Inhomogeneity during deflation of excised canine lungs. I. Alveolar pressures

Factors both intrinsic and extrinsic to the lung may cause inhomogeneity of alveolar pressures during deflation. Wilson et al. (J. Appl. Physiol. 59: 1924-1928, 1985) predicted that any such inhomogeneity would be limited by interdependence of regional expiratory flows. To test this hypothesis and to explore how the pleural pressure gradient might affect inhomogeneity of alveolar pressures, we deflated at submaximal flows excised canine lobes that first were suspended in air and then were immersed in foams that simulated the vertical gradient of pleural pressure. Interregional inhomogeneity of regional transpulmonary pressures was measured with use of an alveolar capsule technique. Flow-dependent inhomogeneity of alveolar pressures was present, with differences in alveolar pressure quickly relaxing to a constant limiting value at each flow. Foam immersion increased inhomogeneity at a given flow. We conclude that factors intrinsic to the lung cause significant inhomogeneity of alveolar pressures at submaximal expiratory flows and that this inhomogeneity is enhanced by the extrinsic gradient of pleural pressure. These observations are consistent with the interdependence of flow proposed by Wilson et al.     

Alveolar pressure inhomogeneity during low-frequency oscillation of excised canine lobes

To quantify the inhomogeneity of alveolar pressures (PA) during cyclic changes in lung volume similar to those present during spontaneous breathing, inhomogeneity of PA was measured with an alveolar capsule technique in six excised canine lungs. The lungs were ventilated by a quasi-sinusoidal pump with a constant end-expiratory lung volume and tidal volumes of 10, 20, and 40% of vital capacity at breathing frequencies ranging from 5 to 45 breaths/min. Inhomogeneity of PA was quantified as the sample standard deviation of pressures measured in three capsules. A component of inhomogeneity in phase with flow and a smaller component out of phase with flow were present. The in-phase component increased approximately linearly with flow. The ratio of inhomogeneity to flow was smaller at large tidal volumes and, at the two higher tidal volumes studied, the ratio was greater during inspiration than during expiration. If these data are interpreted in terms of a simple circuit model, this degree of inhomogeneity implies an approximately twofold variation in regional time constants. Despite these considerable differences in time constants, the absolute amount of inhomogeneity as defined by the sample standard deviation of the three PA's was small (maximum 0.57 +/- 0.32 cmH2O at the highest breathing frequency and tidal volume) because airway resistance in the canine lung was small.     

Interdependence of flow between lobes reduces maximal emptying postresection in dogs.

The effect of pulmonary resection on the maximal emptying of the remaining lobes was examined in an open-chest preparation in normal canine lungs and in a unilobar papain emphysema model. The objectives were to determine whether, compared with when both lungs were deflated (BL), maximal emptying of the normal lower lobes or the emphysematous right lower lobe would be altered 1) when acute pneumonectomy of the contralateral lung was performed (OL) and 2) when the lower lobe deflated alone (LA). The alveolar capsule technique was used to measure alveolar pressures (Palv) at 75, 50, and 30% lobar vital capacity (VC). During forced deflation, the maximal rates of deflation (dPalv/dt) and flows (lobarV(max)) of the lower lobes were determined under the three different conditions. The Pitot-static tube technique was used to measure intrabronchial pressures and to estimate bronchial area and compliance in which values were obtained at the same central airway during the conditions studied. The results showed that, compared with BL and OL, dPalv/dt and lobar V(max) decreased during LA (P < 0.05). These findings were due to a reduction in bronchial area during LA that limited flow at a lower maximal value compared with BL. This decrease in area appeared to be due to a change in bronchial pressure area behavior that resulted in a smaller bronchial area during LA for similar transmural pressures between conditions. There were no differences in findings between normal and emphysematous lobes. This study suggested that removal of lobes may alter the pressure area behavior of central airways. Possible mechanisms considered were differences in axial tension between conditions, negative effort dependence, or parenchymal-bronchial interdependence that may be relevant to understanding the dynamic collapsibility of central as well as intraparenchymal airways.     

Heterogeneous lung emptying during forced expiration

Several lines of evidence suggest that the healthy mammalian lung empties homogeneously during a maximally forced deflation. Nonetheless, such behavior would appear to be implausible if for no other reason than that airway structure is known to be substantially heterogeneous among parallel pathways of gas conduction. To resolve this paradox we reexamined the degree to which lung emptying is homogeneous, and considered mechanisms that might control differential regional emptying. Twelve excised canine lungs were studied. Regional alveolar pressure relative to pleural pressure was used as an index of regional lung volume. By use of a capsule technique, alveolar pressure was measured simultaneously in each of six regions during flow-limited deflations; flow from the lung was measured plethysmographically. The standard deviation of interregional pressure differences, which was taken as an index of nonuniformity, was 0.0, 0.74, 0.64, and 0.90 cmH2O at mean recoil pressures of 30, 8.4, 4.5, and 2.1 cmH2O (0, 25, 50, and 75% expired vital capacity), indicating that interregional pressure differences increased more rapidly earlier in the deflation. When we examined the time rate of change of regional alveolar pressure as an index of regional flow, we observed an intricate pattern of differential regional behavior that was inapparent in the maximum expiratory flow-volume (MEFV) curve. The most plausible interpretation of these findings is that regions of the healthy excised canine lung empty heterogeneously to a small degree, but in an interdependent compensatory pattern that is inapparent in the configuration of the maximum expiratory flow-volume curve.     

Alveolar septal folding and lung inflation history.

On the basis of microscopic appearance of excised lungs, it has been thought that alveolar septa may fold and unfold during deflation and inflation. We suspected that this appearance might depend heavily on the inflation history of the lung preparation. We therefore studied, by light and electron microscopy, dog, rabbit, and rat lungs fixed over a range of inflation pressures and after a variety of inflation histories. Septal folding, as suggested by the configurations of the air spaces, by the placement of the fine and coarse connective tissue elements, and by the pattern of infolding of alveolar epithelium, was readily seen with some inflation protocols but was absent with others. Pressure at fixation was not as important as events before fixation; deflation to 3 cmH2O did not induce folding, and inflation to 16 cmH2O did not undo the folds. This range corresponds with concepts of critical opening and closing pressures. We suggest that folds form de novo during experimental preparation; one need not postulate that septal folding was present in vivo.     

Alveolar pressure inhomogeneity and gas exchange during constant-flow ventilation in dogs

Analysis of momentum transfer between inflow jets and resident gas during constant-flow ventilation (CFV) predicts inhomogeneity of alveolar pressures (PA) and volume, which might account for specific ventilation-variance in the lung. Using alveolar needles to measure pressures (PA) during CFV in eight anesthetized dogs with wide thoracotomy, we observed random dispersion of PA among lobes of up to 12.5 cmH2O. Within each lobe, the PA dispersion was up to 10 cmH2O at CFV of 90 l/min; when flow decreased, PA at all sites decreased, as did the intralobar dispersion. These pressure differences were not observed during conventional mechanical ventilation (CMV). During CFV with room air, dogs were hypoxemic [arterial PO2 (Pao2) 54 +/- 15 Torr] and the venous admixture (Qva/QT) was 50 +/- 15%. When inspiratory O2 fraction was increased to 0.4, Pao2 increased to 172 +/- 35 Torr and Qva/QT dropped to 13.5 +/- 8.4%, confirming considerable ventilation-perfusion (VA/Q) variance not observed during CMV. We conclude that momentum transfer between the inflow stream and resident gas caused inhomogeneities of alveolar pressures, volumes, and ventilation responsible for VA/Q variance and hypoxemia during CFV. Conceivably, the abnormal ventilation distribution is minimized by collateral ventilation and forces of interdependence between regions of high and low alveolar pressures. Momentum transfer also predicted the mucosal damage observed on histological evaluation of the bronchial walls near the site of inflow jet impact.     

Inhomogeneity during deflation of excised canine lungs. III. Single-breath O2 tests

Both interregional and intraregional mechanisms may cause changes in N2 concentration of expired gas during the phases of the single-breath O2 test (SBO2) that follow dead-space washout. To evaluate the possible importance of each mechanism, we performed the SBO2 in excised canine lungs that were first suspended in air and then immersed in stable foams that simulated the vertical gradient of pleural pressure. The lungs were deflated at constant submaximal flows. The slope of phase III diminished with increasing expiratory flow and increased with foam immersion. The onset of phase IV depended on flow, and a terminal decrease in N2 concentration (phase V) was often observed. Simultaneously measured estimates of regional flows and volumes (J. Appl. Physiol. 65: 1764-1774, 1988) were used to further interpret these results. The onset of phase IV at flows greater than quasi-static signified the onset of flow limitation of dependent regions. The onset of phase V corresponded to flow limitation of nondependent regions.     

Microsphere maps of regional blood flow and regional ventilation.

Systematically mapped samples cut from lungs previously labeled with intravascular and aerosol microspheres can be used to create high-resolution maps of regional perfusion and regional ventilation. With multiple radioactive or fluorescent microsphere labels available, this methodology can compare regional flow responses to different interventions without partial volume effects or registration errors that complicate interpretation of in vivo imaging measurements. Microsphere blood flow maps examined at different levels of spatial resolution have revealed that regional flow heterogeneity increases progressively down to an acinar level of scale. This pattern of scale-dependent heterogeneity is characteristic of a fractal distribution network, and it suggests that the anatomic configuration of the pulmonary vascular tree is the primary determinant of high-resolution regional flow heterogeneity. At approximately 2-cm(3) resolution, the large-scale gravitational gradients of blood flow per unit weight of alveolar tissue account for <5% of the overall flow heterogeneity. Furthermore, regional blood flow per gram of alveolar tissue remains relatively constant with different body positions, gravitational stresses, and exercise. Regional alveolar ventilation is accurately represented by the deposition of inhaled 1.0-microm fluorescent microsphere aerosols, at least down to the approximately 2-cm(3) level of scale. Analysis of these ventilation maps has revealed the same scale-dependent property of regional alveolar ventilation heterogeneity, with a strong correlation between ventilation and blood flow maintained at all levels of scale. The ventilation-perfusion (VA/Q) distributions obtained from microsphere flow maps of normal animals agree with simultaneously acquired multiple inert-gas elimination technique VA/Q distributions, but they underestimate gas-exchange impairment in diffuse lung injury.     

Effect of ventilation-perfusion inhomogeneity and N(2)O on oxygenation: physiological modeling of gas exchange.

Ventilation-perfusion (VA/Q) inhomogeneity was modeled to measure its effect on arterial oxygenation during maintenance-phase anesthesia involving an inspired mixture of 30% O(2) and either N(2)O or N(2). A multialveolar compartment computer model was constructed based on a log normal distribution of VA/Q inhomogeneity. Increasing the log SD of the distribution of blood flow from 0 to 1.75 produced a progressive fall in arterial PO(2) (Pa(O(2))). The fall was less steep in the presence of N(2)O than when N(2) was present instead. This was due mainly to the concentrating effect of N(2)O uptake on alveolar PO(2) in moderately low VA/Q compartments. The improvement in Pa(O(2)) when N(2)O was present instead of N(2) was greatest when the degree of VA/Q inhomogeneity was in the range typically seen in anesthetized patients. Models based on distributions of expired and inspired alveolar ventilation give quantitatively different results for Pa(O(2)). In the presence of VA/Q inhomogeneity, second-gas and concentrating effects may have clinically significant effects on arterial oxygenation even at "steady-state" levels of N(2)O uptake.     

Spatial distribution of ventilation and perfusion in anesthetized dogs in lateral postures.

We aimed to assess the influence of lateral decubitus postures and positive end-expiratory pressure (PEEP) on the regional distribution of ventilation and perfusion. We measured regional ventilation (VA) and regional blood flow (Q) in six anesthetized, mechanically ventilated dogs in the left (LLD) and right lateral decubitus (RLD) postures with and without 10 cmH(2)O PEEP. Q was measured by use of intravenously injected 15-microm fluorescent microspheres, and VA was measured by aerosolized 1-microm fluorescent microspheres. Fluorescence was analyzed in lung pieces approximately 1.7 cm(3) in volume. Multiple linear regression analysis was used to evaluate three-dimensional spatial gradients of Q, VA, the ratio VA/Q, and regional PO(2) (Pr(O(2))) in both lungs. In the LLD posture, a gravity-dependent vertical gradient in Q was observed in both lungs in conjunction with a reduced blood flow and Pr(O(2)) to the dependent left lung. Change from the LLD to the RLD or 10 cmH(2)O PEEP increased local VA/Q and Pr(O(2)) in the left lung and minimized any role of hypoxia. The greatest reduction in individual lung volume occurred to the left lung in the LLD posture. We conclude that lung distortion caused by the weight of the heart and abdomen is greater in the LLD posture and influences both Q and VA, and ultimately gas exchange. In this respect, the smaller left lung was the most susceptible to impaired gas exchange in the LLD posture.     

Alveolar air-tissue interface and nuclear magnetic resonance behavior of lung

Inflated lungs are characterized by a short nuclear magnetic resonance (NMR) free induction decay (rapid disappearance of NMR signal), likely due to internal (tissue-induced) magnetic field inhomogeneity produced by the alveolar air-tissue interface. This phenomenon can also be detected using temporally symmetric and asymmetric NMR spin-echo sequences; these sequences generate a pair of NMR images from which a difference signal (delta) is obtained (reflecting the signal from lung water experiencing the air-tissue interface effect). We measured delta in normal excised rat lungs at inflation pressures of 0-30 cmH2O for asymmetry times (a) of 1-6 ms. Delta was low in degassed lungs and increased markedly with alveolar opening when measured at a = 6 ms (delta 6 ms); delta 6 ms varied little during the rest of the inflation-deflation cycle. Delta 1 ms (a = 1 ms) did not vary significantly on inflation and deflation. Measurements of delta at a = 3 and 5 ms generally lay between those of delta 1 ms and delta 6 ms. These findings, which are consistent with theoretical predictions, suggest that measurements of delta at appropriate asymmetry times are particularly sensitive to alveolar opening and may provide a means of distinguishing alveolar recruitment from alveolar distension in the pressure-volume behavior of the lung.     

Alveolar liquid pressures in newborn and adult rabbit lungs

To study the effects of lung maturation and inflation on alveolar liquid pressures, we isolated lungs from adult and newborn rabbit pups (1-11 days old). We used the micropuncture technique to measure alveolar liquid pressure at several transpulmonary pressures on lung deflation. Alveolar liquid pressure was greater than pleural pressure but less than airway pressure at all transpulmonary pressures. Alveolar liquid pressure decreased further below airway pressure with lung inflation. At high transpulmonary pressure, alveolar liquid pressure was less in newborn than in adult lungs. To study the effects of edema, we measured alveolar liquid pressures in newborn lungs with different wet-to-dry weight ratios. Alveolar liquid pressure increased with progressive edema. In addition, we compared alveolar liquid and perivenular interstitial pressures in perfused newborn lungs and found that they were similar. Thus alveolar liquid pressure can be used to estimate perivenular interstitial pressure. We conclude that the transvascular pressure gradient for fluid flux into the interstitium might increase with lung inflation and decrease with progressive edema. Furthermore, this gradient might be greater in newborn than adult lungs at high inflation pressures.     

Heterogeneity of maximal lobar emptying rates in dogs with compensatory lung growth

Five dogs underwent left pneumonectomy at 10 wk of age, whereas four littermates underwent a sham operation. At 26 wk of age the postpneumonectomy dogs had total lung vital capacity (VC) and lung weight similar to controls, but maximum expiratory flow was reduced. Pressure capsules were glued to right lower (RLL) and right cardiac (RCL) lobes, and alveolar pressures (PA) were measured during forced expiration. In postpneumonectomy dogs RLL and RCL both emptied more slowly than in control dogs, and emptying was especially delayed in RCL, which underwent the most growth. When both lobes deflated together, PA in RCL and RLL were similar in control dogs, but in postpneumonectomy dogs PA in RCL exceeded that in RLL by approximately 3 cmH2O from 80 to 20% VC. Because the higher driving pressure in RCL compensated for the relatively high resistance of RCL, the pattern of lobar emptying was relatively uniform over these lung volumes. This result was compatible with interdependence of lobar maximum expiratory flows. In addition, at PA of 6-10 cmH2O in postpneumonectomy dogs, maximum emptying rates of RCL were less when RCL deflated alone than when RCL and RLL emptied together, again demonstrating interdependence of lobar maximum expiratory flow.     

Gas density dependence of regional VA/V and VA/Q inequality during constant-flow ventilation

Constant-flow ventilation (CFV) is achieved by delivering a constant stream of inspiratory gas through cannulas aimed down the main stem bronchi at flow rates totaling 1-3 l.kg-1.min-1 in the absence of tidal lung motion. Previous studies have shown that CFV can maintain a normal arterial PCO2, although significant ventilation-perfusion (VA/Q) inequality appears. This VA/Q mismatch could be due to regional differences in lung inflation that occur during CFV secondary to momentum transfer from the inflowing stream to resident gas in the lung. We tested the hypothesis that substitution of a gas with lower density might attenuate regional differences in alveolar pressure and reduce the VA/Q inequality during CFV. Gas exchange was studied in seven anesthetized dogs by the multiple inert gas elimination technique during ventilation with intermittent positive-pressure ventilation, CFV with O2-enriched nitrogen (CFV-N2), or CFV with O2-enriched helium (CFV-He). As an index of VA/Q inequality independent of shunt, the log SD blood flow increased from 0.757 +/- 0.272 during intermittent positive-pressure ventilation to 1.54 +/- 0.36 (P less than 0.001) during CFV-N2. Switching from CFV-N2 to CFV-He at the same flow rate did not improve log SD blood flow (1.45 +/- 0.21) (P greater than 0.05) but tended to increase arterial PCO2. In excised lungs with alveolar capsules attached to the pleural surface, CFV-He significantly reduced alveolar pressure differences among lobes compared with CFV-N2 as predicted. Regional alveolar washout of Ar after a stap change of inspired concentration was slower during CFV--He than during CFV-N2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lung inflation does not increase maximal expiratory flow during induced obstruction in the dog

A deep inflation (DI) reverses induced bronchoconstriction in normal human subjects whether assessed by airway resistance before and after a DI or by isovolumic maximal expiratory flows (Vmax) from partial expiratory flow-volume (PEFV) vs. maximum expiratory flow-volume (MEFV) maneuvers. These observations suggest that with induced constriction the hysteresis of airways exceeds that of the parenchyma. In contrast with humans, a previous study of ours on dogs indicated that induced increases in airway resistance were unaffected by DI, suggesting that hysteresis of airways and parenchyma were equal. We hypothesized therefore that in constricted dog lungs, any differences that might arise in isovolumic Vmax between PEFV and MEFV maneuvers would not be due to changes in airway caliber but rather would be wholly determined by isovolumic differences in deflational recoil pressures. Recoil pressures were dynamically measured using six separate alveolar capsules in each of six dogs. At base line there were no significant differences between isovolumic recoil pressures or maximal flows with volume history, suggesting equal degrees of airway and parenchymal hysteresis. After histamine-induced constriction there were also no isovolumic differences in flows, but due to striking nonhomogeneities in dynamic recoil pressure among alveolar capsules, it was not possible to express a single meaningful recoil pressure pertinent to the lungs as a whole. These findings are consistent with the idea that isovolumic comparisons of Vmax serve as a reasonable indicator of changes in the relative degree of airway and parenchymal hysteresis.     

Expiratory flow limitation in dogs with regional changes in lung mechanical properties

We examined maximum expiratory flow (Vmax) in two canine preparations in which regional changes in lung mechanical properties were produced. In one experiment serial bronchial obstructions were made to determine whether flow-limiting sites (choke points, CP) would occur in series. With the right lung tied off, constrictions were placed at the left lower lobar bronchus (LLL) and left main-stem bronchus. On deflation from total lung capacity, the obstructed LLL and nonobstructed left upper lobe (LUL) emptied into the obstructed left main-stem bronchus. Although a CP common to both lobes was identified at the main-stem obstruction, which limited total Vmax, we questioned whether there was also a CP at the lobar obstruction that fixed LLL flow. In that case the rate of LLL emptying would not be dependent on the presence of the common (i.e., central) CP and thus the flow contribution of the LUL. We found that when the LUL was removed, the LLL increased its rate of emptying. Thus a lobar CP did not fix LLL flow and CP did not occur in series. In a second experiment emphysema was produced in the left lung to reduce lung recoil, whereas the right lung was normal. CP were identified at approximately lobar bronchi of each lung, and the lungs were emptied at different rates. A CP common to both lungs was not identified. Our results indicate that in localized lung disease, if flows from the different regions are high enough, then wave speed is reached in proximal airways, and a CP occurs centrally rather than peripherally. On the other hand, if flows are low, then wave speed is reached peripherally and a CP common to all lung regions does not occur.     

Heterogeneity of mean alveolar pressure during high-frequency oscillations

Mean alveolar pressure may exceed mean airway pressure during high-frequency oscillations (HFO). To assess the magnitude of this effect and its regional heterogeneity, we studied six excised dog lungs during HFO [frequency (f) 2-32 Hz; tidal volume (VT) 5-80 ml] at transpulmonary pressures (PL) of 6, 10, and 25 cmH2O. We measured mean pressure at the airway opening (Pao), trachea (Ptr), and four alveolar locations (PA) using alveolar capsules. Pao was measured at the oscillator pump, wherein the peak dynamic head was less than 0.2 cmH2O. Since the dynamic head was negligible here, and since these were excised lungs, Pao thus represented true applied transpulmonary pressure. Ptr increasingly underestimated Pao as f and VT increased, with Pao - Ptr approaching 8 cmH2O. PA (averaged over all locations) and Pao were nearly equal at all PL's, f's, and VT's, except at PL of 6, f 32 Hz, and VT 80 ml, where (PA - Pao) was 3 cmH2O. Remarkably, mean pressure in the base exceeded that in the apex increasingly as f and VT increased, the difference approaching 3 cmH2O at high f and VT. We conclude that, although global alveolar overdistension assessed by PA - Pao is small during HFO under these conditions, larger regional heterogeneity in PA's exists that may be a consequence of airway branching angle asymmetry and/or regional flow distribution.     

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)     

Correlation between ventilation and perfusion determines VA/Q heterogeneity in endotoxemia.

Endotoxin increases ventilation-to-perfusion ratio (VA/Q) heterogeneity in the lung, but the precise changes in alveolar ventilation (VA) and perfusion that lead to VA/Q heterogeneity are unknown. The purpose of this study was to determine how endotoxin affects the distributions of ventilation and perfusion and the impact of these changes on VA/Q heterogeneity. Seven anesthetized, mechanically ventilated juvenile pigs were given E. coli endotoxin intravenously, and regional ventilation and perfusion were measured simultaneously by using aerosolized and injected fluorescent microspheres. Endotoxemia significantly decreased the correlation between regional ventilation and perfusion, increased perfusion heterogeneity, and redistributed perfusion between lung regions. In contrast, ventilation heterogeneity did not change, and redistribution of ventilation was modest. The decrease in correlation between regional ventilation and perfusion was responsible for significantly more VA/Q heterogeneity than were changes in ventilation or perfusion heterogeneity. We conclude that VA/Q heterogeneity increases during endotoxemia primarily as a result of the decrease in correlation between regional ventilation and perfusion, which is in turn determined primarily by changes in perfusion.     

Alveolar pressure measurement in open-chest rats.

In open-chest rats, alveolar pressure was measured with alveolar capsules connected via pliable tubing to inductive pressure transducers. By means of the interrupter technique during constant-flow inflation, it was possible to determine pulmonary static elastance (Est,L) and tissue and airway resistances (Rdiff,L and Rinit,L, respectively). In eight anesthetized paralyzed mechanically ventilated rats, 118 measurements of Rdiff,L and Est,L were performed over a wide range of flows and tidal volumes. There was excellent agreement between the data calculated using transpulmonary pressures and those computed using capsule pressures, the latter being measured at different points of the lung. In another group of rats studied under the same experimental conditions, two capsules were simultaneously placed on different pulmonary lobes. No regional differences in pulmonary mechanics could be detected in either experiment. In addition, alveolar pressure could also be measured accurately by a catheter inserted into lung parenchyma.