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[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center].

Experiments were conducted on cats under nembutal anesthesia; a study was made of pulse activity of bulbar respiratory neurons, electrical activity of the diaphragm and of the intercostal muscles; pO2, pCO2, pH, arterial blood oxygen saturation were determined in combined action of hypoxia and hypercapnia. When hypoxic gaseous mixture was given for respiration the developing hypocapnia disturbed the discharge rhythmic activity of the respiratory neurons, the respiration acquiring a pathological character of the Cheyne--Stokes type. After addition to the hypoxic gaseous mixture of 2% CO2 the gaseous composition of the arterial blood approached the initial values; this addition prevented the development of hypercapnia and disturbances of rhythmic discharge activity of the respiratory neurons. Addition of 5% CO2 to the hypoxic gaseous mixture produced a negative effect: at first it intensified and then depressed the pulse activity of the respiratory neurons, caused metabolic and respiratory acidosis, and promoted asphyxia.

Animals↗

Inspiratory facilitation and inhibition from pulmonary stretch receptors in rabbits.

In anesthetized rabbits firing rate (FR) of single fibers of diaphragm and of parasternal intercostal muscles (PIM) was determined at 30, 50 and 70% of control inspiratory time. During first inspiratory effort after airway occlusion at end expiration it increased on the average by 12.1 +/- 0.6 and 43.0 +/- 2.2% relative to control. Under pulmonary stretch receptor (PSR) block with SO2 this increase disappeared in diaphragm and fell to 28.3 +/- 1.8% in PIM. During first inspiratory efforts under PSR block FR decreased by 11.3 +/- 2.2% in diaphragm and 18.3 +/- 1.6 in PIM relative to unblocked efforts. In open inspirations FR under block did not decrease significantly either in diaphragm or PIM relative to unblocked inspirations. Moving average electromyography of diaphragm and of PIM showed similar trends. These results suggest that PSR discharge at FRC activates a mechanism facilitating inspiratory activity while during inspiration it also activates a mechanism inhibiting this activity since early inspiration. Both effects are greater on PIM.

Animals↗

Pulmonary interstitial pressure in intact in situ lung: transition to interstitial edema.

In anesthetized rabbits (n = 25) subject to slow intravenous saline loading (0.4 ml.min-1.kg-1) for 3 h, we measured pulmonary interstitial pressure (Pip) in intact in situ lungs with glass micropipettes inserted directly into the lung parenchyma via a "pleural window." Measurements were done in apneic animals at the end-expiratory volume with O2 delivered in the trachea. Pip was -10 +/- 1.5 (SD) cmH2O in control and increased to 0.6 +/- 3.8 and 5.7 +/- 3.3 cmH2O at 66 and 180 min, respectively. The wet-to-dry weight ratio (W/D) of the lung was 5.04 +/- 0.2 in the control group and 5.34 +/- 0.7 at 180 min (+6%); the corresponding W/D for intercostal muscles were 3.25 +/- 0.03 and 4.19 +/- 0.5 (+28%). Pulmonary interstitial compliance was 0.47 ml.mmHg-1.100 g wet wt-1. Pulmonary arterial and left atrial pressures were 18.4 +/- 2 and 3 +/- 1 cmH2O in control and increased to 19.5 +/- 2.9 and 4.6 +/- 1.7 cmH2O at 180 min, respectively. Aortic flow (cardiac output) increased from 103 +/- 35 to 131 +/- 26 ml/min; pulmonary resistance fell from 0.17 +/- 0.06 to 0.14 +/- 0.05 cmH2O.min.ml-1 (-18%), suggesting that the increase in Pip did not limit blood flow. The pulmonary capillary-to-interstitium filtration pressure gradient decreased sharply from a control value of 10 cmH2O to 0 cmH2O within 60 min because of the increase in Pip and remained unchanged for < or = 180 min. Data suggest that the pulmonary interstitial matrix can withstand fluid pressures above atmospheric, preventing the development of pulmonary alveolar flooding.

Air Pressure↗

Generation and detection of lung stress waves from the chest surface.

In anesthetized pigs, we generated stress' waves by imposing a distortion on the intercostal muscle between the 5th and 6th ribs. Stress waves were detected by two accelerometers, 5-7 cm apart, oriented in either the ventral-dorsal or cranial-caudal direction. Cross-spectral analysis was used to calculate transit time. Waves of velocities similar to those of lung shear waves were detected at transpulmonary pressures (Ptp) above 15 cmH2O in the nonedematous lung and above 25 cmH2O Ptp in the edematous lung. Waves were detected in the frequency range 9-40 Hz. Stress wave velocity increased from 287 +/- 24 (SD) cm/sec at 18 cmH2O Ptp to 342 +/- 41 cm/sec at 26 cmH2O Ptp, consistent with shear waves propagating in the lung having a shear modulus of 0.9 Ptp and lung density of 0.20 g/cm3. Stress wave velocities at 25 cmH2O Ptp decreased with the increases in lung density induced by alveolar edema, consistent with elasticity theory. An elasticity analysis showed the existence of lung-rib cage interfacial waves with properties similar to the measured stress waves.

Anesthesia↗

Development of the mouse neuromuscular junction in the absence of regulated secretion.

To investigate the role of neurotransmitter secretion in the development and stabilization of synapses, the innervation of the diaphragm and intercostal muscles was studied in munc18-1 null mutant mice, which lack regulated secretion. We found that this mutant is completely devoid of both spontaneous and evoked neuromuscular transmission throughout embryonic development. At embryonic day (E) 14, axonal targeting and main branching of the phrenic nerve were normal in this mutant, but tertiary branches were elongated and no terminal branches were observed at this stage, in contrast to control littermates. Acetylcholinesterase staining was observed in the endplate region of mutant muscle from E14 onwards, but not as dense and confined to spots as in controls. Acetylcholine receptor staining was also present in the endplate region of the mutant muscle. In this case, the staining density and the concentration in spots (clusters) were similar to controls, but the distribution of these clusters was less organized. Starting at E15, some receptor clusters co-localized with nerve terminal staining, suggesting synapses, but most clusters remained a-neural. Electron microscopical analysis confirmed the presence of synaptic structures in the mutant. Between E14 and birth, the characteristic staining pattern of nerve branches gradually disappeared in the mutant until, at E18, an elaborate meshwork of nerve fibers with no apparent organization remained. In the same period, most of the motor neuronal cell bodies in the spinal cord degenerated. In contrast, sensory ganglia in the dorsal root showed no obvious degeneration. These data suggest that regulated secretion is not essential for initial axon path finding, clustering of acetylcholine receptors, acetylcholinesterase or the formation of synapses. However, in the absence of regulated secretion, the maintenance of the motor neuronal system, organization of nerve terminal branches and stabilization of synapses is impaired and a-neural postsynaptic elements persist.

Acetylcholinesterase↗

Cranio-caudal rib cage distortion with increasing inspiratory airflow in man.

Changes in anteroposterior and transverse diameters of the chest wall, in cranial and caudal esophageal pressure (delta Pes), and diaphragm (Adi) and cranial intercostal muscle activity (Aic) were measured in supine and seated subjects during relaxation and full inspirations from FRC at constant slow or high flow rates. No distortion of the rib cage occurred during relaxation of slow inspirations. During fast inspirations cranial part of rib cage expanded relatively more than caudal one because of greater Aic for any level of Adi. Rib cage distortion during fast inspirations, as well as the occurring between seated and supine posture, was directionally consistent with flow or posture related redistribution of apicobasal lung expansion, suggesting that changes in rib cage shape affect regional lung expansion also in man. During relaxation or slow inspirations cranio-caudal difference in delta Pes (delta Pc-c) was essentially nil over all the inspiratory capacity. During fast inspirations delta Pc-c was negative (seated posture) or nil (supine posture) for small lung volume increments, positive for large volume increments. Delta Pc-c dependence on lung volume is compatible with the response of a model consisting of two parallel compartments with different degree of expansion at FRC and equal volume dependent mechanical properties.

Diaphragm↗

Benefit of in-phase chest wall vibration on the pulmonary hemodynamics in patients with chronic obstructive pulmonary disease.

OBJECTIVE: Chest wall vibration of contracting intercostal muscles (in-phase vibration, (IPV)) improves O2 saturation in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate the effect of IPV on the pulmonary hemodynamics in patients with COPD. METHODOLOGY: Twelve patients with COPD (FEV1%, 43.7 +/- 14.4%) underwent pulmonary artery catheterization in the supine position; hemodynamic variables as well as arterial and mixed venous gas tension were measured at baseline and after 15 min of IPV with IPV continued during the measurement. RESULTS: Mean pulmonary arterial pressure (Ppa, 21.3 +/- 5.0-19.1 +/- 4.8 mmHg and pulmonary vascular resistance (PVR, 294.6 +/- 196.0-228.5 +/- 101.7 dyne.sec.cm-5) decreased significantly, but there was no change in heart rate, cardiac index or systemic blood pressure. PaO2 increased (66.5 +/- 10.3-70.0 +/- 9.7 Torr) and PaCO2 decreased (46.6 +/- 8.9-45.0 +/- 10.1 Torr) significantly. Minute ventilation and tidal volume increased significantly in five out of the eight patients in whom ventilation was monitored throughout the study. CONCLUSION: IPV improves gas exchange and pulmonary circulation without affecting systemic circulation.

Aged↗

The temperature sensitivity of miniature endplate currents is mostly governed by channel gating: evidence from optimized recordings and Monte Carlo simulations.

The temperature dependence of miniature endplate current (MEPC) amplitude (A(c)), 20-80% rise time (t(r)), and 90-33% fall-time (t(f)) was determined for lizard (Anolis carolinensis) intercostal muscle using broadband extracellular (EC) and voltage clamp (VC) recordings. Voltage clamp methods were optimized for the fast MEPC rising phase using custom electronics. From 0-43 degrees C, A(c) increased by approximately 4.2-fold, while t(r) and t(f) decreased by approximately 3.6- and approximately 9.5-fold, respectively. Arrhenius plots were smoothly curved, with small apparent Q(10) (A(c)) or (Q(10))(-1) (t(r) and t(f)) values mostly well below 2.0. Nearly identical extracellular and voltage clamp results ruled out measurement artifacts, even for the shortest t(r) values (<60 microseconds). Monte Carlo simulation of MEPCs showed that a single underlying rate cannot determine the observed temperature dependence. To quantitatively reproduce the experimental t(f) results, a minimal model required activation energies of 46.0 (Q(10) approximately 2.0) and 63.6 (Q(10) approximately 2.5) kJ mol(-1) for channel opening and closing, respectively, and accounted for most of the observed changes in A(c) and t(r) as well. Thus, relatively large but offsetting temperature sensitivities of channel gating mostly govern and minimize the temperature dependence of MEPCs, preserving the safety factor for neuromuscular transmission. Additional temperature-sensitive parameters that could fine-tune the minimal model are discussed.

Acetylcholinesterase↗

Plethysmographic estimation of thoracic gas volume in apneic mice.

Electrical stimulation of intercostal muscles was employed to measure thoracic gas volume (TGV) during airway occlusion in the absence of respiratory effort at different levels of lung inflation. In 15 tracheostomized and mechanically ventilated CBA/Ca mice, the value of TGV obtained from the spontaneous breathing effort available in the early phase of the experiments (TGVsp) was compared with those resulting from muscle stimulation (TGVst) at transrespiratory pressures of 0, 10, and 20 cmH2O. A very strong correlation (r2= 0.97) was found, although with a systematically (approximately 16%) higher estimation of TGVst relative to TGVsp, attributable to the different durations of the stimulated (approximately 50 ms) and spontaneous (approximately 200 ms) contractions. Measurements of TGVst before and after injections of 0.2, 0.4, and 0.6 ml of nitrogen into the lungs in six mice resulted in good agreement between the change in TGVst and the injected volume (r2= 0.98). In four mice, TGVsp and TGVst were compared at end expiration with air or a helium-oxygen mixture to confirm the validity of isothermal compression in the alveolar gas. The TGVst values measured at zero transrespiratory pressure in all CBA/Ca mice [0.29 +/- 0.05 (SD) ml] and in C57BL/6 (N = 6; 0.34 +/- 0.08 ml) and BALB/c (N = 6; 0.28 +/- 0.06 ml) mice were in agreement with functional residual capacity values from previous studies in which different techniques were used. This method is particularly useful when TGV is to be determined in the absence of breathing activity, when it must be known at any level of lung inflation or under non-steady-state conditions, such as during pharmaceutical interventions.

Animals↗

Triggered electromyographic threshold for accuracy of thoracic pedicle screw placement in a porcine model.

STUDY DESIGN: A porcine model of thoracic pedicle screw insertion was used to determine the effect of screw position on triggered electromyographic response. OBJECTIVE: To develop a model of intraoperative detection of misplaced thoracic pedicle screws. SUMMARY OF BACKGROUND DATA: Triggered electromyographic stimulation has been a valuable aid in determining appropriate placement of lumbar pedicle screws. The use of pedicle screws is increasing in the thoracic spine. Misplaced thoracic pedicle screws may have significant implications if the spinal cord is injured. This study was an attempt to determine whether the established lumbar model can be used for thoracic pedicle screws. METHODS: Five 120- to 150-lb domestic pigs had 85 pedicle screws placed bilaterally in the thoracic spine at each level from T6 to T15. Screws were inserted entirely in the pedicle (Group A). After removal of the medial pedicle wall, the screws were reinserted in the pedicle with no neural contact (Group B). The screws were then placed with purposeful contact with the neural elements (Group C). The screws were stimulated, eliciting an electromyographic response in the intercostal muscles for each instrumented level. The type of response noted was classified as either primary (response from appropriate nerve root), secondary (response at different root) or no response (response at different root, no response at appropriate root). RESULTS: Two hundred fifty responses were recorded. A primary response was noted in 72% of recordings. There was a relatively consistent decrease in the triggered electromyographic response from Group A (mean 4.15 +/- 1.80 mA) to Group C (mean 3.02 +/- 2.53 mA) screws (P = 0.0003). There was little difference in the response obtained from Group A to Group B (mean 4.37 +/- 2.48 mA) screws (P > 0.05). When a primary response was recorded, the mean threshold electromyographic response recorded was significantly lower than recordings with secondary and no response recordings (P < 0.05). CONCLUSION: Even though there was a consistent decrease between the A and C screws that was more definitively separated when a primary response was elicited, it was not possible to determine a cutoff trigger electromyographic level that would consistently differentiate intraosseous from epidural pedicle screw placement. Furthermore, this method could not differentiate screws clearly in the pedicle from screws with medial pedicle wall breakthrough. A more direct method of spinal cord monitoring must be established to provide the surgeon with early warning of the potential of neural injury in the placement of thoracic pedicle screws.

Animals↗

GABAA and glycine receptors in regulation of intercostal and abdominal expiratory activity in vitro in neonatal rat.

The roles played by GABAA and glycine receptors in inspiratory-expiratory motor co-ordination and in tonic inhibitory regulation of expiratory motor activity were studied using brainstem-spinal cord (-rib) preparations from neonatal rats. Inspiratory activity was recorded from the C4 ventral root. Expiratory activity in internal intercostal muscle, internal oblique muscle or T13 ventral root was evoked by a decrease in perfusate pH from 7.4 to 7.1 (i.e. from normal to low pH conditions) and was limited to the first part of the expiratory phase. Under low pH conditions, bath application of 10 microM bicuculline, a GABAA receptor antagonist, caused the inspiratory burst to overlap the expiratory burst in 2/7 preparations. Overlapping of the expiratory burst with the inspiratory burst was observed in 7/7 preparations made under 10 microM bicuculline. Furthermore, such preparations exhibited expiratory bursts under bicuculline-containing normal pH conditions. Local application of 10 microM bicuculline to the brainstem under normal pH conditions evoked expiratory bursts, some of which overlapped the inspiratory bursts. Picrotoxin, another antagonist of the GABAA receptor, had similar effects. Under normal pH conditions, application of strychnine (0.2- 2.0 microM; a glycine receptor antagonist) to the brainstem did not evoke expiratory bursts. On subsequent application of strychnine-containing low pH solution, expiratory bursts were evoked and some (0.5 microM) or all (2.0 microM) of these overlapped the inspiratory burst. Simultaneous application of picrotoxin and strychnine to the brainstem evoked expiratory bursts that overlapped the inspiratory bursts and a subsequent decrease in perfusate pH to 7.1 increased the frequency of the respiratory rhythm. It was a characteristic finding that the duration of the expiratory burst exceeded that of the inspiratory burst under control low pH conditions. This remained true during concurrent blockade of GABAA and glycine receptors. The results suggest that in the in vitro preparation from neonatal rats: (1) GABAA and glycine receptors within the brainstem play important roles in the co-ordination between inspiratory and expiratory motor activity, (2) tonic inhibition via GABAA receptors, but not glycine receptors, plays a role in the regulation of expiratory motor activity and (3) inspiratory and expiratory burst termination is independent of both GABAA and glycine receptors.

Abdominal Wall↗

Respiratory muscle activity during vocalization in the squirrel monkey.

In order to find out which muscles are involved in the respiratory component of primate phonation, the activity of 17 abdominal and thoracic muscles was recorded during vocalization in the squirrel monkey. Vocalization-correlated activity was found in the musculi obliquus externus et internus, rectus et transversus abdominis, intercostalis externus et internus and intercartilagineus. It was lacking in the mm. iliocostalis, latissimus dorsi, longissimus dorsi rhomboideus, serratus posterior superior, trapezius, splenius capitis, sternocleidomastoideus, scalenus medius and pectoralis major. There was simultaneous activation of the rib-raising external and rib-lowering internal intercostal muscles during most vocalizations. It is hence concluded that the intercostals, rather than supporting expiratory efforts, serve to stabilize the thorax, thus providing an anchorage against which the abdominal muscles can act.

Abdominal Muscles↗

Changes in histochemical profile of rat respiratory muscles in hypo- and hyperthyroidism.

Rat respiratory muscles underwent considerable changes in histochemical fibre type profile in response to hypo- and hyperthyroidism. Hypothyroidism increased the proportion of type 1 slow oxidative fibres in diaphragm and to a lesser extent in intercostal muscles. Hyperthyroidism resulted in a decreased proportion of type 1 fibres in both diaphragm and intercostals. These changes were broadly comparable to those reported previously in rat limb muscles. In normal rat respiratory muscles, the type 1 fibres were characterized by very high levels of beta-hydroxybutyrate dehydrogenase which was thought to contribute to the fatigue-resistance of these muscles. The type 2B fast glycolytic fibres, and to a lesser extent type 2A fast oxidative fibres, contained high levels of mitochondrial alpha-glycerophosphate dehydrogenase, an enzyme known to be specifically affected in dysthyroid states. The implications of the observed changes in fibre type profile with respect to the oxidative metabolism of rat respiratory muscles are discussed.

Animals↗

Development of innervation of skeletal muscle fibers in man: relation to acetylcholine receptors.

The aim of this study was to establish the time scale of developmental changes in innervation of skeletal muscle fibers in man. Specimens of thigh and intercostal muscle from 19 embryos and 18 infants were examined with histological methods which enabled the discrimination between fetal (gamma) and adult (epsilon) types of acetylcholine receptors (AChRs). At 8 weeks of development, AChRs were distributed diffusely in the myotube membranes. Following onset of innervation in approximately the ninth week the length of the AChR positive area diminished and reached its shortest size at the sixteenth developmental week. At the sixteenth and eighteenth week some nerve terminals opposed the muscle membrane outside the AChR positive area. Decrease in the number of nerve terminals, strongly suggesting elimination of polyneuronal innervation, started in the sixteenth week and was completed in the twenty-fifth week. This fetal (gamma) type of AChR could no longer be demonstrated after the thirty-first week. The length of the end-plates as determined by the presence of AChRs increased again in the last week before birth and reached a plateau size by the end of the first year after birth. It is concluded that in man the transition from poly- to mononeuronal innervation takes place between the sixteenth and twenty-fifth weeks of development. The evidence available suggests that the retraction of nerve terminals is preceded by loss of AChRs from the muscle membrane facing the terminals. There is no relationship between retraction of nerve terminals and the switch from fetal to adult type of AChR. The size of the presynaptic apparatus changes little after the first year of life.

Child↗

Cardiorespiratory response to physical conditioning in children with bronchial asthma.

The relationship of physical conditioning to changes in static lung volumes (hyperinflation) and airway dynamics (bronchoconstriction) as well as to ventilatory gas exchange, heart rate reserve, breathing reserves, and working capacity at a heart rate of 170/min (WC 170) was evaluated in 23 children (16 girls, 7 boys) between 6 and 15 years of age who had perennial asthma. Lung function tests including incremental cycle ergooxymetry were performed before and after a 15-week period of regular physical training (RPT). Lung function data obtained after RPT showed a significant improvement (P less than 0.05) in both hyperinflation and specific airway conductance, whereas oxygen consumption only increased related to lean body mass and heart rate. However, WC 170 and work tolerance during the endurance phase of the exercise test were significantly increased (P less than 0.05 and less than 0.01, respectively). In view of the relationship that has recently been found between exercise tolerance and lung mechanics in adults, the decreased hyperinflation and bronchoconstriction observed in our population after RPT is striking. This finding was presumably a consequence of the effect of RPT on breathing technique and chest wall mechanics. Ventilation of the lungs may improve because of mobilization of the costovertebral articulations, inspiratory muscle relaxation, an optimized force-length relationship of the respiratory muscles, and closer linkage between the diaphragm and intercostal muscles. Therefore, RPT might be an effective addition to standard drug regimens in the management of childhood asthma.

Adolescent↗

Upstream sequences of the myogenin gene convey responsiveness to skeletal muscle denervation in transgenic mice.

Myogenin, as well as other MyoD-related skeletal muscle-specific transcription factors, regulate a large number of skeletal muscle genes during myogenic differentiation. During later development, innervation suppresses myogenin expression in the fetal hind limb musculature. Denervation of skeletal muscle reverses the effects of the nerve, and results in the reactivation of myogenin expression, as well as of other embryonic muscle proteins. Here we report that myogenin upstream sequences confer tissue- and developmental-specific expression in transgenic mice harboring a myogenin/chloramphenicol acetyltransferase (CAT) reporter construct. Using in situ hybridization to analyze serial sections of E12.5 embryos, we found colocalization of CAT and endogenous myogenin transcripts in the primordial muscle of the head and limbs, in the intercostal muscle masses, and in the most caudal somites. Later in development, we observed that the expression of the transgene and endogenous myogenin gene continued to be restricted to skeletal muscle but decreased shortly after birth; a period that coincides with the innervation of secondary myotubes. Furthermore, denervation of the mouse hind limbs induced a 10-fold accumulation of CAT and endogenous myogenin transcripts by 1 day after sciatic nerve resection; a 25-fold increase was observed by 4 days after denervation. Interestingly, we observed that the accumulation of CAT enzyme activity lagged considerably with respect to the increase in CAT transcripts. Our results indicate that the cis-acting elements that temporally and spatially confine transcription of the gene during embryonic development, and that mediate the responses to innervation and denervation of muscle, lie within the upstream sequences analyzed in these studies.

Animals↗

Inferences about respiratory muscle use after cardiac surgery from compartmental volume and pressure measurements.

BACKGROUND: After upper abdominal surgery, patients have been observed to have alterations in respiratory movements of the rib cage and abdomen and respiratory shifts in pleural and abdominal pressure that suggest dysfunction of the diaphragm. The validity of making such deductions about diaphragm function from these observations is open to discussion. METHODS: In eight adult patients, American Society of Anesthesiologists physical status 2, scheduled for elective cardiac surgery, we measured respiratory rate, tidal volume, rib cage and abdominal cross-section changes, and esophageal (Pes) and gastric (Pga) pressures preoperatively, 1 day postoperatively, and 5 days postoperatively. These data were analyzed in detail by following the variables through each respiratory cycle. RESULTS: Mean delta Pga/delta Pes decreased from 0.73 preoperatively to -0.56 1 day postoperatively and recovered to 0.47 5 days postoperatively. Plots of Pes against Pga and rib cage against abdominal expansion (Konno-Mead diagrams) were constructed. Six patients showed a postoperative pattern of breathing similar to that seen in patients who have undergone abdominal surgery: a decrease in the ratio of delta Pga/delta Pes and a shift toward rib cage expansion, with an increase in breathing rate and a decrease in tidal volume. This change was accomplished in most cases by the use of abdominal muscles in expiration with an increase in inspiratory intercostal muscle action without an increase in diaphragm activation, that is, a shift in the normal balance of respiratory muscle use in favor of muscles other than the diaphragm. A different ventilatory pattern was observed in the other two patients, consisting of minimal rib cage excursion and a large abdominal excursion. In these cases tidal volume was generated largely by contraction and relaxation of abdominal muscles with probable reduction in diaphragm activity. In addition, five patients exhibited positive changes in Pes at the end of inspiration that corresponded to closure of the upper airway, relaxation of inspiratory muscles, and subsequent opening of the airway with sudden exhalation, producing a grunt. CONCLUSIONS: Indirect measurements of respiratory muscle action based on pressure and chest wall motion are easier than are assessments based on implanted electromyogram electrodes and sonomicrometers that measure electric activity and muscle length, respectively, directly. Interpretation requires numerous assumptions and detailed analysis of phase relations among the variables. In patients after thoracic surgery, however, these measurements strongly point to a shift in the distribution of motor output toward muscles other than the diaphragm.

Abdominal Muscles↗