Effects of lung volume, volume history, and methacholine on lung tissue viscance

1989 ◽  
Vol 66 (2) ◽  
pp. 977-982 ◽  
Author(s):  
S. T. Kariya ◽  
L. M. Thompson ◽  
E. P. Ingenito ◽  
R. H. Ingram

We examined the effects of lung volume change and volume history on lung resistance (RL) and its components before and during induced constriction. Eleven subjects, including three current and four former asthmatics, were studied. RL, airway resistance (Raw), and, by subtraction, tissue viscance (Vtis) were measured at different lung volumes before and after a deep inhalation and were repeated after methacholine (MCh) aerosols up to maximal levels of constriction. Vtis, which average 9% of RL at base line, was unchanged by MCh and was not changed after deep inhalation but increased directly with lung volume. MCh aerosols induced constriction by increasing Raw, which was reversed by deep inhalation in inverse proportion to responsiveness. such that the more responsive subjects reversed less after a deep breath. Responsiveness correlated directly with the degree of maximal constriction, as more responsive subjects constricted to a greater degree. These results indicate that in humans Vtis comprises a small fraction of overall RL, which is clearly volume-dependent but unchanged by MCh-induced constriction and unrelated to the degree of responsiveness of the subject.

1987 ◽  
Vol 62 (2) ◽  
pp. 807-815 ◽  
Author(s):  
M. S. Ludwig ◽  
I. Dreshaj ◽  
J. Solway ◽  
A. Munoz ◽  
R. H. Ingram

We assessed the relative changes in airways and lung tissue with bronchoconstriction, and the changes in each during and following a deep inhalation (DI). We partitioned pulmonary resistance (RL) into airway (Raw) and tissue (Vtis) components using alveolar capsules in 10 anesthetized, paralyzed, and open-chested dogs ventilated sinusoidally with 350-ml breaths at 1 Hz. We made measurements before and during bronchoconstriction induced by vagal stimulation or inhalation of histamine or prostaglandin F2 alpha (PGF2 alpha), each of which decreased dynamic compliance by approximately 40%. With histamine and PGF2 alpha the rise in RL was predominantly due to Vtis. With vagal stimulation there was a relatively greater increase in Raw than Vtis. At higher lung volumes, Vtis increases offset falls in Raw, producing higher RL at these volumes before and during constriction with PGF2 alpha and histamine. During constriction with vagal stimulation, the fall in Raw with inflation overrode the rise in Vtis, resulting in a lower RL at the higher compared with the lower lung volume. The changes seen after a DI in the control and constricted states were due to alterations in tissue properties, both viscous and elastic. However, the relative hysteresis of the airways and parenchyma were equal, since Raw, our index of airway size, was unchanged after a DI.


1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.


1988 ◽  
Vol 65 (6) ◽  
pp. 2679-2686 ◽  
Author(s):  
S. T. Kariya ◽  
S. A. Shore ◽  
W. A. Skornik ◽  
K. Anderson ◽  
R. H. Ingram ◽  
...  

The maximal effect induced by methacholine (MCh) aerosols on pulmonary resistance (RL), and the effects of altering lung volume and O3 exposure on these induced changes in RL, was studied in five anesthetized and paralyzed dogs. RL was measured at functional residual capacity (FRC), and lung volumes above and below FRC, after exposure to MCh aerosols generated from solutions of 0.1-300 mg MCh/ml. The relative site of response was examined by magnifying parenchymal [RL with large tidal volume (VT) at fast frequency (RLLS)] or airway effects [RL with small VT at fast frequency (RLSF)]. Measurements were performed on dogs before and after 2 h of exposure to 3 ppm O3. MCh concentration-response curves for both RLLS and RLSF were sigmoid shaped. Alterations in mean lung volume did not alter RLLS; however, RLSF was larger below FRC than at higher lung volumes. Although O3 exposure resulted in small leftward shifts of the concentration-response curve for RLLS, the airway dominated index of RL (RLSF) was not altered by O3 exposure, nor was the maximal response using either index of RL. These data suggest O3 exposure does not affect MCh responses in conducting airways; rather, it affects responses of peripheral contractile elements to MCh, without changing their maximal response.


1994 ◽  
Vol 77 (2) ◽  
pp. 789-794 ◽  
Author(s):  
G. E. Tzelepis ◽  
D. L. Vega ◽  
M. E. Cohen ◽  
F. D. McCool

We examined the extent to which training-related increases of inspiratory muscle (IM) strength are limited to the lung volume (VL) at which the training occurs. IM strength training consisted of performing repeated static maximum inspiratory maneuvers. Three groups of normal volunteers performed these maneuvers at one of three lung volumes: residual volume (RV), relaxation volume (Vrel), or Vrel plus one-half of inspiratory capacity (Vrel + 1/2IC). A control group did not train. We constructed maximal inspiratory pressure-VL curves before and after a 6-wk training period. For each group, we found that the greatest improvements in strength occurred at the volume at which the subjects trained and were significantly greater for those who trained at low (36% for RV and 26% for Vrel) than at high volumes (13% for Vrel + 1/2IC). Smaller increments in strength were noted at volumes adjacent to the training volume. The range of vital capacity (VC) over which strength was increased was greater for those who trained at low (70% of VC) than at high VL (20% of VC). We conclude that the greatest improvements in IM strength are specific to the VL at which training occurs. However, the increase in strength, as well as the range of volume over which strength is increased, is greater for those who trained at the lower VL.


2021 ◽  
pp. 57-61
Author(s):  
M. I. Chushkin ◽  
L. A. Popova ◽  
E. A. Shergina ◽  
N. L. Karpina

Interpretation of bronchodilator (BD) test based on reaction of forced expiratory in one second (FEV 1). For assessing bronchodilator responsiveness of lung volumes, airway resistance remains largely unexplored. Therefore, we assessed the response of pulmonary function parameters to BD to reveal the most responsive parameter. 90 patients with chronic airway obstruction (61 male and 29 female; aged 55±11; post-  BD FEV 1 was 63.1+18.3 % predicted) performed spirometry and static lung volume measurements before and after inhalation of BD. We calculated effect size (ES) for each parameter from the difference between two means divided by the standard deviation of baseline score. There was a significant increase both FVC and FEV 1by 8.2 and 12.3 % from baseline (p<0.001). ES were 0.34 for FEV1 and 0.26 for FVC. The ES for lung volumes were from -0.07 (total lung capacity) to -0.31 (residual volume). The ES for sRtot (specific airway resistance) was -0.5 and ES for sGeff (specific effective airway conductance) was 0.95. The parameters of airway resistance and conductance were more responsive for the assessment of pulmonary function changes than spirometry and lung volumes parameters in patients with chronic airway obstruction.


1997 ◽  
Vol 82 (5) ◽  
pp. 1531-1541 ◽  
Author(s):  
David W. Kaczka ◽  
Edward P. Ingenito ◽  
Bela Suki ◽  
Kenneth R. Lutchen

Kaczka, David W., Edward P. Ingenito, Bela Suki, and Kenneth R. Lutchen. Partitioning airway and lung tissue resistances in humans: effects of bronchoconstriction. J. Appl. Physiol. 82(5): 1531–1541, 1997.—The contribution of airway resistance (Raw) and tissue resistance (Rti) to total lung resistance (R l ) during breathing in humans is poorly understood. We have recently developed a method for separating Raw and Rti from measurements of Rland lung elastance (El) alone. In nine healthy, awake subjects, we applied a broad-band optimal ventilator waveform (OVW) with energy between 0.156 and 8.1 Hz that simultaneously provides tidal ventilation. In four of the subjects, data were acquired before and during a methacholine (MCh)-bronchoconstricted challenge. The Rland Eldata were first analyzed by using a model with a homogeneous airway compartment leading to a viscoelastic tissue compartment consisting of tissue damping and elastance parameters. Our OVW-based estimates of Raw correlated well with estimates obtained by using standard plethysmography and were responsive to MCh-induced bronchoconstriction. Our data suggest that Rti comprises ∼40% of total Rlat typical breathing frequencies, which corresponds to ∼60% of intrathoracic Rl. During mild MCh-induced bronchoconstriction, Raw accounts for most of the increase in Rl. At high doses of MCh, there was a substantial increase in Rlat all frequencies and in El at higher frequencies. Our analysis showed that both Raw and Rti increase, but most of the increase is due to Raw. The data also suggest that widespread peripheral constriction causes airway wall shunting to produce additional frequency dependence in El.


1978 ◽  
Vol 54 (3) ◽  
pp. 313-321
Author(s):  
K. B. Saunders ◽  
M. Rudolf

1. We measured changes in peak expiratory flow rate (PEFR), forced expiratory volume in 1 s (FEV1·0), airways resistance (Raw), specific conductance (sGaw), residual volume (RV), functional residual capacity (FRC) and total lung capacity (TLC) in 44 patients with asthma. 2. When asthma was induced by exercise in five patients there were large changes in volumes, but these did not obscure changes in PEFR, which adequately defined the time course of the response. 3. In 70 comparisons before and after inhalation of bronchodilator drug in 33 asthmatic subjects, the responses were classified by the size of the change in lung volumes, which showed a concordant improvement, or no change, in 61 comparisons. Despite these lung volume changes, measurement of both PEFR and FEV1·0, would have detected a bronchodilator response in all but two cases. 4. In 81 comparisons in 23 subjects over time intervals varying from 1 day to 11 months, lung volumes changed in concordance with PEFR and FEV1·0 in 59. In eight of these comparisons, measurement of lung volumes would have altered our interpretation of the changes in PEFR and FEV1·0. 5. In the same 81 comparisons changes in airways resistance were concordant with changes in PEFR and FEV1·0 on 44 occasions, with minor discordant changes in 19. We could not explain the remaining 18 cases showing major discordance between these two types of measurement of airway calibre. 6. We conclude that both FEV1·0, and PEFR should be used for detection of a bronchodilator response, and that measurement of lung volumes will rarely contribute to the interpretation. Over longer periods, lung volumes should be measured if possible. We found no practical use for routine measurement of airways resistance in patients with asthma.


1995 ◽  
Vol 78 (3) ◽  
pp. 875-880 ◽  
Author(s):  
Z. Balassy ◽  
M. Mishima ◽  
J. H. Bates

We measured the effect of lung volume on the time course of regional lung input impedance (ZA) after bolus intravenous administration of 2 mg of histamine in seven open-chest dogs using alveolar capsule oscillators. ZA (24–200 Hz) was obtained during apnea at constant lung volume every 2 s for 80 s at lung inflation pressures of 0.1, 0.2, 0.3, 0.5, 0.7, and 1.0 kPa. Local airway resistance (RA) and elastance of the local lung region were calculated by fitting a four-parameter model to the measured ZA. Total lung resistance and lung elastance were also calculated from tracheal pressure and flow measured during mechanical ventilation (0.3 Hz) just before and after each set of ZA measurements. We found the histamine-induced changes in both lung resistance and lung elastance to decrease with increasing lung volume. RA also showed a large negative dependency on lung volume, and the variation between different RA measurements became markedly increased as lung volume decreased. In contrast, local airway elastance was essentially unaffected by lung volume. These results support the idea that parenchymal tethering of the very distal airways impedes their narrowing during bronchoconstriction. They also indicate that reduced parenchymal tethering causes airway narrowing to become markedly more inhomogeneous.


1993 ◽  
Vol 75 (4) ◽  
pp. 1467-1470 ◽  
Author(s):  
R. J. Martin ◽  
J. Pak ◽  
C. G. Irvin

Previous studies have shown that lung volume decreases and airway resistance increases during sleep in patients with nocturnal asthma. To determine whether the fall in lung volume per se causes the overnight decrement in forced expiratory volume in 1 s (FEV1) and/or increase in bronchial responsiveness, we investigated the effect of preventing this nocturnal decrease in lung volume. The mean volume change on a baseline night was -16.3 +/- 1.6% from presleep values and on the volume maintenance night +7.1 +/- 3.0% (P = 0.0001). However, this maintenance of lung volume did not alter the overnight decrement in FEV1 (-29.6 +/- 5.2% baseline vs. -30.2 +/- 5.8% volume maintenance). Similarly, the increase in bronchial responsiveness was also unaltered from baseline to volume maintenance nights, with presleep provocative concentrations of methacholine producing a 20% decrement in FEV1 of 0.28 +/- 0.15 vs. 0.22 +/- 0.7 mg/ml, respectively, and postsleep values of 0.07 +/- 0.03 vs. 0.04 +/- 0.02 mg/ml, respectively. Thus the fall in lung volume during sleep in the nocturnal asthmatic patient is a result, not a cause, of the overnight worsening of lung function.


1982 ◽  
Vol 53 (3) ◽  
pp. 698-702 ◽  
Author(s):  
P. Helms

In 57 infants and very young children, less than 2 yr of age and with a variety of cardiopulmonary illnesses, problems were encountered in the estimation of lung volume with the plethysmographic technique. In 19 subjects calculated thoracic gas volume (TGV) was found to be consistently larger when airway occlusions were performed at low lung volumes than when performed at higher lung volumes. In 13 infants, changes in intraesophageal pressure (Pes) during airway occlusions were found to be larger than simultaneous changes in mouth pressure. In 25 subjects in whom none of the above changes were observed, total pulmonary resistance (TPR) and airway resistance (Raw) did not differ significantly [mean TPR, 50.1 +/- 27.5 cmH2O X l-1; mean Raw, 48.1 +/- 26.5 (P greater than 0.5)]. In the 13 subjects in whom the delta Pes-to-delta Pm occlusion ratio exceeded 1.05, closest agreement with specific resistance (sRaw) and TPR derived lung volume was found when TGV was calculated with delta Pes rather than mouth pressure change (delta Pm). A similar close agreement with the sRaw TPR derived volume was obtained when TGV was calculated during airway occlusions at the higher lung volume. Two separate lung models are proposed to explain these observations, one with a segmental airway closure and the other with more a generalized airway closure. If plethysmographic techniques are to be used in these young subjects for the estimation of lung volume and airway resistance, possible errors may be reduced by performing airway occlusions at lung volumes above functional residual capacity and noting the delta Pes-to-delta Pm ratio obtained during the occlusion.


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