Chest Wall Strapping Research Articles

Cardiorespiratory Coupling Response to Chest Wall Strapping in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a common lung disease characterized by limited expiratory airflow due to lung destruction or airway obstruction. Chest wall strapping (CWS) is a potential therapy technique that restricts the upper abdomen, inducing breathing at lower lung volumes and opening small airways. Although the respiratory impacts of CWS have been examined, the relationship between CWS and the cardiovascular system, which is closely tied to ventilation, has not been well‐established. Additionally, COPD patients have reduced autonomic nervous system activity, which may be reflected in cardiorespiratory coupling. Cardiorespiratory coupling causes increased heart rate during inhalation to accommodate for increased blood return. The strength of this relationship was evaluated during CWS in five COPD and six control patients by analyzing heart rate changes during ventilation cycles. Heart rate and ventilatory data were collected during baseline, CWS, and post‐CWS removal periods. Average heart rate during each inhalation and exhalation was plotted against tidal volume, with the slope of the linear regression representing the strength of the cardiorespiratory coupling relationship (BPM/L). Multi‐factor ANOVA statistics showed a significantly diminished strength in COPD patients compared to control (p < 0.001). There was no significant change in either group post‐CWS, suggesting that the same‐sized breaths will cause the heart to respond similarly regardless of the total lung capacity. A potential consequence of diminished cardiorespiratory coupling in COPD patients is strain on the right side of the heart, which then has to pump larger stroke volumes. Blunted cardiorespiratory coupling is not further impaired by CWS.

Effect of increased positive end-expiratory pressure on intracranial pressure and cerebral oxygenation: impact of respiratory mechanics and hypovolemia

BackgroundTo evaluate the impact of positive end-expiratory pressure (PEEP) on intracranial pressure (ICP) in animals with different respiratory mechanics, baseline ICP and volume status.MethodsA total of 50 male adult Bama miniature pigs were involved in four different protocols (n = 20, 12, 12, and 6, respectively). Under the monitoring of ICP, brain tissue oxygen tension and hemodynamical parameters, PEEP was applied in increments of 5 cm H2O from 5 to 25 cm H2O. Measurements were taken in pigs with normal ICP and normovolemia (Series I), or with intracranial hypertension (via inflating intracranial balloon catheter) and normovolemia (Series II), or with intracranial hypertension and hypovolemia (via exsanguination) (Series III). Pigs randomized to the control group received only hydrochloride instillation while the intervention group received additional chest wall strapping. Common carotid arterial blood flow before and after exsanguination at each PEEP level was measured in pigs with intracranial hypertension and chest wall strapping (Series IV).ResultsICP was elevated by increased PEEP in both normal ICP and intracranial hypertension conditions in animals with normal blood volume, while resulted in decreased ICP with PEEP increments in animals with hypovolemia. Increasing PEEP resulted in a decrease in brain tissue oxygen tension in both normovolemic and hypovolemic conditions. The impacts of PEEP on hemodynamical parameters, ICP and brain tissue oxygen tension became more evident with increased chest wall elastance. Compare to normovolemic condition, common carotid arterial blood flow was further lowered when PEEP was raised in the condition of hypovolemia.ConclusionsThe impacts of PEEP on ICP and cerebral oxygenation are determined by both volume status and respiratory mechanics. Potential conditions that may increase chest wall elastance should also be ruled out to avoid the deleterious effects of PEEP.

Intracranial pressure responsiveness to positive end-expiratory pressure in different respiratory mechanics: a preliminary experimental study in pigs

BackgroundRespiratory mechanics affects the effect of positive end-expiratory pressure (PEEP) on intracranial pressure (ICP). Respiratory mechanics of the lung and the chest wall was not differentiated in previous studies. In the present study, we investigated the influence of the following possible determinants of ICP responsiveness to PEEP: chest wall elastance (ECW), lung elastance (EL), and baseline ICP.MethodsEight healthy Bama miniature pigs were studied. The increase of EL was induced by instillation of hydrochloride, and the increase of ECW was induced by strapping the animals’ chest wall and abdomen. A balloon-tipped catheter was placed intracranially for inducing intracranial hypertension. Six experimental conditions were investigated in sequence: 1) Normal; 2) Stiff Chest Wall; 3) Lung Injury; 4) Lung Injury + Stiff Chest Wall; 5) Lung Injury + Stiff Chest Wall + Intracranial Hypertension and 6) Lung Injury + Intracranial Hypertension. PEEP was gradually increased in a 5 cm H2O interval from 5 to 25 cm H2O in each condition. Blood pressure, central venous pressure, ICP, airway pressure and esophageal pressure were measured.ResultsHydrochloride instillation significantly increased EL in conditions with lung injury. ECW significantly increased in the conditions with chest wall and abdomen strapping (all p < 0.05). ICP significantly increased with increments of PEEP in all non-intracranial hypertension conditions (p < 0.001). The greatest cumulative increase in ICP was observed in the Stiff Chest Wall condition (6 [5.3, 6.8] mm Hg), while the lowest cumulative increase in ICP was observed in the Lung Injury condition (2 [1.3, 3.8] mm Hg). ICP significantly decreased when PEEP was increased in the intracranial hypertension conditions (p < 0.001). There was no significant difference in cumulative ICP change between the two intracranial hypertension conditions (p = 0.924).ConclusionsDifferent respiratory mechanics models can be established via hydrochloride induced lung injury and chest wall and abdominal strapping. The effect of PEEP on ICP is determined by respiratory mechanics in pigs with normal ICP. However, the responsiveness of ICP to PEEP is independent of respiratory mechanics when there is intracranial hypertension.

Effect of Inhaled Nebulized Furosemide (40 and 120 mg) on Breathlessness during Exercise in the Presence of External Thoracic Restriction in Healthy Men.

Inhalation of nebulized furosemide has been shown to alleviate breathlessness provoked experimentally in health and disease; however, it remains unclear whether the efficacy of nebulized furosemide on breathlessness is dose-dependent. We tested the hypothesis that inhaled nebulized furosemide would be associated with a dose-dependent relief of breathlessness during exercise testing in the setting of abnormal restrictive constraints on tidal volume (VT) expansion. In a randomized, double-blind, crossover study, 24 healthy men aged 25.3 ± 1.2 years (mean ± SE) completed a symptom-limited constant-load cycle endurance exercise test in the setting of external thoracic restriction via chest wall strapping to reduce vital capacity by ~20% following single-dose inhalation nebulized furosemide (40 and 120 mg) and 0.9% saline. Compared with 0.9% saline, neither 40 nor 120 mg of inhaled nebulized furosemide had an effect on ratings of perceived breathlessness during exercise or an effect on cardiometabolic, ventilatory, breathing pattern, or dynamic operating lung volume responses during exercise. Urine production rate, the percentage of participants reporting an “urge to urinate” and the intensity of perceived “urge to urinate” were all significantly greater after inhaling the 120 mg furosemide solution compared with both 0.9% saline and 40 mg furosemide solutions. We concluded that, under the experimental conditions of this study, inhalation of nebulized furosemide at doses of 40 and 120 mg did not alleviate breathlessness during exercise in healthy men.

Chest wall strapping increases expiratory airflow and detectable airway segments in computer tomographic scans of normal and obstructed lungs.

Chest wall strapping (CWS) induces breathing at low lung volumes but also increases parenchymal elastic recoil. In this study, we tested the hypothesis that CWS dilates airways via airway-parenchymal interdependence. In 11 subjects (6 healthy and 5 with mild to moderate COPD), pulmonary function tests and lung volumes were obtained in control (baseline) and the CWS state. Control and CWS-CT scans were obtained at 50% of control (baseline) total lung-capacity (TLC). CT lung volumes were analyzed by CT volumetry. If control and CWS-CT volumetry did not differ by more than 25%, airway dimensions were analyzed via automated airway segmentation. CWS-TLC was reduced on average to 71% of control-TLC in normal subjects and 79% of control-TLC in subjects with COPD. CWS increased expiratory airflow at 50% of control-TLC by 41% (3.50 ± 1.6 vs. 4.93 ± 1.9 l/s, P = 0.04) in normals and 316% in COPD(0.25 ± 0.05 vs 0.79 ± 0.39 l/s, P = 0.04). In 10 subjects (5 normals and 5 COPD), control and CWS-CT scans at 50% control-TLC did not differ more than 25% on CT volumetry and were included in the airway structure analysis. CWS increased the mean number of detectable airways with a diameter of ≤2 mm by 32.5% (65 ± 10 vs. 86 ± 124, P = 0.01) in normal subjects and by 79% (59 ± 19 vs. 104 ± 16, P = 0.01) in subjects with COPD. There was no difference in the number of detectable airways with diameters 2-4 mm and >4 mm in normal or in COPD subjects. In conclusion, CWS enhances the detection of small airways via automated CT airway segmentation and increases expiratory airflow in normal subjects as well as in subjects with mild to moderate COPD. NEW & NOTEWORTHY In normal and COPD subjects, chest wall strapping(CWS) increased the number of detectable small airways using automated CT airway segmentation. The concept of dysanapsis expresses the physiological variation in the geometry of the tracheobronchial tree and lung parenchyma based on development. We propose a dynamic concept to dysanapsis in which CWS leads to breathing at lower lung volumes with a corresponding increase in the size of small airways, a potentially novel, nonpharmacological treatment for COPD.

Exertional dyspnea associated with chest wall strapping is reduced when external dead space substitutes for part of the exercise stimulus to ventilation.

Chest wall strapping has been used to assess mechanisms of dyspnea with restrictive lung disease. This study examined the hypothesis that dyspnea with restriction depends principally on the degree of reflex ventilatory stimulation. We compared dyspnea at the same (iso)ventilation when added dead space provided a component of the ventilatory stimulus during exercise. Eleven healthy men undertook a randomized controlled crossover trial that compared four constant work exercise conditions: 1) control (CTRL): unrestricted breathing at 90% gas exchange threshold (GET); 2) CTRL+dead space (DS): unrestricted breathing with 0.6-l dead space, at isoventilation to CTRL due to reduced exercise intensity; 3) CWS: chest wall strapping at 90% GET; and 4) CWS+DS: chest strapping with 0.6-l dead space, at isoventilation to CWS with reduced exercise intensity. Chest strapping reduced forced vital capacity by 30.4 ± 2.2% (mean ± SE). Dyspnea at isoventilation was unchanged with CTRL+DS compared with CTRL (1.93 ± 0.49 and 2.17 ± 0.43, 0-10 numeric rating scale, respectively; P = 0.244). Dyspnea was lower with CWS+DS compared with CWS (3.40 ± 0.52 and 4.51 ± 0.53, respectively; P = 0.003). Perceived leg fatigue was reduced with CTRL+DS compared with CTRL (2.36 ± 0.48 and 2.86 ± 0.59, respectively; P = 0.049) and lower with CWS+DS compared with CWS (1.86 ± 0.30 and 4.00 ± 0.79, respectively; P = 0.006). With unrestricted breathing, dead space did not change dyspnea at isoventilation, suggesting that dyspnea does not depend on the mode of reflex ventilatory stimulation in healthy individuals. With chest strapping, dead space presented a less potent stimulus to dyspnea, raising the possibility that leg muscle work contributes to dyspnea perception independent of the ventilatory stimulus.NEW & NOTEWORTHY Chest wall strapping was applied to healthy humans to simulate restrictive lung disease. With chest wall strapping, dyspnea was reduced when dead space substituted for part of a constant exercise stimulus to ventilation. Dyspnea associated with chest wall strapping depended on the contribution of leg muscle work to ventilatory stimulation. Chest wall strapping might not be a clinically relevant model to determine whether an alternative reflex ventilatory stimulus mimics the intensity of exertional dyspnea.

Does nebulized fentanyl relieve dyspnea during exercise in healthy man?

Few therapies exist for the relief of dyspnea in restrictive lung disorders. Accumulating evidence suggests that nebulized opioids selective for the mu-receptor subtype may relieve dyspnea by modulating intrapulmonary opioid receptor activity. Our respective primary and secondary objectives were to test the hypothesis that nebulized fentanyl (a mu-opioid receptor agonist) relieves dyspnea during exercise in the presence of abnormal restrictive ventilatory constraints and to identify the physiological mechanisms of this improvement. In a randomized, double-blind, placebo-controlled crossover study, we examined the effect of 250 μg nebulized fentanyl, chest wall strapping (CWS), and their interaction on detailed physiological and perceptual responses to constant work rate cycle exercise (85% of maximum incremental work rate) in 14 healthy, fit young men. By design, CWS decreased vital capacity by ∼20% and mimicked the negative consequences of a mild restrictive lung disorder on exercise endurance time and on dyspnea, breathing pattern, dynamic operating lung volumes, and diaphragmatic electromyographic and respiratory muscle function during exercise. Compared with placebo under both unrestricted control and CWS conditions, nebulized fentanyl had no effect on exercise endurance time, integrated physiological response to exercise, sensory intensity, unpleasantness ratings of exertional dyspnea. Our results do not support a role for intrapulmonary opioids in the neuromodulation of exertional dyspnea in health nor do they provide a physiological rationale for the use of nebulized fentanyl in the management of dyspnea due to mild restrictive lung disorders, specifically those arising from abnormalities of the chest wall and not affiliated with airway inflammation.

Chest wall strapping. An old physiology experiment with new relevance to small airways diseases.

Chest wall strapping (CWS) induces breathing at low lung volumes. Mild to moderate obesity can lead to similar changes in lung volumes, due to chest wall and abdominal restriction. Chest wall strapping is also conceptually similar to a mismatch between significantly oversized donor lungs transplanted into a recipient with a smaller chest cavity. Chest wall strapping increases lung elastic recoil, reduces pulmonary compliance, and substantially increases maximal expiratory flows. The interactions between elastic properties of the lung parenchyma and small airways are critical for pulmonary function. Chest wall strapping lowers residual volume and closing volume, likely from the interdependence between increased elastic recoil and airways, leading to greater radial distending forces on small airways and small airway dilation. Chronic obstructive pulmonary disease (COPD) and chronic rejection of the transplanted lung, bronchiolitis obliterans syndrome (BOS), are primarily diseases of the small airways, and are characterized by progressive obstruction and subsequent loss of small airways. In COPD, higher body mass index (BMI) (conceptually like being more tightly strapped) is associated with lower lung volumes, increased airway conductance, and lower risk of progression to emphysema or death. Likewise, in lung transplantation, oversized donor lungs have been linked to higher expiratory airflows, lower risk of bronchiolitis obliterans syndrome, and improved survival. This article reviews the physiology of chest wall strapping and explores how it could enhance the understanding or even the treatment of small airway diseases, such as COPD and bronchiolitis obliterans syndrome.

Physiological mechanisms of dyspnea during exercise with external thoracic restriction: Role of increased neural respiratory drive

We tested the hypothesis that neuromechanical uncoupling of the respiratory system forms the mechanistic basis of dyspnea during exercise in the setting of "abnormal" restrictive constraints on ventilation (VE). To this end, we examined the effect of chest wall strapping (CWS) sufficient to mimic a "mild" restrictive lung deficit on the interrelationships between VE, breathing pattern, dynamic operating lung volumes, esophageal electrode-balloon catheter-derived measures of the diaphragm electromyogram (EMGdi) and the transdiaphragmatic pressure time product (PTPdi), and sensory intensity and unpleasantness ratings of dyspnea during exercise. Twenty healthy men aged 25.7 ± 1.1 years (means ± SE) completed symptom-limited incremental cycle exercise tests under two randomized conditions: unrestricted control and CWS to reduce vital capacity (VC) by 21.6 ± 0.5%. Compared with control, exercise with CWS was associated with 1) an exaggerated EMGdi and PTPdi response; 2) no change in the relationship between EMGdi and each of tidal volume (expressed as a percentage of VC), inspiratory reserve volume, and PTPdi, thus indicating relative preservation of neuromechanical coupling; 3) increased sensory intensity and unpleasantness ratings of dyspnea; and 4) no change in the relationship between increasing EMGdi and each of the intensity and unpleasantness of dyspnea. In conclusion, the increased intensity and unpleasantness of dyspnea during exercise with CWS could not be readily explained by increased neuromechanical uncoupling but likely reflected the awareness of increased neural respiratory drive (EMGdi) needed to achieve any given VE during exercise in the setting of "abnormal" restrictive constraints on tidal volume expansion.

Short-term variability in respiratory impedance and effect of deep breath in asthmatic and healthy subjects with airway smooth muscle activation and unloading

Inspiratory resistance (RINSP) and reactance (XINSP) were measured for 7 min at 5 Hz in 10 subjects with mild asymptomatic asthma and 9 healthy subjects to assess the effects of airway smooth muscle (ASM) activation by methacholine (MCh) and unloading by chest wall strapping (CWS) on the variability of lung function and the effects of deep inspiration (DI). Subjects were studied at control conditions, after MCh, with CWS, and after MCh with CWS. In all experimental conditions XINSP was significantly more negative in subjects with asthma than in healthy subjects, suggesting greater inhomogeneity in the former. However, the variability in both RINSP and XINSP was increased by either ASM activation or CWS, without significant difference between groups. DI significantly reversed MCh-induced changes in RINSP both in subjects with asthma and healthy subjects, but XINSP in the former only. This effect was impaired by CWS more in subjects with asthma than in healthy subjects. The velocity of RINSP and XINSP recovery after DI was faster in subjects with asthma than healthy subjects. In conclusion, these results support the opinion that the short-term variability in respiratory impedance is related to ASM tone or operating length, rather than to the disease. Nevertheless, ASM in individuals with asthma differs from that in healthy individuals in an increased velocity of shortening and a reduced sensitivity to mechanical stress when strain is reduced.

Does increased baseline ventilation heterogeneity following chest wall strapping predispose to airway hyperresponsiveness?

Baseline ventilation heterogeneity is associated with airway hyperresponsiveness (AHR) in asthma; however, it is unknown whether increased baseline ventilation heterogeneity leads to AHR or both are independent effects of similar disease pathophysiology. Reducing functional residual capacity (FRC) in healthy subjects increases baseline ventilation heterogeneity and airway responsiveness, but the relationship between the two is unclear. The aim was to determine whether an increase in baseline ventilation heterogeneity due to a reduction in FRC correlated with the increase in response to methacholine. In 13 healthy male subjects, ventilation heterogeneity was measured by multiple-breath N(2) washout before a cumulative high-dose (0.79-200 μmol) methacholine challenge. On a separate day, the protocol was performed with chest wall strapping (CWS) to reduce FRC. Indexes of ventilation heterogeneity in the convection-dependent (Scond) and diffusion-convection-dependent (Sacin) airways were calculated from the multiple-breath N(2) washout. CWS decreased FRC by 15.6 ± 2.7% (P < 0.0001). CWS increased the percent fall in forced expiratory volume in 1 s during bronchial challenge (P = 0.006), and the magnitude of this effect was independently determined by the effect of CWS on Sacin and FRC (r(adj)(2) = 0.55, P = 0.02). This suggests that changes in baseline ventilation heterogeneity in healthy subjects are sufficient to increase airway responsiveness, independent of the presence of disease pathology.

Airway hyperresponsiveness with chest strapping: A matter of heterogeneity or reduced lung volume?

Chest wall strapping has been recently shown to be associated with an increase in airway responsiveness to methacholine. To investigate whether this is the result of the decreased lung volume or an increased heterogeneity due to chest wall distortion, ten healthy volunteers underwent a methacholine challenge at control conditions and after selective strapping of the rib cage, the abdomen or the whole chest wall resulting in similar decrements of functional residual capacity and total lung capacity but causing different distribution of the bronchoconstrictor. Methacholine during strapping reduced forced expiratory flow, dynamic compliance, and reactance at 5Hz and increased pulmonary resistance and respiratory resistance at 5Hz that were significantly greater than at control and associated with a blunted bronchodilator effect of the deep breath. However, no significant differences were observed between selective and total chest wall strapping, suggesting that the major mechanism for increasing airway responsiveness with chest wall strapping is the breathing at low lung volume rather than regional heterogeneities.

Effects of chest wall strapping on mechanical response to methacholine in humans

We examined the effects of chest wall strapping (CWS) on the response to inhaled methacholine (MCh) and the effects of deep inspiration (DI). Eight subjects were studied on 1 day with MCh inhaled without CWS (CTRL), 1 day with MCh inhaled during CWS (CWSon/on), and 1 day with MCh inhaled during temporary removal of CWS (CWSoff/on). On the CWSon/on day, MCh caused greater increases in pulmonary resistance, upstream resistance, dynamic elastance, residual volume, and greater decreases in maximal expiratory flow than on the CTRL day. On the CWSoff/on day, the changes in these parameters with MCh were not different from the CTRL day. Six of the subjects were again studied using the same protocol on CTRL and CWSon/on days, except that, on a third day, MCh was given after applying the CWS, but the measurements before and after the inhalation were made without CWS (CWSon/off). The latter sequence was associated with more severe airflow obstruction than during CTRL, but less than with CWSon/on. The bronchodilator effects of a DI were blunted when CWS was applied during measurements (CWSon/on and CWSoff/on) but not after it was removed (CWSon/off). We conclude that CWS is capable of increasing airway responsiveness only when it is applied during the inhalation of the constrictor agent. We speculate that breathing at low lung volumes induced by CWS enhances airway narrowing because the airway smooth muscle is adapted at a length at which the contractile apparatus is able to generate a force greater than normal.

Influence of Posture and Sustained Loss of Lung Volume on Pulmonary Function in Awake Asthmatic Subjects

Nocturnal worsening occurs commonly in the asthmatic patient population and contributes substantially to the morbidity and even mortality of asthma. However, no physiologic process has yet been identified as the major contributor to this pattern. Sleep is typically associated with both the supine posture and substantial decrements in lung volume, and both have been proposed to have a role in the pattern of nocturnal worsening. To assess the effects of posture and sleep-associated reductions in functional residual capacity on pulmonary function, eight asthmatic patients were first monitored overnight in a horizontal volume-displacement body plethysmograph to determine mean FRC during sleep for each subject. We then compared, during wakefulness, the effects on FEV1 and methacholine responsiveness from chest wall and abdomen strapping (to maintain FRC at mean sleep levels) for 6 h in the supine and upright postures. FEV1 was significantly decreased after strapping in the supine posture (2.54 +/- 0.36 versus 3.38 +/- 0.29 L on control day, p = 0.0001) but was not affected by strapping in the upright posture (3.07 +/- 0.30 versus 3.34 +/- 0.31 L on control day, not significant, NS). Bronchial responsiveness to methacholine was not altered after strapping in either posture. These observations suggest that the supine posture, in conjunction with the reduction in lung volume associated with sleep, may contribute to the nocturnal worsening of asthma.

Rib cage mobility in pectus excavatum.

Pectus excavatum is generally regarded as a cosmetic deformity; however, some children with pectus excavatum complain of chest pain and exercise limitation. Physiologic studies sometimes show mild restrictive changes and suggest an increased oxygen cost of breathing. Limitation of rib cage mobility related to the deformity may explain these findings. If rib cage mobility is limited, the ability of the actively inspiring rib cage to lower abdominal pressure would be decreased. If this were so, increased swings in abdominal pressure would be seen during the respiratory cycle, especially at times of stress such as during exercise. To test the hypothesis that pectus excavatum is associated with decreased rib cage mobility, we studied 11 patients with pectus excavatum and 11 control subjects. Four control subjects were also studied with rib cage mobility restricted by chest wall strapping sufficient to decrease vital capacity by 5, 10, and 40%. Gastric pressure was measured using balloon catheters and was used as an index of abdominal pressure. Flow at the mouth was recorded and integrated to give volume. Measurements were made at rest, immediately after exercise, and during graded voluntary inspiration to total lung capacity. Gastric pressure was related to tidal volume, and pressure-volume loops were constructed. There were no differences in abdominal pressure swings during respiration between the patients with pectus excavatum and the control subjects. Both groups showed moderate increase in gastric pressure during inspiration at rest and smaller increases or even decreases in abdominal pressure at end inspiration after exercise and at total lung capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchial closure with Mecholyl in excised dog lobes.

ArticleBronchial closure with Mecholyl in excised dog lobes.P S Murtagh, D F Proctor, S Permutt, B Kelly, and S EveringP S Murtagh, D F Proctor, S Permutt, B Kelly, and S EveringPublished Online:01 Sep 1971https://doi.org/10.1152/jappl.1971.31.3.409MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByIt's Not All Smooth Muscle: Non-Smooth-Muscle Elements in Control of Resistance to AirflowAnnual Review of Physiology, Vol. 72, No. 1The role of the large airways on smooth muscle contraction in asthmaSolbert Permutt1 October 2007 | Journal of Applied Physiology, Vol. 103, No. 4Effects of chest wall strapping on mechanical response to methacholine in humansRoberto Torchio, Carlo Gulotta, Claudio Ciacco, Alberto Perboni, Marco Guglielmo, Flavio Crosa, Mario Zerbini, Vito Brusasco, Robert E. Hyatt, and Riccardo Pellegrino1 August 2006 | Journal of Applied Physiology, Vol. 101, No. 2The structural basis of airways hyperresponsiveness in asthmaRobert H. Brown, David B. Pearse, George Pyrgos, Mark C. Liu, Alkis Togias, and Solbert Permutt1 July 2006 | Journal of Applied Physiology, Vol. 101, No. 1Invited Review: Understanding airway pathophysiology with computed tomograpyRobert H. Brown, and Wayne Mitzner1 August 2003 | Journal of Applied Physiology, Vol. 95, No. 2Methacholine-Induced Temporal Changes in Airway Geometry and Lung Density by CTChest, Vol. 119, No. 6High-Resolution Computed Tomographic Evaluation of Airway Distensibility and the Effects of Lung Inflation on Airway Caliber in Healthy Subjects and Individuals with AsthmaAmerican Journal of Respiratory and Critical Care Medicine, Vol. 163, No. 4Effect of transpulmonary pressure on airway diameter and responsiveness of immature and mature rabbitsX. Shen, R. Ramchandani, B. Dunn, R. Lambert, S. J. Gunst, and R. S. Tepper1 October 2000 | Journal of Applied Physiology, Vol. 89, No. 4Potent bronchoprotective effect of deep inspiration and its absence in asthmaTrisevgeni Kapsali, Solbert Permutt, Beth Laube, Nicola Scichilone, and Alkis Togias1 August 2000 | Journal of Applied Physiology, Vol. 89, No. 2Differences in Airway Closure between Normal and Asthmatic Subjects Measured with Single-Photon Emission Computed Tomography and TechnegasAmerican Journal of Respiratory and Critical Care Medicine, Vol. 158, No. 6PhysiologyNEW TECHNIQUES AND DEVELOPMENTS IN PHYSIOLOGIC IMAGING OF AIRWAYSRadiologic Clinics of North America, Vol. 36, No. 1Interaction between airway edema and lung inflation on responsiveness of individual airways in vivoRobert H. Brown, Wayne Mitzner, and Elizabeth M. Wagner1 August 1997 | Journal of Applied Physiology, Vol. 83, No. 2Effect of lung inflation in vivo on airways with smooth muscle tone or edemaRobert H. Brown, Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner1 February 1997 | Journal of Applied Physiology, Vol. 82, No. 2The relevance of pharmacological dose—response curves to airway narrowingTrends in Pharmacological Sciences, Vol. 10, No. 12Bronchial HyporesponsivenessChest, Vol. 91, No. 6Bronchial HyporesponsivenessChest, Vol. 87, No. 5Influence of lung inflation on the elastic properties of intra- and extrapulmonary airways in manRespiration Physiology, Vol. 37, No. 3Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2Relation Between Pulmonary Arterial Pressure and Pleural Pressure During the Acute Asthmatic AttackChest, Vol. 63, No. 4 More from this issue > Volume 31Issue 3September 1971Pages 409-15 https://doi.org/10.1152/jappl.1971.31.3.409PubMed5111859History Published online 1 September 1971 Published in print 1 September 1971 Metrics