scholarly journals Potent bronchoprotective effect of deep inspiration and its absence in asthma

2000 ◽  
Vol 89 (2) ◽  
pp. 711-720 ◽  
Author(s):  
Trisevgeni Kapsali ◽  
Solbert Permutt ◽  
Beth Laube ◽  
Nicola Scichilone ◽  
Alkis Togias
Keyword(s):  
Single Dose ◽  
Healthy Subjects ◽  
Alternative Hypothesis ◽  
Forced Expiratory Volume ◽  
Deep Inspiration ◽  
Healthy Individuals ◽  
Lung Inflation ◽  
Airway Caliber ◽  
Physiologic Function ◽  
Rule Out

In the absence of deep inspirations, healthy individuals develop bronchoconstriction with methacholine inhalation. One hypothesis is that deep inspiration results in bronchodilation. In this study, we tested an alternative hypothesis, that deep inspiration acts as a bronchoprotector. Single-dose methacholine bronchoprovocations were performed after 20 min of deep breath inhibition, in nine healthy subjects and in eight asthmatics, to establish the dose that reduces forced expiratory volume in 1 s by >15%. The provocation was repeated with two and five deep inspirations preceding methacholine. Additional studies were carried out to assess optimization and reproducibility of the protocol and to rule out the possibility that bronchoprotection may result from changes in airway geometry or from differential spasmogen deposition. In healthy subjects, five deep inspirations conferred 85% bronchoprotection. The bronchoprotective effect was reproducible and was not attributable to increased airway caliber or to differential deposition of methacholine. Deep inspirations did not protect the bronchi of asthmatics. We demonstrated that bronchoprotection is a potent physiologic function of lung inflation and established its absence, even in mild asthma. This observation deepens our understanding of airway dysfunction in asthma.

Effect of deep inspiration avoidance on ventilation heterogeneity and airway responsiveness in healthy adults

2011 ◽  
Vol 110 (5) ◽  
pp. 1400-1405 ◽  
Author(s):  
David G. Chapman ◽  
Norbert Berend ◽  
Gregory G. King ◽  
Cheryl M. Salome
Keyword(s):  
Healthy Subjects ◽  
Forced Expiratory Volume ◽  
Airway Responsiveness ◽  
Deep Inspiration ◽  
Airway Closure ◽  
Airway Narrowing ◽  
Before And After ◽  
Ventilation Heterogeneity ◽  
Peripheral Airway ◽  
Diffusion Convection

The mechanisms by which deep inspiration (DI) avoidance increases airway responsiveness in healthy subjects are not known. DI avoidance does not alter respiratory mechanics directly; however, computational modeling has predicted that DI avoidance would increase baseline ventilation heterogeneity. The aim was to determine if DI avoidance increased baseline ventilation heterogeneity and whether this correlated with the increase in airway responsiveness. Twelve healthy subjects had ventilation heterogeneity measured by multiple-breath nitrogen washout (MBNW) before and after 20 min of DI avoidance. This was followed by another 20-min period of DI avoidance before the inhalation of a single methacholine dose. The protocol was repeated on a separate day with the addition of five DIs at the end of each of the two periods of DI avoidance. Baseline ventilation heterogeneity in convection-dependent and diffusion-convection-dependent airways was calculated from MBNW. The response to methacholine was measured by the percent fall in forced expiratory volume in 1 s/forced vital capacity (FVC) (airway narrowing) and percent fall in FVC (airway closure). DI avoidance increased baseline diffusion-convection-dependent airways ( P = 0.02) but did not affect convection-dependent airways ( P = 0.9). DI avoidance increased both airway closure ( P = 0.002) and airway narrowing ( P = 0.02) during bronchial challenge. The increase in diffusion-convection-dependent airways due to DI avoidance did not correlate with the increase in either airway narrowing ( rs = 0.14) or airway closure ( rs = 0.12). These findings suggest that DI avoidance increases diffusion-convection-dependent ventilation heterogeneity that is not associated with the increase in airway responsiveness. We speculate that DI avoidance reduces surfactant release, which increases peripheral ventilation heterogeneity and also predisposes to peripheral airway closure.

Airway response to deep inspiration: role of inflation pressure

2001 ◽  
Vol 91 (6) ◽  
pp. 2574-2578 ◽  
Author(s):  
Robert H. Brown ◽  
Wayne Mitzner
Keyword(s):  
Healthy Subjects ◽  
Total Lung Capacity ◽  
Qualitative Change ◽  
Intrinsic Properties ◽  
High Resolution Computed Tomography ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Airway Caliber ◽  
Airway Response

Deep inspirations (DIs) have been shown to have both bronchoprotective and bronchodilator effects in healthy subjects; however, the bronchodilator effects of a DI appear to be impaired in asthmatic compared with healthy subjects. Because the ability to generate high transpulmonary pressures at total lung capacity depends on both the lung properties and voluntary effort, we wondered how the response of airways to DI might be altered if the maneuver were done with less than maximal inflation. The present work was undertaken to examine the effects of varying the magnitude of lung inflation during the DI maneuver on subsequent airway caliber. In five anesthetized and ventilated dogs during methacholine infusion, changes in airway size after DIs of increasing magnitude were measured over the subsequent 5-min period using high-resolution computed tomography. Results show that the magnitude of lung inflation is extremely important, leading to a qualitative change in the airway response. A large DI (45 cmH2O airway pressure) caused subsequent airway dilation, whereas smaller DIs (≤35 cmH2O) caused bronchoconstriction. The precise mechanism underlying these observations is uncertain, but it seems to be related to an interaction between intrinsic properties of the contracted airway smooth muscle and the response to mild stretch.

Enhanced airway dilation by positive-pressure inflation of the lungs compared with active deep inspiration in patients with asthma

2008 ◽  
Vol 105 (6) ◽  
pp. 1725-1732 ◽  
Author(s):  
Annelies M. Slats ◽  
Kirsten Janssen ◽  
Ronald C. de Jeu ◽  
Dirk T. van der Plas ◽  
Robert Schot ◽  
...  
Keyword(s):  
Forced Oscillation ◽  
Forced Expiratory Volume ◽  
Positive Pressure ◽  
Forced Oscillation Technique ◽  
Deep Inspiration ◽  
Respiratory Resistance ◽  
Airway Wall ◽  
Lung Inflation ◽  
Significant Difference ◽  
Response Group

Deep inspiration temporarily reduces induced airways obstruction in healthy subjects. This bronchodilatory effect of deep inspiration is impaired in asthma. Passive machine-assisted lung inflation may augment bronchodilation compared with an active deep inspiration in patients with asthma by either opening closed airways or by reducing fluid flux across the airway wall during deep inspiration, and thereby increasing the tethering forces on the airway wall. We recruited 24 patients with asthma [18–46 yr old, forced expiratory volume in 1 s (FEV1) > 70% predicted; provocative concentration of methacholine inducing a 20% fall in FEV1 (PC20) < 8 mg/ml], with either an impaired ( n = 12) or an intact ( n = 12) bronchodilatory response to deep inspiration. Two methacholine challenges were performed on separate days. At a 50% increase in respiratory resistance (forced oscillation technique at 8 Hz), the change in resistance by a positive-pressure inflation (computer-driven syringe) or an active deep inspiration was measured in randomized order. The reduction in resistance by positive-pressure inflation was significantly greater than by active deep inspiration in the impaired deep inspiration response group (mean change ± SE: −0.6 ± 0.1 vs. −0.03 ± 0.2 cmH2O·l−1·s, P = 0.002). No significant difference was found between positive-pressure inflation and active deep inspiration in the intact deep inspiration response group (−0.6 ± 0.2 vs. −1.0 ± 0.3 cmH2O·l−1·s, P = 0.18). Positive-pressure inflation of the lungs can significantly enhance deep inspiration-induced bronchodilation in patients with asthma.

Effects of exercise training on airway closure in asthmatics

2012 ◽  
Vol 113 (5) ◽  
pp. 714-718 ◽  
Author(s):  
Nicola Scichilone ◽  
Giuseppe Morici ◽  
Daniele Zangla ◽  
Rita Arrigo ◽  
Irene Cardillo ◽  
...  
Keyword(s):  
Single Dose ◽  
Exercise Training ◽  
Healthy Subjects ◽  
Vital Capacity ◽  
Maximal Exercise ◽  
Forced Expiratory Volume ◽  
Airway Responsiveness ◽  
Short Course ◽  
Exercise Training Program ◽  
Similar Beneficial Effect

We previously reported that responsiveness to methacholine (Mch) in the absence of deep inspiration (DI) decreased in healthy subjects after a short course of exercise training. We assessed whether a similar beneficial effect of exercise on airway responsiveness could occur in asthmatics. Nine patients (male/female: 3/6; mean age ± SD: 24 ± 2 yr) with mild untreated asthma [forced expiratory volume in 1 s (FEV1): 100 ± 7.4% pred; FEV1/vital capacity (VC): 90 ± 6.5%] underwent a series of single-dose Mch bronchoprovocations in the absence of DI in the course of a 10-wk training rowing program (6 h/wk of submaximal and maximal exercise), at baseline ( week 0), and at week 5 and 10. The single-dose Mch was established as the dose able to induce ≥15% reduction in inspiratory vital capacity (IVC) and was administered to each subject at every challenge occasion. Five asthmatics (male/female: 1/4; mean age ± SD: 26 ± 3 yr) with similar baseline lung function (FEV1: 102 ± 7.0% predicted; FEV1/VC: 83 ± 6.0%; P = 0.57 and P = 0.06, respectively) not participating in the exercise training program served as controls. In the trained group, the Mch-induced reduction in IVC from baseline was 22 ± 10% at week 0, 13 ± 11% at week 5 ( P = 0.03), and 11 ± 8% at week 10 ( P = 0.028). The Mch-induced reduction in FEV1 did not change with exercise ( P = 0.69). The reduction in responsiveness induced by exercise was of the same magnitude of that previously obtained in healthy subjects (50% with respect to pretraining). Conversely, Mch-induced reduction in IVC in controls remained unchanged after 10 wk (%reduction IVC at baseline: 21 ± 20%; after 10 wk: 29 ± 14%; P = 0.28). This study indicates that a short course of physical training is capable of reducing airway responsiveness in mild asthmatics.

Airway distensibility and volume recruitment with lung inflation in COPD

2010 ◽  
Vol 109 (4) ◽  
pp. 1019-1026 ◽  
Author(s):  
Simonetta Baldi ◽  
Raffaele Dellacà ◽  
Leonardo Govoni ◽  
Roberto Torchio ◽  
Andrea Aliverti ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Lung Volume ◽  
Muscle Tone ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
High Resolution Computed Tomography ◽  
Lung Inflation ◽  
Control Subjects ◽  
Airway Caliber

The effects of full lung inflation on respiratory conductance (Grs) and reactance (Xrs) were measured in 15 subjects with moderate to severe chronic obstructive pulmonary disease (COPD) and 11 matched healthy control subjects. Airway distensibility was estimated from the ratio of the difference of Grs between functional residual capacity and total lung capacity to the relevant changes in lung volume (ΔGrs/ΔVl) or transpulmonary pressure (ΔGrs/ΔPtp). Similar analysis was applied to Xrs to estimate lung volume recruitment (ΔXrs/ΔVl or ΔXrs/ΔPtp). The extent of emphysema in COPD subjects was estimated from the percentage of low attenuation area (LAA) at high-resolution computed tomography. At baseline, ΔGrs/ΔVl and ΔXrs/ΔVl were significantly less in COPD than control subjects, indicating less distensibility and volume recruitment in the former. In COPD, ΔGrs/ΔPtp and ΔXrs/ΔPtp were uncorrelated with LAA but correlated with 1-s forced expiratory volume and with each other. After albuterol, both ΔGrs/ΔPtp and ΔGrs/ΔVl became significantly and negatively correlated with LAA, while ΔXrs/ΔPtp and ΔXrs/ΔVl decreased significantly independently of LAA. Moreover, ΔGrs/ΔPtp and ΔXrs/ΔPtp with lung inflation were no longer correlated with each other, suggesting that airway distensibility and volume recruitment were affected differently by airway smooth muscle tone. Assuming that Grs mainly reflects airway caliber and Xrs the number of ventilated lung units, we conclude that airway smooth muscle contributes to airway stiffness and ventilation inhomogeneities in COPD subjects with prevailing bronchitis but only to the latter in those with more emphysema. We suggest that changes of airway distensibility and volume recruitment with a bronchodilator may be useful for disease phenotyping.

Mechanisms for isolated volume response to a bronchodilator in patients with COPD

2000 ◽  
Vol 88 (6) ◽  
pp. 1989-1995 ◽  
Author(s):  
Isa Cerveri ◽  
Riccardo Pellegrino ◽  
Roberto Dore ◽  
Angelo Corsico ◽  
Paola Fulgoni ◽  
...  
Keyword(s):  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Cube Root ◽  
High Resolution Computed Tomography ◽  
Obstructive Pulmonary Disease ◽  
Lung Inflation ◽  
Severe Emphysema ◽  
Airway Caliber ◽  
Volume Response ◽  
Residual Capacity

We hypothesized that an altered effect of lung inflation on airway caliber may in part explain the isolated volume response to bronchodilators, i.e., an increase of forced vital capacity (FVC) without change in 1-s forced expiratory volume (FEV1). Small-airway caliber was measured by high-resolution computed tomography at functional residual capacity and total lung capacity in five chronic obstructive pulmonary disease patients with an isolated increase of FVC (FVC responders) and five with an increase of both FVC and FEV1(FVC-FEV1 responders) after inhalation of salbutamol. In FVC-FEV1 responders, the airway diameter increased with the cube root of increase in lung volume but was unchanged or even decreased in four of five FVC responders. FVC responders had more severe emphysema, as inferred from lung function and imaging studies, than FVC-FEV1 responders. We speculate that longitudinal traction or space competition (Verbeken EK, Cauberghs M, and Van de Woestijne KP, J Appl Physiol 81: 2468–2480, 1996) are possible underlying mechanisms. We conclude that the isolated volume response to bronchodilators is associated with severe emphysema and likely results from an altered effect of lung inflation on airway caliber.

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