Regulation of bronchomotor tone by lung inflation in asthmatic and nonasthmatic subjects

1981 ◽  
Vol 50 (5) ◽  
pp. 1079-1086 ◽  
Author(s):  
J. E. Fish ◽  
M. G. Ankin ◽  
J. F. Kelly ◽  
V. I. Peterman

We examined the effects of lung inflation on induced airway obstruction in 14 atopic asthmatic and 14 atopic nonasthmatic subjects. Subjects were challenged with aerosols of methacholine (MCh) and pollen antigen (Ag), and the effects of inflation were assessed with partial ad full flow-volume curves and by comparing airway conductance measurements before and after deep inspiration to total lung capacity (TLC). Whereas bronchoconstriction was transiently abolished or reduced with inspiration in nonasthmatics, these effects were absent or diminished in asthmatic subjects. Dissimilarities could not be explained by differences in base-line lung function or degree of obstruction produced. Deep inspiration had a greater effect in reducing airway obstruction produced with MCh than with Ag in nonasthmatics. In addition, atropine pretreatment had no effect on inspiration responses in asthmatics given Ag, suggesting that vagal reflexes were not the cause of an impaired ability to reduce bronchomotor tone by lung inflation. Our findings reveal the existence of an intrinsic means of regulating bronchomotor toe by active changes in lung volume and that such a mechanism is impaired in asthma. We suggest that airway hyperactivity in asthma is perhaps less a reflection of enhanced end-organ responsiveness than a reflection of this impaired capacity.

Author(s):  
Ynuk Bossé

The deep inspiration (DI) maneuver entices a great deal of interest because of its ability to temporarily ease the flow of air into the lungs. This salutary effect of a DI is proposed to be mediated, at least partially, by momentarily increasing the operating length of airway smooth muscle (ASM). Concerningly, this premise is largely derived from a growing body of in vitro studies investigating the effect of stretching ASM by different magnitudes on its contractility. The relevance of these in vitro findings remains uncertain, as the real range of strains ASM undergoes in vivo during a DI is somewhat elusive. In order to understand the regulation of ASM contractility by a DI and to infer on its putative contribution to the bronchodilator effect of a DI, it is imperative that in vitro studies incorporate levels of strains that are physiologically relevant. This review summarizes the methods that may be used in vivo in humans to estimate the strain experienced by ASM during a DI from functional residual capacity (FRC) to total lung capacity (TLC). The strengths and limitations of each method, as well as the potential confounders, are also discussed. A rough estimated range of ASM strains is provided for the purpose of guiding future in vitro studies that aim at quantifying the regulatory effect of DI on ASM contractility. However, it is emphasized that, owing to the many limitations and confounders, more studies will be needed to reach conclusive statements.


1980 ◽  
Vol 48 (2) ◽  
pp. 389-393 ◽  
Author(s):  
G. Hayatdavoudi ◽  
J. D. Crapo ◽  
F. J. Miller ◽  
J. J. O'Neil

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.


1988 ◽  
Vol 74 (3) ◽  
pp. 311-317 ◽  
Author(s):  
Allan R. Glanville ◽  
Richard A. Yeend ◽  
James Theodore ◽  
Eugene D. Robin

1. The time course and magnitude of the effect of single slow and rapid respiratory manoeuvres on specific airway conductance (sGaw) was assessed in seven normal control subjects and in seven heart–lung transplant (HLT) recipients before and after experimentally induced bronchoconstriction. 2. Neither full inspiration, full exhalation nor vital capacity manoeuvres significantly altered sGaw in normal controls or HLT recipients under baseline conditions despite the presence of hyper-responsiveness to methacholine (MC) in the latter group. 3. After induced bronchoconstriction, single slow and rapid inspirations to total lung capacity transiently abolished or attenuated the bronchoconstriction in normal controls. This effect was absent in the HLT recipients. 4. In HLT recipients, the combination of hyper-responsiveness to MC, the absence of bronchoconstriction with respiratory manoeuvres and the absence of significant bronchodilatation after deep inspiration suggest lack of normal pulmonary innervation.


1991 ◽  
Vol 70 (2) ◽  
pp. 701-707 ◽  
Author(s):  
B. R. Boynton ◽  
D. Villanueva ◽  
M. D. Hammond ◽  
P. N. Vreeland ◽  
B. Buckley ◽  
...  

We studied the effect of mean airway pressure (Paw) on gas exchange during high-frequency oscillatory ventilation in 14 adult rabbits before and after pulmonary saline lavage. Sinusoidal volume changes were delivered through a tracheostomy at 16 Hz, a tidal volume of 1 or 2 ml/kg, and inspired O2 fraction of 0.5. Arterial PO2 and PCO2 (PaO2, PaCO2), lung volume change, and venous admixture were measured at Paw from 5 to 25 cmH2O after either deflation from total lung capacity or inflation from relaxation volume (Vr). The rabbits were lavaged with saline until PaO2 was less than 70 Torr, and all measurements were repeated. Lung volume change was measured in a pressure plethysmograph. Raising Paw from 5 to 25 cmH2O increased lung volume by 48-50 ml above Vr in both healthy and lavaged rabbits. Before lavage, PaO2 was relatively insensitive to changes in Paw, but after lavage PaO2 increased with Paw from 42.8 +/- 7.8 to 137.3 +/- 18.3 (SE) Torr (P less than 0.001). PaCO2 was insensitive to Paw change before and after lavage. At each Paw after lavage, lung volume was larger, venous admixture smaller, and PaO2 higher after deflation from total lung capacity than after inflation from Vr. This study shows that the effect of increased Paw on PaO2 is mediated through an increase in lung volume. In saline-lavaged lungs, equal distending pressures do not necessarily imply equal lung volumes and thus do not imply equal PaO2.


1982 ◽  
Vol 53 (3) ◽  
pp. 737-743 ◽  
Author(s):  
S. J. Lai-Fook ◽  
K. C. Beck

Micropipettes (2–5 microns), in conjunction with a servo-nulling system, were used to measure liquid pressure (Pliq) in subpleural alveoli of lobes of dog lungs made edematous by perfusing with plasma to a constant extravascular weight gain (W). Pliq was measured at fixed transpulmonary pressure (Ptp) in lungs whose W was more than 0.5 that of the initial weight (Wi). In six lobes at W/Wi = 0.6, Pliq, relative to alveolar pressure (Palv), was -2.6 +/- 0.4 cmH2O (mean +/- SE), -11.8 +/- 0.6, and -17.5 +/- 1.7 at deflation Ptp values of 5, 15, and 25 cmH2O, respectively. The Pliq increased to -2, -7, and -13.7, respectively, at W/Wi = 2.8. Based on a mean alveolar radius of 50 micron at Ptp at 25 cmH2O and values of Palv - Pliq, values for alveolar surface tension (tau) at W/Wi = 0.6 were 6, 30, and 44 dyn/cm at Ptp of 5, 15, and 25 cmH2O, respectively. In five other lobes at W/Wi = 0.5 and at 65 and 84% total lung capacity, tau was much higher on lung inflation than on deflation. If pericapillary interstitial fluid pressure (Pi) and Pliq were identical under edematous conditions, tau would be the main determinant of Pi.


1985 ◽  
Vol 59 (3) ◽  
pp. 884-889 ◽  
Author(s):  
H. Baier ◽  
L. Yerger ◽  
R. Moas ◽  
A. Wanner

The influence of lung inflation on lung elasticity and pulmonary resistance (RL) and on pulmonary and bronchial hemodynamics was examined in five anesthetized, mechanically ventilated adult sheep before and after treatment with the cyclooxygenase inhibitor indomethacin (2 mg/kg). Lung inflation was accomplished by increasing levels of positive end-expiratory pressure (PEEP). Measurements of pulmonary vascular resistance (PVR), bronchial blood flow (Qbr), and RL were obtained with a Swan-Ganz catheter, with an electromagnetic flow probe placed around the carinal artery, and by relating airflow to transpulmonary pressure (Ptp), respectively. Before indomethacin, increasing PEEP from 5 to 15 cmH2O increased mean lung volume (VL) to 135% (P less than 0.01), Ptp to 165% (P less than 0.005), and PVR to 132% (P less than 0.05) of base line and decreased mean Qbr (normalized for cardiac output) to 53% (P less than 0.05) of base line. Mean RL showed a tendency to decrease with a mean value of 67% of base line at 15 cmH2O PEEP. After indomethacin the corresponding values were 121% for VL, 155% for Ptp, 124% for PVR, 35% for Qbr, and 31% for RL. The PEEP-dependent changes were not different before and after indomethacin except for mean VL, which increased less (P less than 0.05) after indomethacin. The failure of indomethacin to modify PEEP-induced changes in RL, PVR, and Qbr was also present when these parameters were expressed as a function of Ptp. These findings suggest that the cyclooxygenase products elaborated during lung inflation reduce lung elasticity but fail to influence airflow resistance and pulmonary and bronchial hemodynamics.


2016 ◽  
Vol 1 (60) ◽  
pp. 117-124 ◽  
Author(s):  
Савушкина ◽  
Olga Savushkina ◽  
Черняк ◽  
Aleksandr Chernyak

One of the methods to evaluate lung function is body plethysmography. Body plethysmography allows to measure indicators that cannot be obtained during spirometry, that is: total lung capacity (TLC), bronchial resistance (Raw), and functional residual capacity (FRC). FRC measured by body plethysmography reflects thoracic gas volume (TGV or VTG), and includes both ventilated and poorly ventilated volume. Plethysmographic measurements are based on the principle of the relationship between pressure and volume at constant temperature and fixed amount of gas. This principle states that the absolute pressure exerted by a given mass of an ideal gas is inversely proportional to the volume it occupies if the temperature and amount of gas remain unchanged within a closed system (Boyle-Mariotte Law). In body plethysmography, the following parameters: TGV, vital capacity (VC), expiratory reserve volume (ERV), tidal volume (TV), inspiratory reserve volume (IRV), inspiratory capacity (IC), Raw are obtained. TLC, residual volume (RV) and its share in total lung capacity can be calculated. Reduced TLC allows to diagnose restrictive disorders of pulmonary ventilation. The RV and its share in TLC increase together with airway obstruction indicates air trapping. The TGV increase together with airway obstruction indicates hyperinflation. In the analysis of lung volumes predictive values, which are calculated by the formulas recommended by ATS/ERS statement, are used. The results are expressed as a percentage of the predicted value. Thus, body plethysmography is an important addition to spirometry and image methods of research, allowing to assess the functional state of the lungs more objectively; it helps to conduct the differential diagnosis and control the course of the disease.


1983 ◽  
Vol 54 (6) ◽  
pp. 1618-1623 ◽  
Author(s):  
C. H. Fanta ◽  
D. E. Leith ◽  
R. Brown

Normal subjects can increase their vital capacity by appropriate training. We tested whether that change can be achieved by greater maximal shortening of the inspiratory muscles without concomitant increases in peak static inspiratory pressures. Sixteen healthy volunteers participated in the study: eight were randomly assigned to make 20 inhalations to total lung capacity, held for 10 s with the glottis open, each day for 6 wk; the remainder served as nontraining controls. Before and after the 6-wk study period, we made multiple determinations of lung volumes and of curves relating lung volume to maximal static inspiratory (and expiratory) pressure. Control subjects had no significant changes from base line in any variable. In the training group, the mean vital capacity increased 200 +/- 74 ml (P less than 0.05) or 3.9 +/- 1.3% (P less than 0.02), without a significant change in residual volume. After training, the mean maximal inspiratory pressure at the airway opening (PI) at a lung volume equal to the base-line total lung capacity was 27 +/- 8 cmH2O in this group (vs. zero before training; P less than 0.02). Values of PI in the mid-vital capacity range did not change. We conclude that in response to appropriate training stimuli inspiratory muscles can contract to shorter minimal lengths, a capacity potentially important in progressive pulmonary hyperinflation.


2001 ◽  
Vol 91 (6) ◽  
pp. 2574-2578 ◽  
Author(s):  
Robert H. Brown ◽  
Wayne Mitzner

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.


1983 ◽  
Vol 55 (4) ◽  
pp. 1051-1056 ◽  
Author(s):  
R. Winn ◽  
J. Stothert ◽  
B. Nadir ◽  
J. Hildebrandt

Pressure-volume curves were obtained from excised left lungs of goats at 4, 24, and 48 h after tracheal instillation of 2.5 ml/kg of 0.1 N HCl. Air total lung capacity (TLC) at transpulmonary pressure (PL) = 35 cmH2O was 38.8 ml/kg body weight before acid, and was reduced sharply to 21.1 at 4 h, then increased to 25.6 at 24 h and 32.1 at 48 h. Excess extravascular lung water (EVLW) could account for only part of the volume reductions. Specific compliance ratio of transpulmonary pressure to total lung capacity (CL/TLC) between PL of 5 and 0 cmH2O was reduced from 0.074/cmH2O to 0.050, 0.048, and 0.053/cmH2O, respectively. Saline TLC (PL = 10 cmH2O) changed from 44.8 to 32.4, 34.3, and 45.4 ml/kg, respectively, but CL/TLC did not, suggesting airway obstruction. After injury, trapped volume at PL = 0 increased from 24.9 to 29.2, 43.3, and 37.3% TLC with air, and from 20.3 to 38.5, 33.1, and 28.5%, respectively, with saline. Air volume at a PL = 10 cmH2O on deflation fell from 82.0 to 72.1% TLC at 4 h, but was near control at 24 and 48 h. The reduction in ventilated volume was not reflected in proportionately increased shunt; therefore, some compensatory vasoconstriction must have occurred. We suggest that in affected regions increased surface forces, increased EVLW, and airway obstruction caused reductions of lung volume.


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