Effect of transpulmonary and driving pressures on collateral gas flow in dog lungs

The effect of changing segment pressure (Ps) and airway opening pressure (Pao) on flow through a collaterally ventilating lung segment was evaluated in intact and excised dog lungs. He, N2, and SF6 were passed through the lung segment distal to a catheter wedged in a peripheral airway at driving pressures (Ps - Pao) between 0.25 and 2 cm H2O. Eight excised caudal lobes were studied at Pao = 5, 10, and 15 cm H2O. Flow was directly related to Ps - Pao and Pao and inversely related to the density of the gas. A dimensionless plot of the driving pressure normalized to a reference dynamic pressure as a function of Reynolds number (Re) indicated that flow through the segment behaved as if it were laminar at Re less than 100 and that increasing Pao increased the dimension of the pathways conducting flow as shown previously. Small changes in Ps had no effect on pathway geometry or on the pattern of flow through the segment at Pao = 10 and 15 cmH2O. At Pao = 5 cm H2O increasing segment pressure appeared to increase the dimensions of the flow pathways slightly. Similar changes in Ps - Pao had no consistent effect on flow pattern or pathway geometry in six anesthetized, paralyzed, vagotomized dogs at functional residual capacity or after widely opening the chest (Pao = 5 cm H2O). These results suggest that, at large lobe volumes, airways (including collateral pathways) are maximally dilated and therefore relatively insensitive to small changes in segment pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased surface tension decreases pulmonary capillary volume and compliance.

Increased surface tension is an important component of several respiratory diseases, but its effects on pulmonary capillary mechanics are incompletely understood. We measured capillary volume and specific compliance before and after increasing surface tension with nebulized siloxane in excised dog lungs. The change in surface tension was sufficient to increase lung recoil 5 cm H(2)O at 50% total lung capacity. Increased surface tension decreased both capillary volume and specific compliance. The changes in capillary volume and compliance were greatest at the lung volumes at which the surface tension change was greatest. Near functional residual capacity, capillary volume postsiloxane was approximately 30% of control. Presiloxane capillary specific compliance was approximately 7%/cm H(2)O near functional residual capacity and approximately 2.5%/cm H(2)O near total lung capacity. Postsiloxane capillary-specific compliance was 3%/cm H(2)O, and was independent of lung volume. We conclude that in addition to their well-known effects on lung mechanics, changes in surface tension also have important effects on capillary mechanics. We speculate that these changes may in turn affect ventilation and perfusion, worsen gas exchange, and alter leukocyte sequestration.     

Effect of flow direction on collateral ventilation in excised dog lung lobes

We determined the effect of flow direction on the relationship between driving pressure and gas flow through a collaterally ventilating lung segment in excised cranial and caudal dog lung lobes. He, N2, and SF6 were passed through the lung segment distal to a catheter wedged in a peripheral airway. Gases were pushed through the segment by raising segment pressure (Ps) relative to airway opening pressure (Pao) and pulled from the segment by ventilating the lobe with the test gas, then lowering Ps relative to Pao. Driving pressures (Ps - Pao) between 0.25 and 2 cmH2O were evaluated at Pao values of 5, 10, and 15 cmH2O. Results were similar in cranial and caudal lobes. Flow increased as Ps - Pao increased and was greatest at Pao = 15 cmH2O for the least-dense gas (He). Although flow direction was not a significant first-order effect, there was significant interaction between volume, driving pressure, and flow direction. Dimensional analysis suggested that, although flow direction had no effect at Pao = 10 and 15 cmH2O, at Pao = 5 cmH2O, raising Ps relative to Pao increased the characteristic dimension of the flow pathways, and reducing Ps relative to Pao reduced the dimension. These data suggest that at large lobe volumes, airways (including collateral pathways) within the segment are maximally dilated and the stiffness of the parenchyma prevents any significant distortion when Ps is altered. At low lobe volumes, these pathways are affected by changes in transmural pressure due to the increased airway and parenchymal compliance.     

Spectral content of forced expiratory wheezes during air, He, and SF6 breathing in normal humans.

The effect of gas density on the spectral content of forced expiratory wheezes was studied in the search for additional information on the mechanism of generation of respiratory wheezes. Five normal adults performed forced vital capacity maneuvers through four or five orifice resistors (0.4-1.92 cm ID) after breathing air, 80% He-20% O2, or 80% SF6-20% O2. Tracheal lung sounds, flow, volume, and airway opening (Pao) and esophageal (Pes) pressures were measured during duplicate runs for each orifice and gas. Wheezes were detected in running spectra of lung sounds by use of a frequency domain peak detection algorithm. The wheeze spectrograms were presented along side expiratory flow rate and transpulmonary pressure (Ptp = Pao - Pes) as function of volume. The frequencies and patterns of wheeze spectrograms were evaluated for gas density effects. We found that air, He, and SF6 had similar wheeze spectrograms. Both wheeze frequency and patterns (as function of volume) did not exhibit consistent changes with gas density. Speech tone, however, was substantially affected in the usual pattern. These observations support the hypothesis that airway wall vibratory motion, rather than gas phase oscillations, is the source of acoustic energy of wheezes.     

Hysteresivity of the lung and tissue strip in the normal rat: effects of heterogeneities.

We measured lung impedance in rats in closed chest (CC), open chest (OC), and isolated lungs (IL) at four transpulmonary pressures with a optimal ventilator waveform. Data were analyzed with an homogeneous linear or an inhomogeneous linear model. Both models include tissue damping and elastance and airway inertance. The homogeneous linear model includes airway resistance (Raw), whereas the inhomogeneous linear model has a continuous distribution of Raw characterized by the mean Raw and the standard deviation of Raw (SDR). Lung mechanics were compared with tissue strip mechanics at frequencies and operating stresses comparable to those during lung impedance measurements. The hysteresivity (eta) was calculated as tissue damping/elastance. We found that 1) airway and tissue parameters were different in the IL than in the CC and OC conditions; 2) SDR was lowest in the IL; and 3) eta in IL at low transpulmonary pressure was similar to eta in the tissue strip. We conclude that eta is primarily determined by lung connective tissue, and its elevated estimates from impedance data in the CC and OC conditions are a consequence of compartment-like heterogeneity being greater in CC and OC conditions than in the IL.     

Partitioning of pulmonary resistance in dogs: effect of tidal volume and frequency

To determine the sensitivity of pulmonary resistance (RL) to changes in breathing frequency and tidal volume, we measured RL in intact anesthetized dogs over a range of breathing frequencies and tidal volumes centering around those encountered during quiet breathing. To investigate mechanisms responsible for changes in RL, the relative contribution of airway resistance (Raw) and tissue resistance (Rti) to RL at similar breathing frequencies and tidal volumes was studied in six excised, exsanguinated canine left lungs. Lung volume was sinusoidally varied, with tidal volumes of 10, 20, and 40% of vital capacity. Pressures were measured at three alveolar sites (PA) with alveolar capsules and at the airway opening (Pao). Measurements were made during oscillation at five frequencies between 5 and 45 min-1 at each tidal volume. Resistances were calculated by assuming a linear equation of motion and submitting lung volume, flow, Pao, and PA to a multiple linear regression. RL decreased with increasing frequency and decreased with increasing tidal volume in both isolated and intact lungs. In isolated lungs, Rti decreased with increasing frequency but was independent of tidal volume. Raw was independent of frequency but decreased with tidal volume. The contribution of Rti to RL ranged from 93 +/- 4% (SD) with low frequency and large tidal volume to 41 +/- 24% at high frequency and small tidal volume. We conclude that the RL is highly dependent on breathing frequency and less dependent on tidal volume during conditions similar to quiet breathing and that these findings are explained by changes in the relative contributions of Raw and Rti to RL.     

Mechanism of action of ozone on the human lung

Fourteen healthy normal volunteers were randomly exposed to air and 0.5 ppm of ozone (O3) in a controlled exposure chamber for a 2-h period during which 15 min of treadmill exercise sufficient to produce a ventilation of approximately 40 l/min was alternated with 15-min rest periods. Before testing an esophageal balloon was inserted, and lung volumes, flow rates, maximal inspiratory (at residual volume and functional residual capacity) and expiratory (at total lung capacity and functional residual capacity) mouth pressures, and pulmonary mechanics (static and dynamic compliance and airway resistance) were measured before and immediately after the exposure period. After the postexposure measurements had been completed, the subjects inhaled an aerosol of 20% lidocaine until response to citric acid aerosol inhalation was abolished. All of the measurements were immediately repeated. We found that the O3 exposure 1) induced a significant mean decrement of 17.8% in vital capacity (this change was the result of a marked fall in inspiratory capacity without significant increase in residual volume), 2) significantly increased mean airway resistance and specific airway resistance but did not change dynamic or static pulmonary compliance or viscous or elastic work, 3) significantly reduced maximal transpulmonary pressure (by 19%) but produced no changes in inspiratory or expiratory maximal mouth pressures, and 4) significantly increased respiratory rate (in 5 subjects by more than 6 breaths/min) and decreased tidal volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

On the respiratory function of the ribs.

To assess the respiratory function of the ribs, we measured the changes in airway opening pressure (Pao) induced by stimulation of the parasternal and external intercostal muscles in anesthetized dogs, first before and then after the bony ribs were removed from both sides of the chest. Stimulating either set of muscles with the rib cage intact elicited a fall in Pao in all animals. After removal of the ribs, however, the fall in Pao produced by the parasternal intercostals was reduced by 60% and the fall produced by the external intercostals was eliminated. The normal outward curvature of the rib cage was also abolished in this condition, and when the curvature was restored by a small inflation, external intercostal stimulation consistently elicited a rise rather than a fall in Pao. These findings thus confirm that the ribs play a critical role in the act of breathing by converting intercostal muscle shortening into lung volume expansion. In addition, they carry the compression that is required to balance the pressure difference across the chest wall.     

Mechanical properties of small airways in excised pony lungs.

We evaluated the pressure-flow relationships in collaterally ventilating segments of excised pony lungs by infusing N2, He, Ne, or SF6 at known flows (V) through a catheter wedged in a peripheral airway. Measurements were made at segment- (Ps) to-airway opening (Pao) pressure differentials of 3-15 cmH2O when the lungs were held at transpulmonary pressures of 5, 10, and 15 cmH2O. The data were analyzed both by calculating collateral resistance (Ps-Pao/V) and by constructing Moody-type plots of normalized pressure drop [(Ps-Pao)/(1/2 rho U2, where rho is density and U is velocity)] against Reynolds number to assess the pattern of flow through the segment and the change in dimension of the flow channels as Ps and Pao were changed. The interpretations from these analyses were compared with radiographic measurements of the diameters of small airways within the collaterally ventilating lung segment at similar pressures. Collateral resistance increased as Ps-Pao increased at high Reynolds numbers, i.e., high flows or dense gas (SF6). Analysis of the Moody-type plots revealed that flow was density dependent at Reynolds number greater than 100, which frequently occurred when N2 was the inflow gas. The radiographic data revealed that small airway diameter increased as Ps-Pao increased at all lung volumes. In addition, at 5 cmH2O Pao, small-airway diameter was smaller for a given Ps in the nonhomogeneous case (Ps greater than Pao) than small-airway diameter for the same Ps in the homogeneous case (Ps = Pao). We interpret these data to suggest that the surrounding lung prevented the segment from expanding in the nonhomogeneous case.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanics of edematous lungs.

Using the parenchymal marker technique, we measured pressure (P)-volume (P-V) curves of regions with volumes of approximately 1 cm3 in the dependent caudal lobes of oleic acid-injured dog lungs, during a very slow inflation from P = 0 to P = 30 cmH2O. The regional P-V curves are strongly sigmoidal. Regional volume, as a fraction of volume at total lung capacity, remains constant at 0.4-0.5 for airway P values from 0 to approximately 20 cmH2O and then increases rapidly, but continuously, to 1 at P = approximately 25 cmH2O. A model of parenchymal mechanics was modified to include the effects of elevated surface tension and fluid in the alveolar spaces. P-V curves calculated from the model are similar to the measured P-V curves. At lower lung volumes, P increases rapidly with lung volume as the air-fluid interface penetrates the mouth of the alveolus. At a value of P = approximately 20 cmH2O, the air-fluid interface is inside the alveolus and the lung is compliant, like an air-filled lung with constant surface tension. We conclude that the properties of the P-V curve of edematous lungs, particularly the knee in the P-V curve, are the result of the mechanics of parenchyma with constant surface tension and partially fluid-filled alveoli, not the result of abrupt opening of airways or atelectatic parenchyma.     

Differential effects of ozone on airway and tissue mechanics in obese mice.

Obesity is an important risk factor for asthma. We recently reported increased ozone (O(3))-induced hyperresponsiveness to methacholine in obese mice (Shore SA, Rivera-Sanchez YM, Schwartzman IN, and Johnston RA. J Appl Physiol 95: 938-945, 2003). The purpose of this study was to determine whether this increased hyperresponsiveness is the result of changes in the airways, the lung tissue, or both. To that end, we examined the effect of O(3) (2 parts/million for 3 h) on methacholine-induced changes in lung mechanics with the use of a forced oscillation technique in wild-type C57BL/6J mice and mice obese because of a genetic deficiency in leptin (ob/ob mice). In ob/ob mice, O(3) increased baseline values for all parameters measured in the study: airway resistance (Raw), lung tissue resistance (Rtis), lung tissue damping (G) and elastance (H), and lung hysteresivity (eta). In contrast, no effect of O(3) on baseline mechanics was observed in wild-type mice. O(3) exposure significantly increased Raw, Rtis, lung resistance (Rl), G, H, and eta responses to methacholine in both groups of mice. For G, Rtis, and Rl there was a significant effect of obesity on the response to O(3). Our results demonstrate that both airways and lung tissue contribute to the hyperresponsiveness that occurs after O(3) exposure in wild-type mice. Our results also demonstrate that changes in the lung tissue rather than the airways account for the amplification of O(3)-induced hyperresponsiveness observed in obese mice.     

Effects of elastase-induced emphysema on airway responsiveness to methacholine in rats

We examined the effects of elastase-induced emphysema on lung volumes, pulmonary mechanics, and airway responses to inhaled methacholine (MCh) of nine male Brown Norway rats. Measurements were made before and weekly for 4 wk after elastase in five rats. In four rats measurements were made before and at 3 wk after elastase; in these same animals the effects of changes in end-expiratory lung volume on the airway responses to MCh were evaluated before and after elastase. Airway responses were determined from peak pulmonary resistance (RL) calculated after 30-s aerosolizations of saline and doubling concentrations of MCh from 1 to 64 mg/ml. Porcine pancreatic elastase (1 IU/g) was administered intratracheally. Before elastase RL rose from 0.20 +/- 0.02 cmH2O.ml-1.s (mean +/- SE; n = 9) to 0.57 +/- 0.06 after MCh (64 mg/ml). A plateau was observed in the concentration-response curve. Static compliance and the maximum increase in RL (delta RL64) were significantly correlated (r = 0.799, P less than 0.01). Three weeks after elastase the maximal airway response to MCh was enhanced and no plateau was observed; delta RL64 was 0.78 +/- 0.07 cmH2O.ml-1.s, significantly higher than control delta RL64 (0.36 +/- 0.7, P less than 0.05). Before elastase, increase of end-expiratory lung volume to functional residual capacity + 1.56 ml (+/- 0.08 ml) significantly reduced RL at 64 mg MCh/ml from 0.62 +/- 0.05 cmH2O.ml-1.s to 0.50 +/- 0.03, P less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alveolar pressure nonhomogeneity during small-amplitude high-frequency oscillation

In six excised canine lungs, regional alveolar pressures (PA) were measured during small-amplitude high-frequency oscillations applied at the airway opening. Both the regional distribution of PA's and their relationship to pressure excursions at the airway opening (Pao) were assessed in terms of amplitude and phase. PA was sampled in several capsules glued to the pleural surface and communicating with alveolar gas via pleural punctures. Pao and PA were measured over the frequency (f) range 1-60 Hz, at transpulmonary pressures (PL) of 5, 10, and 25 cmH2O. The amplitude of PA excursions substantially exceeded Pao excursions at frequencies near the resonant frequency. At resonance the ratio [PA/Pao] was 1.9, 2.9, and 4.8 at PL's of 5, 10, and 25 cmH2O, respectively. Both spatial homogeneity and temporal synchrony of PA's between sampled lung regions decreased with f and increased with PL. Interregional variability of airway impedance [(Pao - PA)/Vao] and tissue impedance (PA/Vao) tended to be larger than differences due to changing PL but not as large as between-dog variability. These data define the baseline nonhomogeneity of the normal canine lung and also suggest that there may be some advantage in applying high-frequency ventilation at frequencies at least as high as lung resonant frequency.     

Differential effect of recruitment maneuvres on pulmonary blood flow and oxygenation during HFOV in preterm lambs.

The effects of lung volume recruitment manouvres on pulmonary blood flow (PBF) during high-frequency oscillatory ventilation (HFOV) in preterm neonates are unknown. Since increased airway pressure adversely affects PBF, we compared the effects of two HFOV recruitment strategies on PBF and oxygenation index (OI). Preterm lambs (128+/-1 day gestation; term approximately 150 days) were anesthetized and ventilated using HFOV (10 Hz, 33% tI) with a mean airway pressure (Pao) of 15 cmH2O. Lung volume was recruited by either increasing Pao to 25 cmH2O for 1 min, repeated five times at 5-min intervals (Sigh group; n=5) or stepwise (5 cmH2O) changes in Pao at 5-min intervals incrementing up to 30 cmH2O then decrementing back to 15 cmH2O (Ramp group; n=6). Controls (n=5) received constant HFOV at 15 cmH2O. PBF progressively decreased (by 45+/-4%) and OI increased (by 15+/-6%, indicating reduced oxygenation) in controls during HFOV, which was similar to the changes observed in the Sigh group of lambs. In the Ramp group, PBF fell (by 54+/-10%) as airway pressure increased (r2=0.99), although the PBF did not increase again as the Pao was subsequently reduced. The OI decreased (by 47+/-9%), reflecting improved oxygenation at high Pao levels during HFOV in the Ramp group. However, high Pao restored retrograde PBF during diastole in four of six lambs, indicating the restoration of right-to-left shunting through the ductus arteriosus. Thus the choice of volume recruitment maneuvre influences the magnitude of change in OI and PBF that occurs during HFOV. Despite significantly improving OI, the ramp recruitment approach causes sustained changes in PBF.     

Small airway pressure-diameter relationships during nonhomogeneous lung lobe inflation

The pressure-diameter behavior of airways within a collaterally ventilating segment of lung was evaluated radiographically in 12 excised dog lung lobes. The results were compared with the pressure-diameter behavior of airways in a lung region adjacent to the collaterally ventilating segment. Airways in each lung region were dusted with powdered tantalum, and airway diameters were measured during homogeneous and nonhomogeneous lobe inflation. Intrasegmental and extrasegmental airways behaved similarly during homogeneous lobe inflation; airway diameter increased as alveolar pressure increased. The lobe was inflated nonhomogeneously by raising pressure in the collaterally ventilating segment (Ps) while maintaining pressure at the lobar bronchus (Pao) constant at 5, 10, or 15 cmH2O. Increasing Ps at constant Pao reciprocally affected intrasegmental and extrasegmental airways. When Pao was low, intrasegmental airways were expanded, and extrasegmental airways were compressed when Ps was raised. When Pao was high, airway diameter was unaffected by increasing Ps presumably because the airways were already maximally expanded. A comparison of diameters during homogenous and nonhomogenous lobe inflation suggests a very small interdependence effect from the parenchyma surrounding the collaterally ventilating segment. These results demonstrate the combined effects of parenchymal properties and airway pressure-diameter relationships in determining the effect of local lung distortion on airway function.     

Lung volume and compliance in neonatal rats

Lung volumes and static lung compliance were measured in decapitated three day-old neonatal Long Evans' rat pups. Compliance was measured in situ (open chest method) using a water manometer and syringe system. Mean total lung capacity at 20 cm H2O pressure (TLC20) was 0.678 ml. Minimum lung volume after experimental inflation was 0.197 +/- 0.048 ml, and vital capacity was 0.56 ml (Vmax20). The mean lung compliance value for the approximate tidal loop (between 3 and 12 cm H2O) equalled 26.2 microliters air/cm H2O for the inflation limb and 23.1 microliters/cm H2O for the deflation limb.     

The bimodal quasi-static and dynamic elastance of the murine lung.

The double sigmoidal nature of the mouse pressure-volume (PV) curve is well recognized but largely ignored. This study systematically examined the effect of inflating the mouse lung to 40 cm H2O transrespiratory pressure (Prs) in vivo. Adult BALB/c mice were anesthetized, tracheostomized, and mechanically ventilated. Thoracic gas volume was calculated using plethysmography and electrical stimulation of the intercostal muscles. Lung mechanics were tracked during inflation-deflation maneuvers using a modification of the forced oscillation technique. Inflation beyond 20 cm H2O caused a shift in subsequent PV curves with an increase in slope of the inflation limb and an increase in lung volume at 20 cm H2O. There was an overall decrease in tissue elastance and a fundamental change in its volume dependence. This apparent "softening" of the lung could be recovered by partial degassing of the lung or applying a negative transrespiratory pressure such that lung volume decreased below functional residual capacity. Allowing the lung to spontaneously recover revealed that the lung required approximately 1 h of mechanical ventilation to return to the original state. We propose a number of possible mechanisms for these observations and suggest that they are most likely explained by the unfolding of alveolar septa and the subsequent redistribution of the fluid lining the alveoli at high transrespiratory pressure.     

Asymmetrical action of the canine diaphragm after single-lung inflation

Single-lung transplantation (SLT) in patients with emphysema leads to a cranial displacement of the diaphragm on the transplanted side and a shift of the mediastinum toward the transplanted lung. The objective of the present study was to assess the effect of unilateral lung inflation on the mechanics of the diaphragm. Two endotracheal tubes were inserted in the two main stem bronchi of six anesthetized dogs, and radiopaque markers were attached along muscle fibers in the midcostal region of the two halves of the diaphragm. The animals were then placed in a computed tomographic scanner, the left or the right lung was passively inflated, and the phrenic nerves were stimulated while the two endobronchial tubes were occluded. As lung volume increased, the fall in airway opening pressure (ΔPao) in the inflated lung during stimulation decreased markedly, whereas ΔPao in the noninflated lung decreased only moderately (P < 0.001). Also, the two hemidiaphragms shortened both during relaxation and during phrenic stimulation, but the ipsilateral hemidiaphragm was consistently shorter than the contralateral hemidiaphragm. In addition, the radius of curvature of the ipsilateral hemidiaphragm during stimulation increased, whereas the radius of the contralateral hemidiaphragm remained unchanged. These observations indicate that 1) in the presence of unilateral lung inflation, the respiratory action of the diaphragm is asymmetric; and 2) this asymmetry is primarily determined by the differential effect of inflation on the length and curvature of the two halves of the muscle. These observations also imply that in patients with emphysema, SLT improves the action of the diaphragm on the transplanted side.     

Lung volumes and respiratory mechanics in elastase-induced emphysema in mice

Absolute lung volumes such as functional residual capacity, residual volume (RV), and total lung capacity (TLC) are used to characterize emphysema in patients, whereas in animal models of emphysema, the mechanical parameters are invariably obtained as a function of transrespiratory pressure (Prs). The aim of the present study was to establish a link between the mechanical parameters including tissue elastance (H) and airway resistance (Raw), and thoracic gas volume (TGV) in addition to Prs in a mouse model of emphysema. Using low-frequency forced oscillations during slow deep inflation, we tracked H and Raw as functions of TGV and Prs in normal mice and mice treated with porcine pancreatic elastase. The presence of emphysema was confirmed by morphometric analysis of histological slices. The treatment resulted in an increase in TGV by 51 and 44% and a decrease in H by 57 and 27%, respectively, at 0 and 20 cmH(2)O of Prs. The Raw did not differ between the groups at any value of Prs, but it was significantly higher in the treated mice at comparable TGV values. In further groups of mice, tracheal sounds were recorded during inflations from RV to TLC. All lung volumes but RV were significantly elevated in the treated mice, whereas the numbers and size distributions of inspiratory crackles were not different, suggesting that the airways were not affected by the elastase treatment. These findings emphasize the importance of absolute lung volumes and indicate that tissue destruction was not associated with airway dysfunction in this mouse model of emphysema.     

Effect of rib cage and abdominal restriction on total respiratory resistance and reactance

In 14 healthy male subjects we studied the effects of rib cage and abdominal strapping on lung volumes, airway resistance (Raw), and total respiratory resistance (Rrs) and reactance (Xrs). Rib cage, as well as abdominal, strapping caused a significant decrease in vital capacity (respectively, -36 and -34%), total lung capacity (TLC) (-31 and -27%), functional residual capacity (FRC) (-28 and -28%), and expiratory reserve volume (-40 and -48%) and an increase in specific airway conductance (+24 and +30%) and in maximal expiratory flow at 50% of control TLC (+47 and +42%). The decrease of residual volume (RV) was significant (-12%) with rib cage strapping only. Abdominal strapping resulted in a minor overall increase in Rrs, whereas rib cage strapping produced a more marked increase at low frequencies; thus a frequency dependence of Rrs was induced. A similar pattern, but with lower absolute values, of Rrs was obtained by thoracic strapping when the subject was breathing at control FRC. Xrs was decreased, especially at low frequencies, with abdominal strapping and even more with thoracic strapping; thus the resonant frequency of the respiratory system was shifted toward higher frequencies. Partitioning Rrs and Xrs into resistance and reactance of lungs and chest wall demonstrated that the different effects of chest wall and abdominal strapping on Rrs and Xrs reflect changes mainly of chest wall mechanics.