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.

scholarly journals The airway response to deep inspirations decreases with COPD severity and is associated with airway distensibility assessed by computed tomography

2008 ◽  
Vol 105 (3) ◽  
pp. 832-838 ◽  
Author(s):  
Nicola Scichilone ◽  
Alba La Sala ◽  
Maria Bellia ◽  
Katherine Fallano ◽  
Alkis Togias ◽  
...  
Keyword(s):  
Computed Tomography ◽  
High Resolution ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Chronic Obstructive ◽  
High Resolution Computed Tomography ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Gold Stage ◽  
Computed Tomography Scans

In patients with mild chronic obstructive pulmonary disease (COPD), the effect of deep inspirations (DIs) to reverse methacholine-induced bronchoconstriction is largely attenuated. In this study, we tested the hypothesis that the effectiveness of DI is reduced with increasing disease severity and that this is associated with a reduction in the ability of DI to distend the airways. Fifteen subjects [Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I–II: n = 7; GOLD stage III–IV: n = 8] underwent methacholine bronchoprovocation in the absence of DI, followed by DI. The effectiveness of DI was assessed by their ability to improve inspiratory vital capacity and forced expiratory volume in 1 s (FEV1). To evaluate airway distensibility, two sets of high-resolution computed tomography scans [at residual volume (RV) and at total lung capacity] were obtained before the challenge. In addition, mean parenchymal density was calculated on the high-resolution computed tomography scans. We found a strong correlation between the response to DI and baseline FEV1 %predicted ( r2 = 0.70, P < 0.0001) or baseline FEV1/forced vital capacity ( r2 = 0.57, P = 0.001). RV %predicted and functional residual capacity %predicted correlated inversely ( r2 = 0.33, P = 0.02 and r2 = 0.32, P = 0.03, respectively), and parenchymal density at RV correlated directly ( r2 = 0.30, P = 0.03), with the response to DI. Finally, the effect of DI correlated to the change in large airway area from RV to total lung capacity ( r2 = 0.44, P = 0.01). We conclude that loss of the effects of DI is strongly associated with COPD severity and speculate that the reduction in the effectiveness of DI is due to the failure to expand the lungs because of the hyperinflated state and/or the parenchymal damage that prevents distension of the airways with lung inflation.

Role of alveolar recruitment in lung inflation: influence on pressure-volume hysteresis

1983 ◽  
Vol 55 (4) ◽  
pp. 1321-1332 ◽  
Author(s):  
G. C. Smaldone ◽  
W. Mitzner ◽  
H. Itoh
Keyword(s):  
Lung Volume ◽  
Linear Dimension ◽  
Total Lung Capacity ◽  
Alveolar Recruitment ◽  
Rapid Cycling ◽  
Lung Inflation ◽  
Lung Capacity ◽  
History Of

The behavior of terminal lung units (alveoli) with changes in lung volume is controversial. For example, different investigators using similar techniques have suggested that alveoli expand homogeneously or, conversely, get smaller with increases in lung volume. We studied this problem by filling excised dog lobes with monodisperse aerosol and observing deposition at zero airflow. Under these conditions, the deposition of particles is inversely proportional to a mean alveolar linear dimension (ALD). With this technique, changes in ALD were assessed as the lung ventilated along its pressure-volume (PV) curve. PV curves were generated using a rapid cycling technique that minimized trapping and allowed reversible regulation of inflation-deflation hysteresis. Irreversible changes in PV hysteresis were assessed by rinsing the lung with Tween. With significant PV hysteresis, the ALD progressively decreased with inflation to total lung capacity (TLC). With deflation from TLC, the ALD was unchanged until low volumes were reached, when it decreased markedly. When PV hysteresis was minimized (reversibly or irreversibly), inflation and deflation ALD were superimposed. These data are consistent with progressive alveolar recruitment with inflation to TLC and derecruitment with deflation. The correlation between alveolar dimensions and PV hysteresis suggests that shifts in the PV curve can be accounted for by changes in the population of units. The number open at any given point is determined by the dynamic history of inflation.

Airway responses to inhaled histamine in asymptomatic smokers and nonsmokers

1977 ◽  
Vol 42 (4) ◽  
pp. 508-513 ◽  
Author(s):  
N. E. Brown ◽  
E. R. McFadden ◽  
R. H. Ingram
Keyword(s):  
Vital Capacity ◽  
Total Lung Capacity ◽  
Aerosol Deposition ◽  
Flow Volume ◽  
Maximal Flow ◽  
Airway Reactivity ◽  
Lung Capacity ◽  
Large Airway ◽  
Airway Response ◽  
Airway Responses

Bronchia reactivity to inhaled histamine was assessed in asymptomatic cigarette smokers and in nonsmoking atopic and nonatopic subjects. The only prechallenge between-group difference was the ratio of maximal flow on 80% helium-20% oxygen (Vmax HeO2) to maximal flow on air (Vmax air) from partial expiratory flow volume curves at 25% vital capacity (25% VC PEFV): Mean +/- SEM for smokers 1.18 /+- 0.06, atopics 1.45 +/- 0.08, nonatopics 1.51 +/- 0.03. This suggests that prior to inhalation to total lung capacity, the predominant site of resistance at flow limitation was in smaller airways of the smokers and in larger airways of both groups of nonsmokers. Following inhalation of histamine, smokers and nonatopics had similar changes in lung volumes and Vmax air which were less than in atopics. The Vmax HeO2/Vmax air ratios at 25% VC PEFV increased in smokers and decreased in nonsmokers: smokers 1.48 +/- 0.08, atopics 1.22 +/- 0.10, nontopics 1.16 +/- 0.06. This suggests a predominant large airway response in smokers and a prominent small airway response in nonsmokers. These responses may reflect differences in the predominant site of aerosol deposition rather than in airway reactivity.

Interaction of inhaled LTC4 with histamine and PGD2 on airway caliber in asthma

1989 ◽  
Vol 66 (1) ◽  
pp. 304-312 ◽  
Author(s):  
G. D. Phillips ◽  
S. T. Holgate
Keyword(s):  
Time Course ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Forced Expiratory Volume ◽  
Maximal Flow ◽  
Lung Capacity ◽  
Airway Caliber ◽  
Relevant Interaction

To investigate possible mediator interaction in asthma, the effect of inhaled leukotriene (LT) C4 on bronchoconstriction provoked by histamine and prostaglandin (PG) D2 was studied in nine asthmatic subjects. The provocation doses of histamine, PGD2, and LTC4 required to produce a 12.5% decrease in baseline forced expiratory volume in 1 s (FEV1, PD12.5) and to further this fall to 25% (PD25–12.5) were determined. On three subsequent occasions, subjects inhaled either the PD12.5 LTC4 plus vehicle or vehicle plus the PD25–12.5 of either histamine or PGD2, and FEV1 and maximal flow at 70% of vital capacity below total lung capacity after a forced partial expiratory maneuver (Vp30) followed for 45 min. From these results, predicted time-course curves for LTC4 with histamine and LTC4 with PGD2 were calculated. On two final occasions, airway caliber was followed for 45 min after inhalation of the PD12.5 LTC4 followed by the PD25–12.5 of either histamine or PGD2. During the first 9 min after LTC4-histamine and LTC4-PGD2, the decreases in airway caliber were greater than the calculated predicted response. This interaction, although small, was significant with LTC4-PGD2 for both FEV1 (P = 0.01) and Vp30 (P less than 0.05) and with LTC4-histamine for Vp30 (P less than 0.05) but not for FEV1 (P less than 0.05). We conclude that inhaled LTC4 interacts synergistically with histamine and PGD2 and that this effect, although small, may be a relevant interaction in asthma.

Voluntary activation of the human diaphragm in health and disease

1998 ◽  
Vol 85 (6) ◽  
pp. 2146-2158 ◽  
Author(s):  
Christer Sinderby ◽  
Jennifer Beck ◽  
Jadranka Spahija ◽  
Jan Weinberg ◽  
Alex Grassino
Keyword(s):  
Healthy Subjects ◽  
Total Lung Capacity ◽  
Voluntary Activation ◽  
Chronic Obstructive ◽  
Quiet Breathing ◽  
Obstructive Pulmonary Disease ◽  
Transdiaphragmatic Pressure ◽  
Lung Capacity ◽  
Copd Patients ◽  
Crural Diaphragm

Intersubject comparison of the crural diaphragm electromyogram, as measured by an esophageal electrode, requires a reliable means for normalizing the signal. The present study set out 1) to evaluate which voluntary respiratory maneuvers provide high and reproducible diaphragm electromyogram root-mean-square (RMS) values and 2) to determine the relative diaphragm activation and mechanical and ventilatory outputs during breathing at rest in healthy subjects ( n = 5), in patients with severe chronic obstructive pulmonary disease (COPD, n = 5), and in restrictive patients with prior polio infection (PPI, n = 6). In all groups, mean voluntary maximal RMS values were higher during inspiration to total lung capacity than during sniff inhalation through the nose ( P = 0.035, ANOVA). The RMS (percentage of voluntary maximal RMS) during quiet breathing was 8% in healthy subjects, 43% in COPD patients, and 45% in PPI patients. Despite the large difference in relative RMS ( P = 0.012), there were no differences in mean transdiaphragmatic pressure ( P= 0.977) and tidal volumes ( P = 0.426). We conclude that voluntary maximal RMS is reliably obtained during an inspiration to total lung capacity but a sniff inhalation could be a useful complementary maneuver. Severe COPD and PPI patients breathing at rest are characterized by increased diaphragm activation with no change in diaphragm pressure generation.

Factors determining degree of inflation in intratracheally fixed rat lungs

1980 ◽  
Vol 48 (2) ◽  
pp. 389-393 ◽  
Author(s):  
G. Hayatdavoudi ◽  
J. D. Crapo ◽  
F. J. Miller ◽  
J. J. O'Neil
Keyword(s):  
Slow Rate ◽  
Total Lung Capacity ◽  
Formaldehyde Solution ◽  
Initial Flow ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Final Degree ◽  
Low Rate

The total lung capacity (TLC) of rats was measured in vivo and was compared to the displacement volume of the lungs following intratracheal fixation with glutaraldehyde or formaldehyde solution. When glutaraldehyde was used the speed of infusion of the fixative was an important factor in the final degree of lung inflation achieved. With a low rate of fixative infusion and a final pressure of 20 cm of fixative the glutaraldehyde-fixed lungs inflated to 55% TLC. With a high initial flow of glutaraldehyde and a final pressure of 20 cm of fixative the lungs inflated to 84% TLC. Fixation of lungs inside the intact chest wall was found to result in a higher degree of inflation. With a reservoir height of 20 cm and a low rate of fixative infusion lungs fixed in situ reached 74% TLC, whereas lungs fixed in situ, but from animals that have been exsanguinated prior to fixation, inflated to only 58% TLC. This suggests that the volume of the blood in the lungs prior to infusion of glutaraldehyde influences the degree of inflation achieved. Formaldehyde-fixed lungs required 72 h to be completely fixed and they were inflated to 90% TLC when a reservoir height of 20 cm was used. Because of the slow rate of fixation using with formaldehyde solution the rate of infusion was found not to limit the degree of inflation that could be achieved.

Selected Contribution: Airway caliber in healthy and asthmatic subjects: effects of bronchial challenge and deep inspirations

2001 ◽  
Vol 91 (1) ◽  
pp. 506-515 ◽  
Author(s):  
Andrew Jensen ◽  
Haytham Atileh ◽  
Bela Suki ◽  
Edward P. Ingenito ◽  
Kenneth R. Lutchen
Keyword(s):  
Smooth Muscle ◽  
Healthy Subjects ◽  
Tidal Breathing ◽  
Bronchial Challenge ◽  
Lung Capacity ◽  
Single Breath ◽  
Airway Caliber ◽  
Lung Resistance ◽  
Before And After ◽  
Biological State

In 9 healthy and 14 asthmatic subjects before and after a standard bronchial challenge and a modified [deep inspiration (DI), inhibited] bronchial challenge and after albuterol, we tracked airway caliber by synthesizing a method to measure airway resistance (Raw; i.e., lung resistance at 8 Hz) in real time. We determined the minimum Raw achievable during a DI to total lung capacity and the subsequent dynamics of Raw after exhalation and resumption of tidal breathing. Results showed that even after a bronchial challenge healthy subjects can dilate airways maximally, and the dilation caused by a single DI takes several breaths to return to baseline. In contrast, at baseline, asthmatic subjects cannot maximally dilate their airways, and this worsens considerably postconstriction. Moreover, after a DI, the dilation that does occur in airway caliber in asthmatic subjects constricts back to baseline much faster (often after a single breath). After albuterol, asthmatic subjects could dilate airways much closer to levels of those of healthy subjects. These data suggest that the asthmatic smooth muscle resides in a stiffer biological state compared with the stimulated healthy smooth muscle, and inhibiting a DI in healthy subjects cannot mimic this.

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.

Crural diaphragm activation during dynamic contractions at various inspiratory flow rates

1998 ◽  
Vol 85 (2) ◽  
pp. 451-458 ◽  
Author(s):  
Jennifer Beck ◽  
Christer Sinderby ◽  
Lars Lindström ◽  
Alex Grassino
Keyword(s):  
Chest Wall ◽  
Functional Residual Capacity ◽  
Healthy Subjects ◽  
Total Lung Capacity ◽  
Inspiratory Flow ◽  
Transdiaphragmatic Pressure ◽  
Flow Rates ◽  
Lung Capacity ◽  
Dynamic Contractions ◽  
Residual Capacity

The purpose of this study was to evaluate the influence of velocity of shortening on the relationship between diaphragm activation and pressure generation in humans. This was achieved by relating the root mean square (RMS) of the diaphragm electromyogram to the transdiaphragmatic pressure (Pdi) generated during dynamic contractions at different inspiratory flow rates. Five healthy subjects inspired from functional residual capacity to total lung capacity at different flow rates while reproducing identical Pdi and chest wall configuration profiles. To change the inspiratory flow rate, subjects performed the inspirations while breathing across two different inspiratory resistances (10 and 100 cmH2O ⋅ l−1 ⋅ s), at mouth pressure targets of −10, −20, −40, and −60 cmH2O. The diaphragm electromyogram was recorded and analyzed with control of signal contamination and electrode positioning. RMS values obtained for inspirations with identical Pdi and chest wall configuration profiles were compared at the same percentage of inspiratory duration. At inspiratory flows ranging between 0.1 and 1.4 l/s, there was no difference in the RMS for the inspirations from functional residual capacity to total lung capacity when Pdi and chest wall configuration profiles were reproduced ( n = 4). At higher inspiratory flow rates, subjects were not able to reproduce their chest wall displacements and adopted different recruitment patterns. In conclusion, there was no evidence for increased demand of diaphragm activation when healthy subjects breathe with similar chest wall configuration and Pdi profiles, at increasing flow rates up to 1.4 l/s.

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