rest and during locomotion. However, at any given level of PCO2 peak external intercostal activity was smaller and peak internal intercostal activity larger during locomotion than at rest. With increasing peak quadriceps e.m.g. activity at a constant walking rate, external intercostal activity was progressively inhibited while internal intercostal activity was progressively enhanced. No consistent change in peak phrenic activity was observed with changes in peak quadriceps activity. With increasing walking rate at a constant peak quadriceps e.m.g., peak phrenic and peak internal intercostal activities progressively increased and peak amplitude of external intercostal activity (which was inhibited below the activity observed at rest) also progressively increased. The virtually simultaneous changes in quadriceps activity and respiratory motor activities suggest that the increase in ventilation at exercise onset is neurally mediated. Furthermore, these results suggest that the motor pathways to both the spinal locomotor pattern generators and the pattern-controlling mechanisms for respiration are driven in parallel to provide a quantitative relationship between respiratory motor output and locomotor activity. The functional significance of the alterations in respiratory pattern and participation of the different respiratory muscles is discussed.

Responses of cat's internal intercostal motor units to hypercapnia and lung inflation.

Single motor unit potentials from the eighth internal intercostal (IIC) muscle were recorded along with tracheal pressure and end-tidal CO2 (PETCO2) in spontaneously breathing, Dial-urethane anesthetized cats during hypercapnia (3, 5, or 7% CO2) and during lung inflation (LI, 100 ml above functional residual capacity) before and after vagotomy. Hypercapnia depressed IIC activity in 5 of 7 cats; the higher the PETCO2, the lower was the firing rate and the fewer the number of spikes per breath. LI evoked an initial silent phase (ISP) in 6 of 10 cats followed by a prolonged IIC burst. Hypercapnia combined with LI abolished or diminished the ISP and shortened the prolonged burst with an increase in firing rate and a recruitment of new units. Vagotomy silenced IIC activity in 7 of 10 cats, but LI after vagotomy activated IIC activity in 10 of 10 cats, though neither an ISP nor prolonged activity occurred. Our data suggest that major factors in controlling IIC activity are reciprocal inhibition from bulbospinal inspiratory neurons, excitatory and inhibitory inputs mediated by vagal afferents, and a modulation of IIC activity via gamma-loop. Hypercapnia affects the former two factors.

The interaction between reflex apnoea and bradycardia produced by injecting 5-HT into the nodose ganglion of the cat.

The apnoea, accompanied by bradycardia and hypotension caused by injection of 5-Hydroxytryptamine (5-HT) into the vascularly isolated nodose ganglion is characterised by intense electrical activity in the internal intercostal muscles. No such activity was recorded when apnoea was provoked by electrical stimulation of the central end of the superior laryngeal nerve. The cardiac slowing induced by 5-HT was less marked when the superior laryngeal nerve was concomitantly stimulated with an intensity sufficient to inhibit the internal intercostal activity. When central respiratory drive was depressed by hypocapnic ventilation nodose ganglion-induced bradycardia was comparable to that provoked during electrical stimulation of the superior laryngeal nerve in eupnoea. Unlike chemoreceptor-induced bradycardia the cardiac slowing caused by nodose ganglion stimulation was not reduced by "ramp" inflation of the lungs. The results were similar during hypocapnic depression of the "Respiratory Centre". These findings suggest that: (a) central expiratory activity contributes to the bradycardia induced by nodose ganglion stimulation, and (b) the inhibition of bradycardia by lung expansion occurs before the neural impulses reach the nucleus ambiguus but does not involve the central respiratory neurones.