Vasodilators, aortic elasticity, and ventricular end-systolic stress in nonanesthetized unrestrained rats.

We evaluated the effect of different vasodilators on ventricular end-systolic stress by investigating the impact of sodium nitroprusside, nifedipine, and hydralazine on blood pressure, aortic stiffness, and wave reflection during drug-induced hypotension (to 80 mm Hg mean blood pressure) in normotensive (central aortic mean blood pressure, 116 to 119 mm Hg; systolic pressure, 133 to 137 mm Hg), nonanesthetized, unrestrained rats. Aortic stiffness was evaluated from the slope of the linear regression relating pulse wave velocity (PWV) to central aortic mean or pulse pressure. The fall in central aortic systolic blood pressure was less than the fall in mean pressure, especially after hydralazine (122+/-4 mm Hg; sodium nitroprusside, 107+/-2; and nifedipine, 112+/-3 mm Hg; P<.05). The PWV/mean pressure slope was linear, positive, and similar in all three groups (hydralazine, 3.3+/-0.2; sodium nitroprusside, 3.8+/-0.3; and nifedipine, 3.9+/-0.3 cm x s[-1]x mm Hg[-1]; P>.05). The PWV/pulse pressure slope was linear, negative, and less steep in the case of hydralazine (-4.9+/-0.6; sodium nitroprusside, -15.5+/-3.7; and nifedipine, -13.5+/-2.9 cm x s[-1] x mm Hg[-1]; P<.05). The travel time and augmentation index of the reflected wave were similar in all groups. In conclusion, sodium nitroprusside and nifedipine had a more beneficial effect on end-systolic stress than did hydralazine. This does not appear to be related to any specific effect on wave reflection or the "static" relationship between PWV and aortic mean blood pressure; it may be related to the effects of these drugs on the "dynamic" relationship between PWV and pulse pressure.

Calcification of medial elastic fibers and aortic elasticity.

We tested the hypothesis that a simple change in wall composition (medial calcium overload of elastic fibers) can decrease aortic elasticity. Calcium overload was produced by hypervitaminosis D plus nicotine (VDN) in the young rat. Two months later, measurement of central aortic mean blood pressure in the unanesthetized, unrestrained rat showed that the VDN rat suffered from isolated systolic hypertension but that mean blood pressure was normal. Wall thickness and internal diameter determined after in situ pressurized fixation were unchanged, as was calculated wall stress. Wall stiffness was estimated from (1) elastic modulus (determined with the Moens-Korteweg equation and values for aortic pulse wave velocity in the unanesthetized, unrestrained rat and arterial dimensions) and (2) isobaric elasticity (= slope relating pulse wave velocity to mean intraluminal pressure in the phenylephrine-infused, pithed rat preparation). Both increased after VDN, and both were significantly correlated to the wall content of calcium and the elastin-specific amino acids desmosine and isodesmosine. Left ventricular hypertrophy occurred in the VDN model, and left ventricular mass was related to isobaric elasticity. In conclusion, elastocalcinosis induces destruction of elastic fibers, which leads to arterial stiffness, and the latter may be involved in the development of left ventricular hypertrophy in a normotensive model.

Streptococcus pneumoniae and Staphylococcus aureus surface properties in relation to their adherence to human buccal epithelial cells.

Adherence to host cells by pathogenic bacteria is achieved through both specific and non-specific mechanisms. The former involve bacterial adhesin and corresponding cell receptors (Gibbons and Van Houte, 1980), while the second include electric charges and hydrophobicity of bacterial cell walls. In a previous study (Beck et al., 1988), we showed that these two cell surface characteristics vary during growth of Staphylococcus aureus in a manner which should promote adherence to host cells. The aims of the current study were to assess: (1) whether the same growth-related variations in surface properties were present in another bacterial species, Streptococcus pneumoniae; (2) whether the adherence of the two types of bacteria to epithelial cells was in fact different at different growth times; and (3) whether such differences were consistent with the observed surface properties.

Volume dependence of respiratory system resistance during artificial ventilation in rabbits.

The volume dependence of respiratory resistance (Rrs), usually observed during normal breathing, is expected to be accentuated during expiratory flow limitation (EFL). In order to quantify this dependence we studied the pressure, flow, and volume data obtained from eight New Zealand rabbits, artificially ventilated at different levels of applied expiratory pressure (0-10 hPa), before and during histamine i. v. infusion. EFL was provoked by lowering the expiratory pressure and was detected by the application of an additional negative expiratory pressure and by forced oscillations. The analysis of respiratory system mechanics was performed by multiple regression, using the classical linear first-order model and also a nonlinear model, accounting for volume dependence of Rrs. Both models satisfactorily fitted the data in the absence of EFL. The nonlinear model proved to be more appropriate in the presence of EFL. The coefficient expressing the volume dependence of Rrs (Rvd) was significantly more negative during EFL. Rvd values were highly correlated with the fraction of the tidal volume left to be expired at the onset of EFL. A threshold Rvd value of -1,000 (hPa x s x l(-2)) detected EFL with high sensitivity and specificity. We conclude that a strongly negative volume dependence of Rrs is a reliable and noninvasive index of EFL during artificial ventilation.

Partitioning of airway and respiratory tissue mechanical impedances by body plethysmography.

We have tested the feasibility of separating the airway (Zaw) and tissue (Zti) components of total respiratory input impedance (Zrs,in) in healthy subjects by measuring alveolar gas compression by body plethysmography (Vpl) during pressure oscillations at the airway opening. The forced oscillation set up was placed inside a body plethysmograph, and the subjects rebreathed BTPS gas. Zrs,in and the relationship between Vpl and airway flow (Hpl) were measured from 4 to 29 Hz. Zaw and Zti were computed from Zrs,in and Hpl by using the monoalveolar T-network model and alveolar gas compliance derived from thoracic gas volume. The data were in good agreement with previous observations: airways and tissue resistance exhibited some positive and negative frequency dependences, respectively; airway reactance was consistent with an inertance of 0.015 +/- 0.003 hPa.s2.l-1 and tissue reactance with an elastance of 36 +/- 8 hPa/I. The changes seen with varying lung volume, during elastic loading of the chest and during bronchoconstriction, were mostly in agreement with the expected effects. The data, as well as computer simulation, suggest that the partitioning is unaffected by mechanical inhomogeneity and only moderately affected by airway wall shunting.

Evaluation of a forced oscillation method to measure thoracic gas volume.

The purpose of this study was to test a plethysmographic method of measuring thoracic gas volume (TGV) that, contrary to the usual panting method, would not require any active cooperation from the subject. It is based on the assumption that the out-of-phase component of airway impedance varies linearly with frequency. By using that assumption, TGV may be computed by combining measurements of total respiratory impedance (Zrs) and of the relationship between the plethysmographic signal (Vpl) and airway flow (V) during forced oscillations at several frequencies. Zrs and Vpl/V were measured at 10 noninteger multiple frequencies ranging from 4 to 29 Hz in 15 subjects breathing gas in nearly BTPS conditions. Forced oscillation measurements were immediately followed by determination of TGV by the standard method. The data were analyzed on different frequency ranges, and the best agreement was seen in the 6- to 29-Hz range. Within that range, forced oscillation TGV and standard TGV differed little (3.92 +/- 0.66 vs. 3.83 +/- 0.73 liters, n = 77, P < 0.05) and were strongly correlated (r = 0.875); the differences were not correlated to the mean of the two estimates, and their SD was 0.35 liter. In seven subjects the differences were significantly different from zero, which may, in part, be due to imperfect gas conditioning. We conclude that the method is not highly accurate but could prove useful when, for lack of sufficient cooperation, the panting method cannot be used. The results of computer simulation, however, suggest that the method would be unreliable in the presence of severe airway inhomogeneity or peripheral airway obstruction.

Total respiratory input and transfer impedances in humans.

Total respiratory input (Zrs,in) and transfer (Zrs,tr) impedances were obtained from 4 to 30 Hz in 10 healthy males by simultaneously measuring mouth and chest flow while applying pseudo-random pressure variations at the mouth. Compared with Zrs,in, the real part of Zrs,tr was larger up to 10 Hz but exhibited a much stronger negative frequency dependence. The imaginary part was larger at all frequencies, with a resonant frequency (fn) at 6.0 +/- 0.8 Hz compared with 8.2 +/- 2.9 Hz for Zrs,in. The two impedances were analyzed with a model featuring airway resistance and inertance, alveolar gas compressibility, and tissue resistance, inertance, and compliance. A good fit was generally obtained but, in most cases, with a different partitioning of resistance between airway and tissue for Zrs,in and Zrs,tr. The data were also used to compute separately airway and tissue (Zt) impedances. In most subjects Zt could not be properly fitted with a simple resistance-inertance-compliance unit and was consistent with a slow (fn = 7.4 +/- 2.3 Hz) overdamped compartment in parallel with a fast (fn = 37.1 +/- 5.6 Hz) underdamped one.

Respiratory tissue properties derived from flow transfer function in healthy humans.

Assuming homogeneity of alveolar pressure, the relationship between airway flow and flow at the chest during forced oscillation at the airway opening [flow transfer function (FTF)] is related to lung and chest wall tissue impedance (Zti): FTF = 1 + Zti/Zg, where Zg is alveolar gas impedance, which is inversely proportional to thoracic gas volume. By using a flow-type body plethysmograph to obtain flow rate at body surface, FTF has been measured at oscillation frequencies (f(os)) of 10, 20, 30 and 40 Hz in eight healthy subjects during both quiet and deep breathing. The data were corrected for the flow shunted through upper airway walls and analyzed in terms of tissue resistance (Rti) and effective elastance (Eti,eff) by using plethysmographically measured thoracic gas volume values. In most subjects, Rti was seen to decrease with increasing f(os) and Eti,eff to vary curvilinearly with f(os)2, which is suggestive of mechanical inhomogeneity. Rti presented a weak volume dependence during breathing, variable in sign according to f(os) and among subjects. In contrast, Eti,eff usually exhibited a U-shaped pattern with a minimum located a little above or below functional residual capacity and a steep increase with decreasing or increasing volume (30-80 hPa/l2) on either side. These variations are in excess of those expected from the sigmoid shape of the static pressure-volume curve and may reflect the effect of respiratory muscle activity. We conclude that FTF measurement is an interesting tool to study Rti and Eti,eff and that these parameters have probably different physiological determinants.

Respiratory transfer impedances with pressure input at the mouth and chest.

Two methods of measuring respiratory transfer impedance (Ztr) were compared in 14 normal subjects, from 4 to 30 Hz, 1) studying the relationship between transrespiratory pressure (Prs) and flow at the chest when varying pressure at the mouth (Ztrm) and 2) studying the relationship between Prs and flow at the mouth when varying pressure around the chest wall (Ztrw). The similarity of the two relationships was expected on the basis of a T-network model. Almost identical phase responses were obtained from the two methods. Pressure-flow ratios were slightly larger for Ztrw than for Ztrm, but differences did not exceed 2% on average in 11 of 14 subjects. When the data were analyzed with the six-coefficient model proposed by DuBois et al. (J. Appl. Physiol. 8: 587-594, 1956), similar values were found for tissue compliance and tissue inertance but slightly different values for gaseous inertance in the airways (1.97 +/- 0.35 X 10(-2) cmH2O X l-1 X s2 for Ztrw vs. 1.73 +/- 0.26 for Ztrm; P less than 0.01). Similar results were also found for total respiratory resistance but with a slightly larger contribution of airway resistance for Ztrw (64 +/- 14 vs. 57 +/- 10%; P less than 0.05). As a practical conclusion it is recommended to measure Ztrw, which is technically much easier.

Acute pulmonary response to intravenous histamine at fixed lung volume in dogs.

We measured tracheal pressure (Ptr), tracheal flow, and two alveolar pressures in five open-chest anesthetized and paralyzed dogs. The lungs were maintained at a fixed volume for 50 s while small amplitude oscillations in flow at 6 Hz were applied at the tracheal opening. The measurements of alveolar pressure showed that the resulting oscillations in Ptr were virtually entirely determined by airway resistance (Raw) and consequently gave accurate estimates of the same. A 20-mg bolus of histamine was given intravenously at the start of this period when Ptr was 0.5 kPa. After approximately 10 s the mean Ptr increased sharply by approximately 40% and plateaued after approximately 25 s. Raw, in contrast, continued to increase throughout the oscillation period. Furthermore, the increases in mean Ptr were virtually identical in all dogs, whereas the increases in Raw were highly variable among the dogs. Our results suggest that the increases in mean Ptr caused by histamine were due to contraction of distal elements in the lung, whereas the changes in Raw were due mainly to constriction of more central airways.

Measurement of thoracic gas volume by low-frequency ambient pressure changes.

When the whole body is exposed to sinusoidal variations of ambient pressure (delta Pam) at very low frequencies (f), the resulting compression and expansion of alveolar gas is almost entirely achieved by gas flow through the airways (Vaw). As a consequence thoracic gas volume (TGV) may be computed from the imaginary part (Im) of the delta Pam/Vaw relationship: TGV = PB/[2 pi f X Im(delta Pam/Vaw)], where PB is barometric minus alveolar water vapor pressure. The method was tested in 35 normal subjects and compared with body plethysmography. The subjects sat in a chamber connected to a large-stroke-volume reciprocating pump that brought about pressure swings of 40 cmH2O at 0.05 Hz. delta Pam and Vaw were digitally processed by fast Fourier transform to extract the low-frequency component from the much larger respiratory flow. Total lung capacities (TLC) obtained by ambient pressure changes and by plethylsmography were highly correlated (r = 0.959, p less than 0.001) and not significantly different (6.96 +/- 1.38 l vs. 6.99 +/- 1.38). TLC obtained by ambient pressure changes were not influenced by lowering the frequency to 0.03 Hz, adding an external resistance at the mouth, or increasing abdominal gas volume. We conclude that the method is practical and in agreement with body plethysmography in normal subjects.

Flow and volume dependence of respiratory mechanical properties studied by forced oscillation.

The influence of inspiratory and expiratory flow magnitude, lung volume, and lung volume history on respiratory system properties was studied by measuring transfer impedances (4-30 Hz) in seven normal subjects during various constant flow maneuvers. The measured impedances were analyzed with a six-coefficient model including airway resistance (Raw) and inertance (Iaw), tissue resistance (Rti), inertance (Iti), and compliance (Cti), and alveolar gas compressibility. Increasing respiratory flow from 0.1 to 0.4 1/s was found to increase inspiratory and expiratory Raw by 63% and 32%, respectively, and to decrease Iaw, but did not change tissue properties. Raw, Iti, and Cti were larger and Rti was lower during expiration than during inspiration. Decreasing lung volume from 70 to 30% of vital capacity increased Raw by 80%. Cti was larger at functional residual capacity than at the volume extremes. Preceding the measurement by a full expiration rather than by a full inspiration increased Iaw by 15%. The data suggest that the determinants of Raw and Iaw are not identical, that airway hysteresis is larger than lung hysteresis, and that respiratory muscle activity influences tissue properties.

Respiratory transfer impedance and derived mechanical properties of conscious rats.

A setup is described for measuring the respiratory transfer impedance of conscious rats in the frequency range 16-208 Hz. The rats were placed in a restraining tube in which head and body were separated by means of a dough neck collar. The restraining tube was placed in a body chamber, allowing the application of pseudorandom noise pressure variations to the chest and abdomen. The flow at the airway opening was measured in a small chamber connected to the body chamber. The short-term reproducibility of the transfer impedance was tested by repeated measurements in nine Wistar rats. The mean coefficient of variation for the impedance did not exceed 10%. The impedance data were analyzed using different models of the respiratory system of which a three-coefficient resistance-inertance-compliance model provided the most reliable estimates of respiratory resistance (Rrs) and inertance (Irs). The model response, however, departed systematically from the measured impedance. A nine-coefficient model best described the data. Optimization of this model provided estimates of the respiratory tissue coefficients and upper and lower airway coefficients. Rrs with this model was 13.6 +/- 1.0 (SD) kPa.l-1.s, Irs was 14.5 +/- 1.3 Pa.l-1.s2, and tissue compliance (Cti) was 2.5 +/- 0.5 ml/kPa. The intraindividual coefficient of variation for Rrs and Irs was 11 and 18%, respectively. Because most of the resistance and inertance was located in the airways (85 and 81% of Rrs and Irs, respectively), the partitioning in tissue and upper and lower airway components was rather poor. Our values for Rrs and Irs of conscious rats were much lower and our values for Cti were higher than previously reported values for anesthetized rats.

Effect of expiratory flow limitation on respiratory mechanical impedance: a model study.

Large phasic variations of respiratory mechanical impedance (Zrs) have been observed during induced expiratory flow limitation (EFL) (M. Vassiliou, R. Peslin, C. Saunier, and C. Duvivier. Eur. Respir. J. 9: 779-786, 1996). To clarify the meaning of Zrs during EFL, we have measured from 5 to 30 Hz the input impedance (Zin) of mechanical analogues of the respiratory system, including flow-limiting elements (FLE) made of easily collapsible rubber tubing. The pressures upstream (Pus) and downstream (Pds) from the FLE were controlled and systematically varied. Maximal flow (Vmax) increased linearly with Pus, was close to the value predicted from wave-speed theory, and was obtained for Pus-Pds of 4-6 hPa. The real part of Zin started increasing abruptly with flow (V) > 85% Vmax and either further increased or suddenly decreased in the vicinity of Vmax. The imaginary part of Zin decreased markedly and suddenly above 95% Vmax. Similar variations of Zin during EFL were seen with an analogue that mimicked the changes of airway transmural pressure during breathing. After pressure and V measurements upstream and downstream from the FLE were combined, the latter was analyzed in terms of a serial (Zs) and a shunt (Zp) compartment. Zs was consistent with a large resistance and inertance, and Zp with a mainly elastic element having an elastance close to that of the tube walls. We conclude that Zrs data during EFL mainly reflect the properties of the FLE.

Assessment of respiratory pressure-volume nonlinearity in rabbits during mechanical ventilation.

The volume dependence of respiratory elastance makes it difficult to recognize actual changes in lung and chest wall elastic properties in artificially ventilated subjects. We have assessed in six anesthetized, tracheotomized, and paralyzed rabbits whether reliable information on the static pressure-volume (PV) curve could be obtained from recordings performed during step variations of the end-expiratory pressure without interrupting mechanical ventilation. Pressure and flow data recorded during 5- and 10-hPa positive-pressure steps were analyzed in the time domain with a nonlinear model featuring a sigmoid PV curve and with a model that, in addition, accounted for tissue viscoelastic properties. The latter fitted the data substantially better. Both models provided reasonably reproducible coefficients, but the PV curves obtained from the 5- and 10-hPa steps were systematically different. When the PV curves were used to predict respiratory effective elastance, the best predictor was the curve derived from the 10-hPa step with the viscoelastic model: unsigned differences averaged 8.6 +/- 11.1, 26.9 +/- 36.4, and 5.5 +/- 5.8% at end-expiratory pressures of 0, 5, and 10 hPa, respectively. This approach provides potentially useful, although not highly accurate, estimates of respiratory effective elastance-volume dependence.

Confidence intervals of respiratory mechanical properties derived from transfer impedance.

Short-term intraindividual variability of the parameters derived from respiratory transfer impedance (Ztr) measured from 4 to 32 Hz was studied in 10 healthy subjects. The corresponding 95% confidence intervals (CIo) were compared with those computed from a single set of data (CIL) according to Lutchen and Jackson (J. Appl. Physiol. 62: 403-413, 1987). Ztr was analyzed with the six-coefficient model of DuBois et al. (J. Appl. Physiol. 8: 587-594, 1956), which includes airway resistance (Raw) and inertance (Iaw), tissue resistance (Rti), inertance (Iti), and compliance (Cti), and alveolar gas compressibility (Cg). The lowest variability was seen for Iaw (CIo = 11.1%), closely followed by Raw (14.3%) and Cti (14.8%), and the largest for Rti and Iti (24.6 and 93.6%, respectively). Using a simpler model, where Iti was excluded, significantly decreased the variability of Iaw (P less than 0.01) and Rti (P less than 0.05) but was responsible for a systematic decrease of Raw and Iaw and increase of Rti. Except for Raw with both models and Iaw with the simpler model, CIL was greater than CIo. Whatever the model, a high correlation between both sets of confidence intervals was found for Rti and Iaw, whereas no correlation was seen for Raw. This suggests that the variability of the former coefficients mainly reflects experimental noise, whereas that of the latter is largely due to biological variability.

Respiratory impedance measured with head generator to minimize upper airway shunt.

A new method for measuring total respiratory input impedance (Zrs), which ensures minimal motion of extrathoracic airway walls, was tested over frequencies of 4-30 Hz in 14 normal subjects and 10 patients with airway obstruction. It consists of applying pressure variations around the head, rather than at the mouth, so that transmural pressure across upper airway walls is equal to the small pressure drop across the pneumotachograph. Compared with reference Zrs values obtained by directly measuring airway wall motion with a head plethysmograph and correcting the data for it, the investigated method provided similar values for respiratory resistance at all frequencies (30 Hz, 3.67 +/- 2.24 cmH2O X 1(-1) X s compared with 3.55 +/- 2.00) but slightly overestimated respiratory reactance at the largest frequencies (30 Hz, 2.82 +/- 1.28 cmH2O X 1(-1) X s compared with 2.52 +/- 1.22, P less than 0.01). In contrast, when the data were not corrected for airway wall motion, resistance was largely underestimated, especially in patients (-48% at 30 Hz, P less than 0.001), and the reactance-frequency curve was shifted to the right. The investigated method is almost as accurate as the reference method, provides equally reproducible data, and is much simpler.

Evaluation of phase correction and low gas density to improve thoracic gas volume measurement.

We investigated two methods of decreasing the error on plethysmographic determinations of thoracic gas volume (TGV) related to cheeks movements during panting maneuvers: lowering gas density in the airways with an 80% He-20% O2 mixture and computing TGV from the in-phase component of the plethysmographic signal (TGVr). The methods were tested by measuring how TGV estimates varied when panting frequency was raised from 0.8 to 2.5 Hz during the same occlusion. The measurements were performed in 6 normal subjects and 12 patients with chronic bronchitis with and without cheeks support and when the airway was connected to an external device simulating an increased cheeks compliance. A small negative frequency dependence of TGV (delta TGV/delta f = -1.2 +/- 0.8%/Hz with cheeks support), most probably unrelated to upper airway walls, was found in normal subjects. Delta TGV/delta f was positive and algebraically larger in patients than in normals, reaching 2.2 +/- 3.4%/Hz without cheeks support and 11.8 +/- 8.0%/Hz with the additional cheeks. The latter value was only 20% smaller when computed on the basis of TGVr, demonstrating the limited usefulness of the phase-based correction. In contrast, breathing He-O2 decreased delta TGV/delta f to approximately 50% of its air value (P less than 0.01) and appears as an effective way to diminish the error in obstructive patients.

Small-amplitude pressure oscillations do not modify respiratory mechanics in rabbits.

Changes in respiratory mechanics have occasionally been observed during high-frequency ventilation. In this study we investigated whether small pressure oscillations such as those used for respiratory impedance measurements modified total respiratory resistance (Rrs) and total respiratory elastance (Ers). The latter were measured in six paralyzed artificially ventilated rabbits with and without superimposed pressure oscillations at the airway opening. Rrs and Ers were obtained by least square fitting of low-pass filtered tracheal pressure and flow to the usual first-order model. Pressure oscillations of 2-4 hPa peak-to-peak at 10, 20, and 30 Hz applied for periods of 10 min had virtually no effect on Ers (changes ranging from -2.5 to 2.6%) and Rrs (0-8.2%). Analysis of variance did not show a significant difference on the pooled data. Pressure oscillations were also applied every other minute after a histamine aerosol. Ers and Rrs were similarly unchanged. We conclude that the small pressure oscillations used in respiratory impedance measurements do not modify lung mechanical properties and lung response to bronchomotor agents.

Human lung impedance from spontaneous breathing frequencies to 32 Hz.

Lung impedance (ZL) was measured from 0.1875 to 32 Hz in spontaneously breathing healthy subjects by spectral analysis of the pressure and flow signals generated simultaneously by the muscular generator of breathing and by a forced oscillation system. This method did not require cooperation from the subject to perform panting or special ventilatory maneuvers and therefore allowed us to analyze the frequency dependence of lung resistance, reactance, and elastance (-2 pi.frequency.reactance) at the physiological conditions of normal breathing. Resistance and elastance parameters were also computed by multiple linear regression of the time-domain pressure and flow data on a simple resistance-elastance model. Resistances and elastances computed at the breathing frequency by spectral analysis and by multiple linear regression were similar (nonsignificant differences < 4 and 10%, respectively). The results obtained when comparing ZL from the breathing component (0.1875-0.75 Hz) of the recorded signals and from the forced oscillation component (2-32 Hz) were fairly consistent. ZL (0.1875-10 Hz) was interpreted in terms of a model consisting of an airway compartment, including a resistance and an inertance, in series with a viscoelastic tissue compartment (J. Hildebrandt. J. Appl. Physiol. 28: 365-372, 1970) characterized by two parameters. The model analysis provided parameter values (resistance 2.49 +/- 0.58 hPa.l-1.s, inertance 1.70 +/- 0.29 Pa.l-1.s2, Hildebrandt parameters 4.87 +/- 2.28 and 0.73 +/- 0.99 hPa/l) consistent with the hypothesis that lung tissue in healthy humans during spontaneous breathing behaves as a viscoelastic structure with a hysteresivity of approximately 0.10.