Range Of Lung Volumes Research Articles

Training Specificity of Inspiratory Muscle Training Methods: A Randomized Trial.

IntroductionInspiratory muscle training (IMT) protocols are typically performed using pressure threshold loading with inspirations initiated from residual volume (RV). We aimed to compare effects of three different IMT protocols on maximal inspiratory pressures (PImax) and maximal inspiratory flow (V̇Imax) at three different lung volumes. We hypothesized that threshold loading performed from functional residual capacity (FRC) or tapered flow resistive loading (initiated from RV) would improve inspiratory muscle function over a larger range of lung volumes in comparison with the standard protocol.Methods48 healthy volunteers (42% male, age: 48 ± 9 years, PImax: 110 ± 28%pred, [mean ± SD]) were randomly assigned to perform three daily IMT sessions of pressure threshold loading (either initiated from RV or from FRC) or tapered flow resistive loading (initiated from RV) for 4 weeks. Sessions consisted of 30 breaths against the highest tolerable load. Before and after the training period, PImax was measured at RV, FRC, and midway between FRC and total lung capacity (1/2 IC). V̇Imax was measured at the same lung volumes against a range of external threshold loads.ResultsWhile PImax increased significantly at RV and at FRC in the group performing the standard training protocol (pressure threshold loading from RV), it increased significantly at all lung volumes in the two other training groups (all p < 0.05). No significant changes in V̇Imax were observed in the group performing the standard protocol. Increases of V̇Imax were significantly larger at all lung volumes after tapered flow resistive loading, and at higher lung volumes (i.e., FRC and 1/2 IC) after pressure threshold loading from FRC in comparison with the standard protocol (all p < 0.05).ConclusionOnly training with tapered flow resistive loading and pressure threshold loading from functional residual capacity resulted in consistent improvements in respiratory muscle function at higher lung volumes, whereas improvements after the standard protocol (pressure threshold loading from residual volume) were restricted to gains in PImax at lower lung volumes. Further research is warranted to investigate whether these results can be confirmed in larger samples of both healthy subjects and patients.

Enhancing Swallowing-Respiration Coordination

This review was designed to summarize our current understanding of optimal respiratory-swallowing coordination and to highlight a novel intervention to improve coordination in patients with dysphagia consequent to head and neck cancer and treatment. Additional consideration was given to the challenges of recording respiratory movements for clinical and research purposes surrounding respiratory-swallowing coordination. Our recent findings in normal humans reveal that the respiratory pause to accommodate swallowing interrupts quiet breathing in a restricted range of lung volumes from mid to low tidal volume. We have hypothesized that this “optimal” range imparts significant airway protective and physiological swallowing benefits. Systematic respiratory-swallow training in patients treated for head and neck cancer with refractory dysphagia and less than optimal patterning not only improved respiratory-swallowing coordination but also diminished aspiration and improved key components of swallowing physiology. These data suggest that respiratory-swallow training may be an important treatment tool to re-establish respiratory-swallowing coordination and could be used in conjunction with other swallowing treatments to improve swallowing outcomes in susceptible patients. Future research is needed to explore mechanisms of change and to refine the treatment methodology to further improve swallowing outcomes.

Respiratory-swallowing coordination in normal subjects: Lung volume at swallowing initiation

This study was designed to investigate the significance of bolus types and volumes, delivery methods and swallowing instructions on lung volume at swallowing initiation in normal subjects in a single experiment using a multifactorial approach. Our broad range goal was to determine optimal lung volume range associated with swallowing initiation to provide training targets for dysphagic patients with disordered respiratory-swallow coordination. Our hypothesis was that swallows would be initiated within a limited range of quiet breathing lung volumes regardless of bolus volume, consistency or task. Results confirmed this hypothesis and revealed that swallows were initiated at mean lung volume=244ml. Cued swallows were initiated at lower quiet breathing volumes than un-cued swallows (cued=201ml; un-cued=367ml). Water boluses were initiated at slightly higher quiet breathing volumes than solids. Data suggest that swallows occur within a restricted range of lung volumes with variation due to instructions, bolus type and other experimental variables.

Respiratory Laryngeal Coordination in Airflow Conservation and Reduction of Respiratory Effort of Phonation

This study evaluates the need of airflow conservation and the effect of glottal resistance on respiratory effort of phonation under different phonation conditions. A computational model of the pressure-volume-flow relationship of the respiratory system is developed. Simulations show that increasing the glottal resistance reduces the glottal airflow and allows phonation to be sustained for a longer breath group duration. For a given breath group duration, the reduced airflow also allows phonation to be sustained within a narrow range of lung volumes, thus lowering the overall respiratory effort. This study shows that for breath group durations and subglottal pressures typical of normal conversational speech, airflow conservation or maintaining "effortless" respiratory support does not provide a stricter requirement on the glottal resistance than that required for initiating phonation. However, the need for airflow conservation and respiratory effort reduction becomes relevant when the target subglottal pressure and breath group duration increase as in prolonged speech or singing or in conditions of weakened pulmonary function. In those conditions, the glottal resistance is expected to increase proportionally with increasing subglottal pressure to conserve airflow consumption and reduce respiratory effort.

Measurement of the pressure-volume curve in mouse lungs.

In recent decades the mouse has become the primary animal model of a variety of lung diseases. In models of emphysema or fibrosis, the essential phenotypic changes are best assessed by measurement of the changes in lung elasticity. To best understand specific mechanisms underlying such pathologies in mice, it is essential to make functional measurements that can reflect the developing pathology. Although there are many ways to measure elasticity, the classical method is that of the total lung pressure-volume (PV) curve done over the whole range of lung volumes. This measurement has been made on adult lungs from nearly all mammalian species dating back almost 100 years, and such PV curves also played a major role in the discovery and understanding of the function of pulmonary surfactant in fetal lung development. Unfortunately, such total PV curves have not been widely reported in the mouse, despite the fact that they can provide useful information on the macroscopic effects of structural changes in the lung. Although partial PV curves measuring just the changes in lung volume are sometimes reported, without a measure of absolute volume, the nonlinear nature of the total PV curve makes these partial ones very difficult to interpret. In the present study, we describe a standardized way to measure the total PV curve. We have then tested the ability of these curves to detect changes in mouse lung structure in two common lung pathologies, emphysema and fibrosis. Results showed significant changes in several variables consistent with expected structural changes with these pathologies. This measurement of the lung PV curve in mice thus provides a straightforward means to monitor the progression of the pathophysiologic changes over time and the potential effect of therapeutic procedures.

Validation of a Photoacoustic Gas Analyser for the Measurement of Functional Residual Capacity Using Multiple-Breath Inert Gas Washout

Background: The respiratory mass spectrometer is the current gold-standard technique for performing multiple-breath inert gas washout (MBW), but is expensive and lacks portability. A number of alternative techniques have recently been described. Objectives: We aimed to validate, using an in vitro lung model, an open-circuit MBW system that utilises a portable photoacoustic gas analyser, with sulphur hexafluoride (SF₆) as the inert tracer gas. Methods: An acrylic glass lung model was utilised to assess the accuracy of functional residual capacity (FRC) measurements derived from MBW. Measurements were performed in triplicate at 20 combinations of simulated FRC, tidal volume and respiratory rate. FRC measured using MBW (FRC_mbw) was compared to FRC calculated from the known dimensions of the model (FRC_calc). MBW was also performed in 10 healthy subjects and 14 patients with asthma. Results: The MBW system measured FRC with high precision. The mean bias of FRC_mbw with respect to FRC_calc was -0.4% (95% limits of agreement of -4.6 and 3.9%). The mean coefficient of variation of triplicate FRC measurements was 4.0% in vivo and 1.0% in vitro. MBW slightly underestimated low lung volumes and overestimated high lung volumes, but this did not cause a significant error in lung clearance index except at lung volumes below 1,500 ml. Conclusions: The open-circuit MBW system utilising SF₆ as the inert tracer gas and a photoacoustic gas analyser is both accurate and repeatable within the adult range of lung volumes. Further modifications would be required before its use in young children or infants.

Effect of airway smooth muscle tone on airway distensibility measured by the forced oscillation technique in adults with asthma

Airway distensibility appears to be unaffected by airway smooth muscle (ASM) tone, despite the influence of ASM tone on the airway diameter-pressure relationship. This discrepancy may be because the greatest effect of ASM tone on airway diameter-pressure behavior occurs at low transpulmonary pressures, i.e., low lung volumes, which has not been investigated. Our study aimed to determine the contribution of ASM tone to airway distensibility, as assessed via the forced oscillation technique (FOT), across all lung volumes with a specific focus on low lung volumes. We also investigated the accompanying influence of ASM tone on peripheral airway closure and heterogeneity inferred from the reactance versus lung volume relationship. Respiratory system conductance and reactance were measured using FOT across the entire lung volume range in 22 asthma subjects and 19 healthy controls before and after bronchodilator. Airway distensibility (slope of conductance vs. lung volume) was calculated at residual volume (RV), functional residual capacity (FRC), and total lung capacity. At baseline, airway distensibility was significantly lower in subjects with asthma at all lung volumes. After bronchodilator, distensibility significantly increased at RV (64.8%, P < 0.001) and at FRC (61.8%, P < 0.01) in subjects with asthma but not in control subjects. The increased distensibility at RV and FRC in asthma were not associated with the accompanying changes in the reactance versus lung volume relationship. Our findings demonstrate that, at low lung volumes, ASM tone reduces airway distensibility in adults with asthma, independent of changes in airway closure and heterogeneity.

Deglutitive Subglottic Air Pressure and Respiratory System Recoil

The purpose of this experiment was to confirm the presence of positive subglottic air pressure during swallowing, known as deglutitive subglottic air pressure (DPsub), in a group of healthy individuals. We also sought to determine if respiratory system recoil is responsible for generating the pressure. Ten healthy volunteers underwent direct DPsub measurement via percutaneous puncture of the cricothyroid membrane. Simultaneous DPsub and nasal airflow volumes were recorded while participants swallowed calibrated boluses over a wide range of lung volumes. Body plethysmography was used to determine functional residual capacity and residual volume. A custom respiratory recoil measurement system was used to measure recoil pressures. Regression analysis of lung volume on DPsub and lung volume on recoil pressure yielded strong linear relationships (P<0.0001, R (2)=0.71 and P<0.0001, R (2)=0.69, respectively). A mixed-model analysis of the effect of method (direct puncture or recoil) on pressure showed that there was no effect (F=0.63; P=0.43). By confirming the presence of DPsub in healthy adults and showing that respiratory system recoil is the most likely mechanism that generates DPsub, treatment of persons with dysphagia has even greater potential to be expanded to include consideration of factors that affect respiratory control and recoil forces.

Maximum static inspiratory and expiratory pressures with different lung volumes.

BackgroundMaximum pressures developed by the respiratory muscles can indicate the health of the respiratory system, help to determine maximum respiratory flow rates, and contribute to respiratory power development. Past measurements of maximum pressures have been found to be inadequate for inclusion in some exercise models involving respiration.MethodsMaximum inspiratory and expiratory airway pressures were measured over a range of lung volumes in 29 female and 19 male adults. A commercial bell spirometry system was programmed to occlude airflow at nine target lung volumes ranging from 10% to 90% of vital capacity.ResultsIn women, maximum expiratory pressure increased with volume from 39 to 61 cmH2O and maximum inspiratory pressure decreased with volume from 66 to 28 cmH2O. In men, maximum expiratory pressure increased with volume from 63 to 97 cmH2O and maximum inspiratory pressure decreased with volume from 97 to 39 cmH2O. Equations describing pressures for both sexes are:Pe/Pmax = 0.1426 Ln( %VC) + 0.3402 R2 = 0.95Pi/Pmax = 0.234 Ln(100 - %VC) - 0.0828 R2 = 0.96ConclusionThese results were found to be consistent with values and trends obtained by other authors. Regression equations may be suitable for respiratory mechanics models.

Volume-related and volume-independent effects of posture on esophageal and transpulmonary pressures in healthy subjects

Ventilator management decisions in acute lung injury could be better informed with knowledge of the patient's transpulmonary pressure, which can be estimated using measurements of esophageal pressure. Esophageal manometry is seldom used for this, however, in part because of a presumed postural artifact in the supine position. Here, we characterize the magnitude and variability of postural effects on esophageal pressure in healthy subjects to better assess its significance in patients with acute lung injury. We measured the posture-related changes in relaxation volume and total lung capacity in 10 healthy subjects in four postures: upright, supine, prone, and left lateral decubitus. Then, in the same subjects, we measured static pressure-volume characteristics of the lung over a wide range of lung volumes in each posture by using an esophageal balloon catheter. Transpulmonary pressure during relaxation (PLrel) averaged 3.7 (SD 2.0) cmH2O upright and -3.3 (SD 3.2) cmH2O supine. Approximately 58% of the decrease in PLrel between the upright and supine postures was due to a corresponding decrease in relaxation volume. The remaining 2.9-cmH2O difference is consistent with reported values of a presumed postural artifact. Relaxation volumes and pressures in prone and lateral postures were intermediate. To correct estimated transpulmonary pressure for the effect of lying supine, we suggest adding 3 cmH2O (95% confidence interval: -1 to +7 cmH2O). We conclude that postural differences in estimated transpulmonary pressure at a given lung volume are small compared with the substantial range of PLrel in patients with acute lung injury.

Measurement of Forced Expiratory Flows and Lung Volumes

After completing this article, readers should be able to: 1. Describe the information that measurements of forced expiratory flow can provide in spontaneously breathing and mechanically ventilated infants. 2. Delineate how lung volume can be measured. The measurements of forced expiratory flows and lung volumes are important to the evaluation of patients who have respiratory symptoms. Until recently, measurements have been restricted to adults and children old enough to cooperate with testing maneuvers. Newer techniques have enabled such measurements to be made in infants and led to improved understanding of normal lung and airway growth during infancy and early childhood, when dramatic changes occur. The measurements have had important clinical uses in the evaluation and treatment of infants who have respiratory disease, but their use has been limited because they require specialized equipment and expertise as well as sedation of the infant. In this article, we discuss the techniques required for measurement of forced expiratory flows and lung volumes, their limitations, and applications in clinical practice. Detection of airflow obstruction, by physical examination or by quantitative measurement techniques, is facilitated by increasing expiratory flow rates. Measurement of forced expiratory flows is useful because flow rates are inversely proportional to the fourth power of the radius of the airway and, therefore, are indicative of airway size when flow is limited. Disease states affecting the airways, including asthma, bronchopulmonary dysplasia (BPD), or congenital lesions such as pulmonary hypoplasia or vascular airway compression, are expected to decrease expiratory flow. Infants typically are sedated for testing to maintain relaxed breathing with a face mask placed over the mouth and nose. This sedation often is perceived by parents and physicians as one of the barriers to such testing. (1) However, sedation can be achieved safely using oral chloral hydrate at a dose of 80 to 100 mg/kg. …

Preliminary studies on respiratory activity in speech

Work at Edinburgh University in the 1950s, summarized by Ladefoged [Three Area of Experimental Phonetics (Oxford University Press, Oxford, 1967)] claimed that (1) the mean power for speech was provided by actions of the respiratory muscles. The external intercostals check the outgoing airflow when speaking with high lung volumes, and the internal intercostals, rectus abdominis, and other muscles become more active as lung volume decreases. (2) Stressed syllables are produced by increases of respiratory power above the mean, usually by further activity of the internal intercostals. Hixon and Weismer (1995) pointed out technical limitations of these early studies, but wrongly indicated that they were of little value. These studies have been replicated with modern methods to measure intramuscular EMG and airflow and pressure. The two subjects studied to date follow the pattern previously described. In addition the improved techniques indicate that speakers exercise further control by bringing in stabilizing antagonistic muscles. These results are consistent with the general hypothesis that the central nervous system is able to control subglottal pressure by using various combinations of passive elastic and active muscle forces, thereby achieving motor equivalence and acoustic invariance over a wide range of lung volumes.

Estimation of diaphragm length in patients with severe chronic obstructive pulmonary disease

In patients with advanced chronic obstructive pulmonary disease (COPD) diaphragm function may be compromised because of reduced muscle fibre length. Diaphragm length (L Di) can be estimated from measurements of transverse diameter of the rib cage (D Rc) and the length of the zone of apposition (L Zapp) in healthy subjects, but this method has not been validated in patients with COPD. Postero-anterior chest radiographs were obtained at total lung capacity (TLC), functional residual capacity (FRC) and residual volume (RV) in nine male patients with severe COPD (mean [S.D.]; FEV 1, 23 [6] %pred.; FRC, 199 [15] %pred.). Radiographs taken at TLC were used to identify the lateral costal insertions of the diaphragm (L Zapp assumed to approach zero at TLC). L Di was measured directly and also estimated from measurements of L Zapp and D Rc using a prediction equation derived from healthy subjects. The estimation of L Di was highly accurate with an intraclass correlation coefficient of 0.93 and 95% CI of ∼±8% of the true value. L Di decreased from 426 (64) mm at RV to 305 (31) mm at TLC. As there were only small and variable changes in D Rc across the lung volume range, most of the L Di changes occurred in the zone of apposition. Additional studies showed that measurements of L Di from PA and lateral radiographs performed at different lung volumes were tightly correlated. These results suggest that non-invasive measurements of L Zapp in the coronal plane (e.g. using ultrasonography) and D Rc (e.g. using magnetometers) can be used to provide an accurate estimate of L Di in COPD patients.

Effect of lung volume on the oesophageal diaphragm EMG assessed by magnetic phrenic nerve stimulation.

Previous studies have shown conflicting results on the effect of lung volume on the diaphragm compound muscle action potential (CMAP). Consequently, the ability to quantify the oesophageal diaphragm electromyography (EMG) has been questioned. If lung volume changes have little effect on the diaphragm CMAP the accurate measurement of voluntary EMG, as an index of respiratory drive, may be possible. Furthermore, the measurement of CMAP could provide useful clinical information when evaluating patients with neuromuscular disease. To reassess the effect of lung volume on the oesophageal diaphragm CMAP, six normal subjects were studied using an oesophageal catheter incorporating seven electrodes (number one being proximal and seven distal) that were 1 cm in length and 1 cm apart. Electrode number three was positioned at the centre of the electrically active region of the diaphragm (EARdi) at functional residual capacity (FRC). The diaphragm CMAP elicited by bilateral magnetic stimulation of the phrenic nerves was simultaneously recorded from four electrode pairs. Pair one was created from electrodes one and three, pair two from electrodes two and four, pair three from electrodes three and five, and pair four from electrodes five and seven. Phrenic nerve stimulation was at residual volume (RV), FRC, FRC+1.0 L, FRC+2.0 L, and total lung capacity (TLC). The CMAP recorded from pair one was least influenced by changes in lung volume and the amplitude was 2.41+/-0.39 (mean+/-SD), 2.60+/-0.27, 2.64+/-0.29, and 2.71+/-0.45 mV at RV, FRC, FRC+1.0 L and FRC+2.0 L, respectively. At TLC the CMAP was more variable. The CMAP amplitude recorded from pair two increased with increasing lung volume and at FRC+2.0 L was 3.7 times larger than that at FRC. Pair four usually recorded substantially smaller CMAPs at all lung volumes. This study shows that the diaphragm compound muscle action potential recorded from an oesophageal electrode just above the diaphragm is relatively stable over the lung volume range residual volume to functional residual capacity+2.0 L.

Effects of Lung Volume on Parasternal Pressure-Generating Capacity in Dogs

Previous studies have suggested that the optimum length for force generation of the parasternal intercostal (PS) muscles is well above functional residual capacity (FRC). We further explored this issue by examining the pressure-generating capacity of the PS muscles as a function of lung volume in anaesthetized dogs. Upper thoracic spinal cord stimulation (SCS) was used to electrically activate the PS muscles. Changes in airway pressure and parasternal resting length (LR) during airway occlusion were monitored over a wide range of lung volumes during SCS. To assess the effects of parasternal contraction alone, SCS was performed following phrenicotomy and section of the external intercostal, levator costae and triangularis sterni muscles. With increasing lung volume, there were progressive decrements in the capacity of the PS muscles to produce changes in airway pressure. The relationship between PS pressure generation and lung volume was similar to a previous comparable assessment of the external intercostal muscles. The PS muscles shortened during passive inflation and also shortened further (by > 20 % of LR) during SCS. Total shortening (passive plus active) increased progressively with increasing lung volume. Our results indicate that the capacity of the PS muscles to produce changes in airway pressure (a) falls progressively with increasing lung volume and (b) is similar to that of the external intercostal muscles. We speculate that the fall in PS pressure-generating capacity is related, in part, to progressive reductions in end-inspiratory length.

The effect of lung volume on transdiaphragmatic pressure

Diaphragm strength can be assessed by measurement of transdiaphragmatic pressure (Pdi) in response to stimulation of the phrenic nerves. The length-tension relationship of the diaphragm can be studied by measuring twitch Pdi over the range of lung volume. Previous studies of the relationship between lung volume and diaphragm strength have used the technique of electrical stimulation of the phrenic nerves. In these studies, the phenomenon of twitch potentiation has not been taken into account. It has previously been shown that prior contraction of the diaphragm can greatly enhance the twitch response, thus affecting the measurements. The aim of this study was to investigate the relationship between unpotentiated twitch Pdi and lung volume for volumes ranging from residual volume (RV) to total lung capacity (TLC) in normal subjects. Great care was taken to avoid muscle potentiation. For this purpose, we stimulated the phrenic nerves with a magnetic stimulator. In addition, we used positive pressure to inflate the lungs to high lung volumes. The impact of twitch potentiation on the length-tension relationship was investigated by subjects making maximum inspiratory efforts prior to phrenic nerve stimulation. The unpotentiated twitch Pdi decreased in a linear fashion with increasing lung volume over the full range of vital capacity by 0.54 kPa.L-1. Potentiation increased twitch Pdi by 40% at FRC and the effect was similar, in absolute terms, at all lung volumes. In relative terms, the effect of potentiation became greater as lung volume increased, and more than doubled twitch Pdi at TLC. With increasing lung volume, there is a linear fall in unpotentiated twitch Pdi with a slope that is less steep, over the same range of absolute lung volume, than previously reported. When assessing diaphragm strength by the twitch technique, it is essential to control for lung volume and equally important to control for twitch potentiation.

Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.

Mechanical ventilation may promote overdistension-induced pulmonary lesions in patients with acute respiratory distress syndrome (ARDS). The static pressure-volume (P-V) curve of the respiratory system can be used to determine the lung volume and corresponding static airway pressure at which lung compliance begins to diminish (the upper inflection point, or UIP). This fall in compliance may indicate overdistension of lung units. We prospectively studied 42 patients receiving mechanical ventilation with an FIO2 of 0.5 or more for at least 24 h. According to the Lung Injury Score (LIS), 25 patients were classified as having ARDS (LIS > 2.5), while 17 patients constituted a non-ARDS control group. The P-V curve was obtained every 2 d. Mechanical ventilation initially used standard settings (volume-control mode, a positive end-expiratory pressure [PEEP] adjusted to the lower inflection point on the P-V curve, and a tidal volume [VT] of 10 ml/kg). The end-inspiratory plateau pressure (Pplat) was compared to the UIP, and VT was lowered when the Pplat was above the UIP. In the range of lung volume studied on the P-V curves (up to 1600 ml), a UIP could be shown in only one control patient (at 23 cm H2O). By contrast, a UIP was present on the P-V curve obtained from all patients with ARDS, corresponding to a mean airway pressure of 26 +/- 6 cm H2O, a lung volume of 850 +/- 200 ml above functional residual capacity and 610 +/- 235 ml above PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrical activation of the expiratory muscles to restore cough.

Many patients with spinal cord injury have paralysis of their expiratory muscles and, consequently, lack an effective cough. The purpose of the present study was to evaluate the utility of lower thoracic spinal cord stimulation (SCS) to activate the expiratory muscles. Studies were performed on 15 anesthetized dogs. A quadripolar stimulating electrode (Medtronic Model 3586) was inserted epidurally and on the ventral surface of the lower thoracic spinal cord. Changes in airway pressure, airflow, and internal intercostal and abdominal muscle length were monitored to assess the effects of electrical stimulation. Spinal stimulation applied at the T9-T10 spinal level provided maximal changes in airway pressure generation in preliminary experiments. All subsequent studies were therefore performed with the electrode positioned at this level. The expiratory muscles were stimulated supramaximally over a wide range of lung volumes which were expressed as the corresponding change in airway pressure. The pressure-generating capacity of the expiratory muscles was evaluated by the change in airway pressure produced by SCS during airway occlusion. Peak expiratory airflow was also monitored following release of occlusion. At FRC, deflation (-10 cm H2O) and inflation (+ 30 cm H2O), SCS resulted in positive airway pressures of 44 cm H2O +/- 4 SE, 28 cm H2O +/- 3 SE, and 82 cm H2O +/- 7 SE. The relationship between airway pressure expiratory airflow generation and lung volume was linear (slope = 1.34 +/- 0.04) over the entire vital capacity range. Our results indicate that: (1) a major portion of the expiratory muscles can be activated reproducibly and in concert by electrical stimulation, and (2) this technique may be a clinically useful method of restoring cough in spinal cord injured patients.

Stability of evoked parasternal intercostal muscle electromyogram at increased end-expiratory lung volume.

The diaphragmatic electromyogram has been measured as an index of the level of diaphragmatic activation. The diaphragmatic electromyogram, however, even when measured by intramuscular electrodes, can be artifactually altered by a change in lung volume (A. Brancatisano, S. M. Kelly, A. Tully, S. H. Loring, and L. A. Engel. J. Appl. Physiol. 66: 1699-1705, 1989) or by a change in body position. The parasternal intercostal muscle may be less subject to the mechanisms that are believed to produce this artifactual change. We asked whether the parasternal intercostal electromyographic activity could be reliable when lung volume changes. Six supine rabbits were anesthetized with ketamine and xylazine. Fine bipolar copper wires, with their tips exposed, were inserted into the left parasternal intercostal muscle in the third interspace. A stimulus that was three times maximal was applied to the corresponding intercostal nerve, and the resulting action potential (AP) was photographed. Parasternal intercostal muscle length was measured by sonomicrometry over the vital capacity range. There were small nonsignificant changes in the AP from functional residual capacity (FRC) to total lung capacity. From FRC to residual volume there was variation in the AP. The AP was also quite stable when regional conductivity was altered but showed variation when the parasternal intercostal muscle length change was accentuated by traction on the rib cage. We conclude that the parasternal intercostal electromyographic activity can be reliably used to measure inspiratory motoneuron output to it over the range of lung volumes from FRC to total lung capacity.

Myosin and actin filament lengths in diaphragms from emphysematous hamsters

In vitro studies of the diaphragm from emphysematous animals have, in some instances, shown an alteration in its sarcomere length-tension relationship and a decreased maximal specific tension. To our knowledge, it has never been determined whether such functional changes may be indicative of ultrastructural adaptations, e.g., changes in filament lengths and thus cross-bridge number. To address this, we compared filament lengths in diaphragms from hamsters in which emphysema was induced by endotracheal instillation of elastase (E) 5 mo before the hamsters were killed with those from control hamsters (C; saline instillation). Diaphragms were then fixed by vascular perfusion with buffered glutaraldehyde in situ at airway pressures set to approximate the physiological range of lung volumes from residual volume (RV) to total lung capacity (TLC). Ultrathin sections (50-70 nm) were taken parallel to the muscle fiber axis and examined by electron microscopy (x33,000). Sarcomere and filament length measurements were calibrated using an actin periodicity of 39 nm and an M-band width of 86 nm to correct for dimensional changes during preparation. Emphysema increased the change in lung volume from -20 to +25 cmH2O airway pressure (from RV to TLC) by approximately 88%, and the displacement volume of excised lung at 0 cmH2O airway pressure was increased by approximately 138% on average. Neither myosin (C = 1.592 +/- 0.027; E = 1.572 +/- 0.035 micron; P = 0.72) nor actin (C = 1.210 +/- 0.035; E = 1.221 +/- 0.014 micron; P = 0.76) filament lengths were affected by emphysema. Thus, filament length changes do not underlie the diaphragm functional adaptations observed previously in emphysema.