Parasternal and external intercostal muscle shortening during eupneic breathing

The interosseous external intercostal (EI) muscles of the upper rib cage are electrically active during inspiration, but the mechanical consequence of their activation is unclear. In 16 anesthetized dogs, we simultaneously measured EI (3rd and 4th interspaces) and parasternal intercostal (PA) (3rd interspace) electromyogram and length. Muscle length was measured by sonomicrometry and expressed as a percentage of resting length (%LR). During resting breathing, each muscle was electrically active and shortened to a similar extent. Sequential EI muscle denervation (3rd and 4th interspaces) followed by PA denervation (3rd interspace) demonstrated significant reductions in the degree of inspiratory shortening for each muscle. Mean EI muscle shortening of the third and fourth interspaces decreased from -3.4 +/- 0.5 and -3.0 +/- 0.4% LR (SE) under control conditions to -0.2 +/- 0.2 and -0.8 +/- 0.3% LR, respectively, after selective denervation of each of these muscles (P less than 0.001 for each). After selective denervation of the PA muscle, its shortening decreased from -3.5 +/- 0.3 to +0.6% LR (SE) (P less than 0.001). PA muscle denervation also caused the EI muscle in the third interspace to change from inspiratory shortening of -0.2% to inspiratory lengthening of +0.2% +/- 0.2 (P less than 0.05). We conclude that during eupneic breathing 1) the EI muscles of the upper rib cage, like the PA muscles, are inspiratory agonists and actively contribute to rib cage expansion and 2) PA muscle contraction contributes to EI muscle shortening.     

Inspiratory action of separate external and parasternal intercostal muscle contraction

We have previously shown that electrical stimulation of the thoracic spinal cord produces near maximal activation of the inspiratory intercostal muscles. In the present investigation, we used this technique to evaluate the relative capacity of separate external (EI) and parasternal intercostal (PA) muscle contraction to produce changes in airway pressure and inspired volume. Studies were performed in 23 anesthetized phrenicotomized dogs. Electrical stimuli were applied to the spinal cord after hyperventilation-induced apnea, before and after sequentially severing either the PA or EI muscles from the first through sixth intercostal spaces. During spinal cord stimulation (SCS), measurements were made of inspired volume (delta V) with the airway open and negative airway pressure (delta P) during tracheal occlusion. Compared with control values, sectioning of the PA muscles resulted in a 40.9% reduction in delta P and 35.7% reduction in delta V during SCS. In other animals, initial sectioning of the EI muscles produced reductions in delta P and delta V of 67.4 and 63.0, respectively, during SCS. After subsequent section of the PA muscles, SCS produced only negligible inspired volumes and changes in airway pressure. We conclude that 1) the EI and PA muscles are each capable of generating substantial changes in airway pressure and large inspired volumes and 2) the ventilatory capacity of the EI muscles exceeds that of the PA muscles.     

Effect of inspiratory muscle fatigue on breathing pattern during inspiratory resistive loading

The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.     

Electrical activation of expiratory muscles increases with time in pentobarbital-anesthetized dogs.

Although the pentobarbital-anesthetized dog is often used as a model in studies of respiratory muscle activity during spontaneous breathing, there is no information regarding the stability of the pattern of breathing of this model over time. The electromyograms of several inspiratory and expiratory muscle groups were measured in six dogs over a 4-h period by use of chronically implanted electrodes. Anesthesia was induced with pentobarbital sodium (25 mg/kg iv), with supplemental doses to maintain constant plasma pentobarbital concentrations. Phasic electrical activity increased over time in the triangularis sterni, transversus abdominis, and external oblique muscles (expiratory muscles). The electrical activity of the costal diaphragm, crural diaphragm, and parasternal intercostal muscles (inspiratory muscles) was unchanged. These changes in electrical activity occurred despite stable plasma levels of pentobarbital and arterial PCO2. They were associated with changes in chest wall motion and an increased tidal volume with unchanged breathing frequency. We conclude that expiratory muscle groups are selectively activated with time in pentobarbital-anesthetized dogs lying supine. Therefore the duration of anesthesia is an important variable in studies using this model.     

Parasternal and external intercostal responses to various respiratory maneuvers.

Recent studies suggest that the external intercostal (EI) muscles of the upper rib cage, like the parasternals (PA), play an important ventilatory role, even during eupneic breathing. The purpose of the present study was to further assess the ventilatory role of the EI muscles by determining their response to various static and dynamic respiratory maneuvers and comparing them with the better-studied PA muscles. Applied interventions included 1) passive inflation and deflation, 2) abdominal compression, 3) progressive hypercapnia, and 4) response to bilateral cervical phrenicotomy. Studies were performed in 11 mongrel dogs. Electromyographic (EMG) activities were monitored via bipolar stainless steel electrodes. Muscle length (percentage of resting length) was monitored with piezoelectric crystals. With passive rib cage inflation produced either with a volume syringe or abdominal compression, each muscle shortened; with passive deflation, each muscle lengthened. During eupneic breathing, each muscle was electrically active and shortened to a similar degree. In response to progressive hypercapnia, peak EMG of each intercostal muscle increased linearly and to a similar extent. Inspiratory shortening also increased progressively with increasing PCO2, but in a curvilinear fashion with no significant differences in response among intercostal muscles. In response to phrenicotomy, the EMG and degree of inspiratory shortening of each intercostal muscle increased significantly. Again, the response among intercostal muscles was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory changes in parasternal intercostal intramuscular pressure

In an attempt to obtain insight in the forces developed by the parasternal intercostal muscles during breathing, changes in parasternal intramuscular pressure (PIP) were measured in 14 supine anesthetized dogs using a microtransducer method. In six animals, during bilateral parasternal stimulation a linear relationship between contractile force exerted on the rib and PIP was demonstrated (r greater than 0.95). In eight animals, during quiet active inspiration, substantial (55 +/- 11.5 cmH2O) PIP was developed. During inspiratory resistive loading and airway occlusion the inspiratory rise in PIP increased in proportion to the inspiratory fall in pleural pressure (r = 0.82). Phrenicotomy and vagotomy resulted in an increase in the inspiratory rise in PIP of 21% and 99%, respectively. During passive deflation, when the parasternal intercostals were passively lengthened, large rises (320 +/- 221 cmH2O) in intramuscular pressure were observed. During passive inflation intramuscular pressure remained constant or even decreased slightly (-8 +/- 25 cmH2O) as expected on the basis of the passive shortening of the muscles. PIP thus invariably increased when tension increased either actively or passively. From PIP it is clear that the parasternals exert significant forces on the ribs during respiratory maneuvers.     

Regional distribution of blood flow within the diaphragm

We investigated the regional distribution of blood flow (Q) within the costal and crural portions of the diaphragm in a total of eight anesthetized supine mongrel dogs. Q was measured with 15-microns microspheres, radiolabeled with three different isotopes, injected into the left ventricle during spontaneous breathing (SB), inspiratory resistive loading (IR), and mechanical ventilation after paralysis (P). At necropsy, the costal and crural portions of each hemidiaphragm were arbitrarily subdivided along a sagittal plane into five to seven and three sections, respectively. During P, there was a dorsoventral Q gradient within the costal part of the diaphragm. During SB there was a fourfold increase in the gradient of Q. Furthermore, during IR, in which mouth pressures of -16 +/- 4 cmH2O were generated, there was a further increase in the gradient of Q. During both SB and IR, Q to the most ventral portion of the costal diaphragm was 26 +/- 6% less than the peak value. In two dogs, studied prone and supine, there was no difference in the Q gradients between the two postures. Over the dorsal 80% of the costal diaphragm there was also a dorsoventral gradient of muscle thickness, such that the most dorsal part was 54 +/- 2% (n = 5) that of the ventral portion. In contrast, there was no consistent gradient of Q or muscle thickness within the crural diaphragm. Our results demonstrate a topographical gravity-independent distribution of Q in the costal, but not the crural, diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intercostal muscle action inferred from finite-element analysis

The external and internal intercostal muscles are important respiratory muscles in humans, but their mechanical actions have been controversial. We used finite-element analysis based on anatomic and mechanical measurements in dogs to assess the action of the intercostal and other rib cage muscles in a model of an isolated canine rib cage. When intercostal muscle forces of either the internal or the external layer were applied in a single interspace, they pulled the adjacent ribs together, consistent with published observations in dogs. However, when the forces were applied in all interspaces, the external layer caused an inspiratory motion and the internal layer caused an expiratory motion, consistent with conventional understanding of intercostal muscle actions. Parasternal intercostal, levator costae, and transversus thoracis (triangularis sterni) muscle actions were also simulated. These muscles caused expected movements of the ribs and sternum. We conclude that the actions of intercostal muscles depend on the spatial extent of their activation. Their actions in a single interspace and in multiple interspaces can be observed and explained with three-dimensional finite-element models.     

Electrical and mechanical activity of respiratory muscles during hypercapnia

In nine anesthetized supine spontaneously breathing dogs, we compared moving average electromyograms (EMGs) of the costal diaphragm and the third parasternal intercostal muscles with their respective respiratory changes in length (measured by sonomicrometry). During resting O2 breathing the pattern of diaphragm and intercostal muscle inspiratory shortening paralleled the gradually incrementing pattern of their moving average EMGs. Progressive hypercapnia caused progressive increases in the amount and velocity of respiratory muscle inspiratory shortening. For both muscles there were linear relationships during the course of CO2 rebreathing between their peak moving average EMGs and total inspiratory shortening and between tidal volume and total inspiratory shortening. During single-breath airway occlusions, the electrical activity of both the diaphragm and intercostal muscles increased, but there were decreases in their tidal shortening. The extent of muscle shortening during occluded breaths was increased by hypercapnia, so that both muscles shortened more during occluded breaths under hypercapnic conditions (PCO2 up to 90 Torr) than during unoccluded breaths under normocapnic conditions. These results suggest that for the costal diaphragm and parasternal intercostal muscles there is a close relationship between their electrical and mechanical behavior during CO2 rebreathing, this relationship is substantially altered by occluding the airway for a single breath, and thoracic respiratory muscles do not contract quasi-isometrically during occluded breaths.     

Coronary and systemic vascular response to inspiratory resistive breathing.

To evaluate the coronary and systemic cardiovascular response to graded inspiratory resistive breathing, seven dogs were studied 2-4 wk after chronic instrumentation to measure circumflex coronary artery and ascending aortic blood flows as well as aortic and left ventricular (LV) blood pressures. The experiments were performed under chloralose anesthesia (to exclude any confounding emotional effects by dyspnea on cardiovascular variables) and hyperoxic conditions (to prevent chemoreflex activation by hypoxemia). In a randomized fashion, the dogs were subjected to graded inspiratory resistive breathing (spontaneous breathing alone and moderate and severe resistive loading, corresponding to resistances of approximately 0, 40, and 110 cmH2O.s.l-1, respectively). Each run lasted 10 min. Compared with mechanical ventilation with the respiratory muscles at rest, spontaneous breathing alone and moderate and severe inspiratory resistive loading induced pronounced and significant increases in circumflex coronary blood flow (19, 32, and 62%, respectively), which were almost exclusively accounted for by significant decrements in coronary vascular resistance and were paralleled (r = 0.88, P less than 0.0001) by significant increments (18, 31, and 57%) in heart rate transmural-aortic pressure product, an indicator of LV myocardial O2 demand. An increase in myocardial O2 consumption during resistive breathing was confirmed by analysis of coronary sinus blood samples in additional experiments (n = 3). Cardiac output significantly increased (10, 14, and 35%) because of increases in heart rate (15, 24, and 49%), with LV stroke volume and diastolic dimensions remaining unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Preferential fatigue of the rib cage muscles during inspiratory resistive loaded ventilation

Because the inspiratory rib cage muscles are recruited during inspiratory resistive loaded breathing, we hypothesized that such loading would preferentially fatigue the rib cage muscles. We measured the pressure developed by the inspiratory rib cage muscles during maximal static inspiratory maneuvers (Pinsp) and the pressure developed by the diaphragm during maximal static open-glottis expulsive maneuvers (Pdimax) in four human subjects, both before and after fatigue induced by an inspiratory resistive loaded breathing task. Tasks consisted of maintaining a target esophageal pressure, breathing frequency, and duty cycle for 3-5 min, after which the subjects maintained the highest esophageal pressure possible for an additional 5 min. After loading, Pinsp decreased in all subjects [control, -128 +/- 14 (SD) cmH2O; with fatigue, -102 +/- 18 cmH2O; P less than 0.001, paired t test]. Pdimax was unchanged (control, -192 +/- 23 cmH2O; fatigue, -195 +/- 27 cmH2O). These data suggest that 1) inability to sustain the target during loading resulted from fatigue of the inspiratory rib cage muscles, not diaphragm, and 2) simultaneous measurement of Pinsp and Pdimax may be useful in partitioning muscle fatigue into rib cage and diaphragmatic components.     

Expiratory muscle fatigue in normal subjects

We examined expiratory muscle fatigue during expiratory resistive loading in 11 normal subjects. Subjects breathed against expiratory resistances at their own breathing frequency and tidal volume until exhaustion or for 60 min. Respiratory muscle strength was assessed from both the maximum static expiratory and inspiratory mouth pressures (PEmax and PImax). At the lowest resistance, PEmax and PImax measured after completion of the expiratory loaded breathing were not different from control values. With higher resistance, both PEmax and PImax were decreased (P less than 0.05), and the decrease lasted for greater than or equal to 60 min. The electromyogram high-to-low frequency power ratio for the rectus abdominis muscle decreased progressively during loading (P less than 0.01), but the integrated EMG activity did not change during recovery. Transdiaphragmatic pressure during loading was increased 3.6-fold compared with control (P less than 0.05). These findings suggest that expiratory resistive loaded breathing induces muscle fatigue in both expiratory and inspiratory muscles. Fatigue of the expiratory muscles can be attributed directly to the high work load and that of the inspiratory muscles may be related to increased work due to shortened inspiratory time.     

Involvement of pharyngeal muscles in compensatory responses of the respiration system to inspiration resistance load]

The present study was undertaken to test the hypothesis that recruitment of upper airway muscles in loaded breathing is a result of integration of peripheral chemoreceptor and pulmonary mechanoreceptor afferents. Experiments were performed in spontaneously breathing tracheostomized anesthetized rabbits. It had been studied the effects of inspiratory resistive loading to EMG activity of genioglossus muscle. In the intact rabbits the peak value and duration of inspiratory activity of genioglossus increased in loading. Imposition of resistive load in vagotomized animals did not evoke alteration in inspiratory activity of genioglossus in the first loaded breath. Hyperoxia decreased the response of genioglossus muscle to inspiratory loading and vagatomy. We conclude that hypoxic stimulation of peripheral chemoreceptors and decrease in volume-related afferent activity from pulmonary stretch receptors are major mechanisms of the upper airway muscle recruiment in inspiratory resistive loading.     

Reproducibility and responsiveness of a noninvasive EMG technique of the respiratory muscles in COPD patients and in healthy subjects.

In the present study, we assessed the reproducibility and responsiveness of transcutaneous electromyography (EMG) of the respiratory muscles in patients with chronic obstructive pulmonary disease (COPD) and healthy subjects during breathing against an inspiratory load. In seven healthy subjects and seven COPD patients, EMG signals of the frontal and dorsal diaphragm, intercostal muscles, abdominal muscles, and scalene muscles were derived on 2 different days, both during breathing at rest and during breathing through an inspiratory threshold device of 7, 14, and 21 cm H2O. For analysis, we used the logarithm of the ratio of the inspiratory activity during the subsequent loads and the activity at baseline [log EMG activity ratio (EMGAR)]. Reproducibility of the EMG was assessed by comparing the log EMGAR values measured at test days 1 and 2 in both groups. Responsiveness (sensitivity to change) of the EMG was assessed by comparing the log EMGAR values of the COPD patients to those of the healthy subjects at each load. During days 1 and 2, log EMGAR values of the diaphragm and the intercostal muscles correlated significantly. For the scalene muscles, significant correlations were found for the COPD patients. Although inspiratory muscle activity increased significantly during the subsequent loads in all participants, the COPD patients displayed a significantly greater increase in intercostal and left scalene muscle activity compared with the healthy subjects. In conclusion, the present study showed that the EMG technique is a reproducible and sensitive technique to assess breathing patterns in COPD patients and healthy subjects.     

Inspiratory muscle fatigue increases sympathetic vasomotor outflow and blood pressure during submaximal exercise

The purpose of this study was to elucidate the influence of inspiratory muscle fatigue on muscle sympathetic nerve activity (MSNA) and blood pressure (BP) response during submaximal exercise. We hypothesized that inspiratory muscle fatigue would elicit increases in sympathetic vasoconstrictor outflow and BP during dynamic leg exercise. The subjects carried out four submaximal exercise tests: two were maximal inspiratory pressure (PI(max)) tests and two were MSNA tests. In the PI(max) tests, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without inspiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each set at 0.5 s)]. Before and immediately after exercise, PI(max) was estimated. In MSNA tests, the subjects performed two 15-min exercises (spontaneous breathing for 5 min, with or without inspiratory resistive breathing for 5 min, and spontaneous breathing for 5 min). MSNA was recorded via microneurography of the right median nerve at the elbow. PI(max) decreased following exercise with resistive breathing, whereas no change was found without resistance. The time-dependent increase in MSNA burst frequency (BF) appeared during exercise with inspiratory resistive breathing, accompanied by an augmentation of diastolic BP (DBP) (with resistance: MSNA, BF +83.4%; DBP, +23.8%; without resistance: MSNA BF, +19.2%; DBP, -0.4%, from spontaneous breathing during exercise). These results suggest that inspiratory muscle fatigue induces increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise at mild intensity.     

Dissociation between diaphragmatic and rib cage muscle fatigue

To assess rib cage muscle fatigue and its relationship to diaphragmatic fatigue, we recorded the electromyogram (EMG) of the parasternal intercostals (PS), sternocleidomastoid (SM), and platysma with fine wire electrodes and the EMG of the diaphragm (DI) with an esophageal electrode. Six normal subjects were studied during inspiratory resistive breathing. Two different breathing patterns were imposed: mainly diaphragmatic or mainly rib cage breathing. The development of fatigue was assessed by analysis of the high-to-low (H/L) ratio of the EMG. To determine the appropriate frequency bands for the PS and SM, we established their EMG power spectrum by Fourier analysis. The mean and SD for the centroid frequency was 312 +/- 16 Hz for PS and 244 +/- 48 Hz for SM. When breathing with the diaphragmatic patterns, all subjects showed a fall in H/L of the DI and none had a fall in H/L of the PS or SM. During rib cage emphasis, four out of five subjects showed a fall in H/L of the PS and five out of six showed a fall in H/L of the SM. Four subjects showed no fall in H/L of the DI; the other two subjects were unable to inhibit diaphragm activity to a substantial degree and did show a fall in H/L of the DI. Activity of the platysma was minimal or absent during diaphragmatic emphasis but was usually strong during rib cage breathing. We conclude that fatigue of either the diaphragm or the parasternal and sternocleidomastoid can occur independently according to the recruitment pattern of inspiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential respiratory muscle recruitment induced by clonidine in awake goats

The purpose of this study was to test thehypothesis that dysrhythmic breathing induced by the₂-agonist clonidine isaccompanied by differential recruitment of respiratory muscles. Inadult goats (n = 14) electromyographic(EMG) measurements were made from inspiratory muscles (diaphragm andparasternal intercostal) and expiratory muscles [triangularissterni (TS) and transversus abdominis (Abd)]. EMG of thethyroarytenoid (TA) muscle was used as an index of upper airway(glottal) patency. Peak EMG activities of all spinal inspiratory andexpiratory muscles were augmented by central and peripheralchemoreceptor stimuli. Phasic TA was apparent in the postinspiratoryphase of the breathing cycle under normoxic conditions. Duringdysrhythmic breathing episodes induced by clonidine, TS and Abdactivities were attenuated or abolished, whereas diaphragm andparasternal intercostal activities were unchanged. There was no tonicactivation of TS or Abd EMG during apneas; however, TA activity becametonic throughout the apnea. We conclude that1) ₂-adrenoceptor stimulationresults in differential recruitment of respiratory muscles duringrespiratory dysrhythmias and 2) apneas are accompanied by active glottic closure in the awake goat.

     

Thyroarytenoid muscle activity during loaded and nonloaded breathing in adult humans

Previous fiber-optic studies in humans have demonstrated narrowing of the glottic aperture in expiration during application of expiratory resistive loads. Nine healthy subjects were studied to determine the effect of expiratory resistive loads on the electromyographic activity of the thyroarytenoid (TA) muscle, a vocal cord adductor. Four of the nine subjects also underwent the application of inspiratory resistive loads and voluntary prolongation of either inspiratory (TI) or expiratory (TE) time. TA activity was recorded by intramuscular hooked-wire electrodes. During quiet breathing in all subjects, the TA was phasically active on expiration and often tonically active throughout the respiratory cycle. TA expiratory activity progressively increased with increasing levels of expiratory load. Inspiratory loads resulted in increased TA "inspiratory" activity. Voluntary prolongation of TE to times similar to those reached during loaded breathing induced increases in TA expiratory activity similar to those reached during the loaded state. Voluntary prolongation of TI was associated with an increase in TA inspiratory activity. Similar increases in TI during inspiratory loading or voluntary conditions were associated with comparable increases in TA inspiratory activity in three of the four subjects. In conclusion, increased activation of TA during the application of expiratory resistive loads implies that the reported narrowing of glottic aperture during expiratory loading is an active phenomenon. Changes in activation of the TA with resistive loads appear to be related to changes in respiratory pattern.     

Triangularis sterni: a primary muscle of breathing in the dog

The isolated action, pattern of neural activation, and mechanical contribution to eupnea of the triangularis sterni (transversus thoracis) muscle were studied in supine anesthetized dogs. Linear displacement transducers were used to measure the axial displacements of the ribs and sternum. Tetanic stimulation of the triangularis sterni in the apneic animal caused a marked caudal displacement of the ribs, a moderate cranial displacement of the sternum, and a decrease in lung volume. During quiet breathing, there was invariably a rhythmic activation of the muscle in phase with expiration that was independent of the presence or absence of activity in the abdominal and internal interosseous intercostal muscles. This phasic expiratory activity in the triangularis sterni was of large amplitude and caused the ribs to be more caudal and the sternum to be more cranial during the spontaneous expiratory pause than during relaxation. Additional studies on awake animals showed that rhythmic activation of the triangularis sterni occurs in all body positions and is not caused by anesthesia. These findings indicate that expiration in the dog is not a passive process and that the end-expiratory volume of the rib cage is not determined by an equilibrium of static forces alone. Rather, it is actively determined and maintained below its relaxation volume by contraction of the triangularis sterni throughout expiration. The use of this muscle is likely to facilitate inspiration by increasing the length of the parasternal intercostals and taking on a portion of their work.     

Mechanical contribution of expiratory muscles to pressure generation during spinal cord stimulation.

Lower thoracic spinal cord stimulation (SCS) results in the generation of large positive airway pressures (Paw) and may be a useful method of restoring cough in patients with spinal cord injury. The purpose of the present study was to assess the mechanical contribution of individual respiratory muscles to pressure generation during SCS. In anesthetized dogs, SCS was applied at different spinal cord levels by using a 15-lead multicontact electrode before and after sequential ablation of the external and internal obliques, transversus abdominis (TA), rectus abdominis, and internal intercostal muscles. Paw was monitored after tracheal occlusion. SCS at the T(9) spinal cord level resulted in maximal changes in Paw (60 +/- 3 cmH(2)O). Section of the oblique muscles resulted in a fall in Paw to 29 +/- 2 cmH(2)O. After subsequent section of the rectus abdominis and TA, Paw fell to 25 +/- 2 and 12 +/- 1 cmH(2)O respectively. There was a small remaining Paw (4 +/- 1 cmH(2)O) after section of the internal intercostal nerves. Stimulation with a two-electrode lead system (T(9) + T(13)) resulted in significantly greater pressure generation compared with a single-electrode lead due to increased contributions from the obliques and transversus muscles. In a separate group of animals, Paw generation was monitored after section of the abdominal muscles and again after section of the external intercostal and levator costae muscles. These studies demonstrated that inspiratory intercostal muscle stimulation resulted in only a small opposing inspiratory action (相似文献