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1 Harvard Medical School, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham & Women's Hospital and 2 Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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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 cmH2O 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 ~30% of control. Presiloxane capillary specific compliance was ~7%/cmH2O near functional residual capacity and ~2.5%/cmH2O near total lung capacity. Postsiloxane capillary-specific compliance was 3%/cmH2O, 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.
lung; mechanics; microcirculation; dog; surfactant; tissue spectroscopy
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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INCREASED SURFACE
TENSION (
) is an important component of the
pathophysiology of several respiratory diseases, including acute
respiratory distress syndrome (1, 12, 27), infant respiratory distress syndrome (2), and industrial exposure to toxic aerosols (11, 24). Changes in may alter
pulmonary capillary mechanics (e.g., their volume, diameter, and
compliance), which in turn affect the pattern of pulmonary perfusion,
matching of ventilation and perfusion and hence gas exchange, and
leukocyte sequestration. However, the direct effects of changes in on the pulmonary capillary bed are incompletely understood, largely because no technique has been available to directly study capillary mechanics in unfixed lungs with altered .
The pressure around a septal capillary could be increased, be
decreased, or remain unchanged by an increase in , even at constant
lung volume, depending on the vessel's geometry (Fig. 1), making the net outcome difficult to
predict. Some have suggested that increased results in increased
capillary volume and compliance and decreased resistance (5, 17,
18, 23). Others have suggested that exerts a compressive
force on capillaries (28, 29, 31), and therefore increased
would decrease capillary volume and compliance and increase
resistance. To resolve these questions in excised perfused lungs, we
estimated the change in pulmonary capillary volume (Vc), after
increasing , at a constant vascular transmural pressure (Ptm). We
also estimated the capillary specific compliance (Cc), both before and
after increasing . Measurements were made at a variety of lung
volumes (VL), and was increased by ventilating the lung
with nebulized polydimethylsiloxane (hereafter referred to as
siloxane). We found that, between ~40 and 80% total lung capacity
(TLC), increasing lowers both Vc and Cc and that after increasing
, Cc was independent of VL. At high VL (at
which postsiloxane was decreased or little changed), Vc
postsiloxane was greater than control.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animal preparation. We studied lower lobes excised from four female mongrel dogs (18-20 kg). Each animal was anesthetized with preservative-free pentobarbital sodium, initial dose ~15 mg/kg iv, with additional doses as needed to maintain adequate anesthesia. The animal was placed supine, a tracheotomy was performed below the larynx, and the trachea was cannulated with a cuffed endotracheal tube. Heparin (1,000-2,000 units/kg iv) was given, and at least 2 min later the dog was exsanguinated via a 14-gauge carotid artery catheter. The blood was collected, and sodium bicarbonate was added periodically as needed to keep the pH near 7.40 (Ciba Corning model 248). After ~1,000 ml of blood had been collected, the animal was killed with an overdose of pentobarbital (iv). A median sternotomy was performed, and the heart and lungs were excised en bloc. Except for momentary episodes during lung excision, lung inflation was maintained by using positive pressure at the airway opening (Pao). The lung was kept moist by spraying it with 0.9% saline.
A lower lobe was isolated, and its bronchus and pulmonary artery (PA) and vein (PV) were cannulated with large-bore catheters. To reduce intravascular air, the PV catheter was initially flushed with saline, and then both the PA and PV cannulas were connected to a perfusion circuit filled with autologous blood. The lobe was suspended by the cannulas. At a transpulmonary pressure (PL) of ~10 cmH2O, three pleural markers (short pieces of black suture) were cemented to the pleural surface with cyanoacrylate glue, ~3.5 cm apart in a triangular pattern. Photographs of the pleural markers and a ruler held parallel to the lobe surface, were used to calculate changes in lung volume (described below). Pulmonary venous pressure and pulmonary arterial pressure, relative to barometric pressure, were measured (Sorenson Abbott Transpac 2), with the transducer heights matched to the height on the lobe where the optical probe was placed (mid lobe and far from any margin). To keep the pleural surface moist and to prevent gas exchange through the pleural surface, a plastic bag, ventilated with the same gas used for ventilating the lobe, was placed around the lobe. Between measurements, described below, the lobe was ventilated with 5-6% CO2 in O2 (Siemens 900, pressure-control mode) and perfused. An adjustable roller pump (Stockert Shiley model 10) pumped blood (at ~100 ml/min) from a reservoir through a 37-38°C heat exchanger into the PA; blood drained passively from the PV back into the reservoir.Optical methods.
Point illumination of the pleural surface results in a distinctive
pattern of backscattered light from an ~1.5-cm3 volume of
lung. The fractional change in blood volume can be derived from this
pattern; the methods have been previously described in detail
(25, 26) and are summarized here. Optical fibers delivered
laser light of two wavelengths (693 and 808 nm) to a point on the lobe
surface and carried backscattered light from three other points on the
lobe back to sensing photodiodes (Fig. 2). The animal end of the two source and
three receiving fibers were held securely in a plastic block (1.9 × 5 cm area), such that the fibers were in a fixed position relative
to each other. The fibers and block were held gently against the lung.
The lasers were cycled alternately on and off with a period of 8 ms.
The signal from each photodiode alternately provided
wavelength-specific light intensity at each known radial distance from
the source fibers.
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VL calculation. VL at each PL was calculated from digital photographs of the pleural markers using the technique of Lehr et al. (16, see also Ref. 6). From each photograph the distance between each pair of pleural markers was measured (NIH Image version 1.61). To reduce variability, all picture analyses were done by the same individual. VL was calculated from the 3/2 power of the triangle area and expressed as a percent of presiloxane (control) TLC, defined as lung volume at PL = 30 cmH2O. (In one animal, one of the three pleural markers was dislodged during the course of the experiment, and VL was calculated from the distance between the remaining two markers.) Note that this VL is the sum of lung tissue and gas volume, and ~44% TLC = functional residual capacity (FRC; end-expiratory VL at rest) (10). Postsiloxane it was not possible to determine VL by using pleural markers below PL = 7 cmH2O because regions of the lobe began to collapse. The absence of atelectasis at higher PL was indicated by the gross appearance of the lung, the uniformity of the pressure-volume (P-V) changes between lungs and within lobes (6), and the smoothness of the light intensity data with changes in position of the optical probe.
The exponential expression of Salazar and Knowles (20),
![V = V<SUB>0</SUB> + VC [1 − exp(−Pao/P<SUB>0</SUB>)]](/content/vol93/issue3/fulltext/1023/img001.gif)
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Experimental protocol.
Data were collected with the perfusion pump off and the PV cannula
occluded, during slow (10-60 s) oscillations in vascular pressure
generated by raising and lowering the blood reservoir, while
PL was held constant at one of several levels (see Fig. 2).
Microcirculatory intravascular pressure was defined as PV pressure,
because the PV cannula was clamped during the maneuver and there was
therefore minimal flow-resistive pressure loss between the capillaries
and the PV. Vascular Ptm was defined as the difference between
microcirculatory intravascular pressure and airway opening pressure.
Vascular Ptm ranged from approximately 
5 to +20 cmH2O. The design of our experiments kept PV pressure 
PA pressure, so
the vasculature was in West's zone 1 when vascular Ptm < 0 and in zone 3 when vascular Ptm > 0 (30). The microvasculature may have transiently gone
through zone 2 conditions as vascular Ptm went through zero.
Before each data collection period, the lung and vasculature were
exposed to standard volume histories; PL was cycled from 2 to 30 cmH2O three times and then deflated from 30 cmH2O to the target PL. Vascular Ptm was cycled
three times from 5 to +30 cmH2O. Just after each set of
optical data was collected, the lobe was photographed.
was altered by ventilating the
lobe with 5 ml of nebulized, constant-, siloxane
(polydimethylsiloxane, = 20.6 dyn/cm; Nye Lubricants, New
Bedford, MA) as described in detail elsewhere (6). This
treatment has been found to change the lung's P-V relationship in a
characteristic and repeatable fashion. The change in lung recoil
pressure at any given VL is an index of the effective dose
of the nebulized siloxane. The change in PL was ~5
cmH2O at 50% TLC and fell to zero at ~90% TLC (Fig.
3). The volume of siloxane deposited has
been determined to be 0.0045 ± 0.0026 ml/g lung (mean ± SD)
(6).
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and lung recoil increased, the positive end-expiratory pressure (initially ~5 cmH2O) was
increased to ~10 cmH2O to maintain end-expiratory
VL at approximately its presiloxane level. During
nebulization, the perfusion pump was off and the vascular reservoir was
below the level of the lung, so vascular pressures were low.
Data acquisition. Raw signals from each pressure transducer (PA, PV, and airway) and the wavelength-specific light intensities at the three known distances from the source fibers were sampled at 100 Hz per channel and stored on a computer using a 12-bit analog-to-digital board and data acquisition software (Dataq Instruments, Akron, OH). All raw data were averaged over 1-s intervals. These averages were used in all subsequent analyses.
Data analysis and statistics.
Diffuse light scattering allows calculation of fractional changes in Vc
(relative to a reference Vc) at any given VL but does not
provide a measure of absolute Vc (25, 26).
Light-scattering data were reduced to two lung volume-specific outcome
variables, both measured at vascular Ptm of 5 cmH2O:
1) microvascular Cc and 2) the microvascular
volume after changes in (Vc postsiloxane), expressed as a percent
of its control values. At each VL, a vascular P-V loop was
made separately before and then after increasing with siloxane
(examples are shown in Fig. 4). Cc is
essentially the slope of each microvascular P-V loop at the reference
vascular Ptm (Fig. 4, point on the upper loop and square on the lower
loop). Specifically, the fractional change in Vc with vascular Ptm was regressed quadratically against vascular Ptm and constrained to equal
zero at the reference Ptm of 5 cmH2O. Cc is the slope of each regression at vascular Ptm = 5 cmH2O.
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are not as robust as our estimates of Cc. Note
that the reference Vc used at each VL to calculate Vc
postsiloxane is the Vc at Ptm 5 cmH2O before siloxane
exposure (e.g., Fig. 4 point on upper loop) and that this is different
from the reference Vc used to calculate Cc postsiloxane, described above.
Data were pooled by nominal PL for analysis of Vc
postsiloxane and Cc, which are presented as means ± SE, and
statistical significance was defined as P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Increasing increased lung elastic recoil at volumes up to
~90% TLC, as demonstrated by the rightward shift of the P-V curves postsiloxane (Fig. 3). The change in PL at VL = 50% TLC was similar in all animals, ~5 cmH2O.
The change in Vc postsiloxane varied significantly with VL
(Fig. 5). At VL where
postsiloxane was increased, Vc postsiloxane was less than control.
At FRC (~45% TLC), Vc postsiloxane was ~30% of control. At high
VL (where postsiloxane was decreased or little
changed), Vc postsiloxane was greater than control.
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In the control state, Cc fell significantly as VL
increased, from ~7%/cmH2O near FRC to
~2.5%/cmH2O at TLC (Fig.
6), similar to our previous results
(25). After siloxane, Cc was ~3%/cmH2O and
did not change significantly with VL. Near TLC (where was little changed by siloxane), Cc was unchanged after siloxane.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Increasing enough to shift the deflation P-V curve 5 cmH2O at 50% TLC caused decreased Cc and capillary volume
(and hence absolute capillary compliance) over most of the vital
capacity. Capillary volume and compliance decreased substantially near
FRC, where the changes in were large. In the following paragraphs, we discuss technical limitations of this study, compare our findings with those of others, and discuss the physiological implications of our findings.
Technical limitations.
The two primary technical issues that affect our estimation of changes
in Vc and Cc using diffuse light scattering are uncertainties about
changes in lung geometry after siloxane and the presence of
noncapillary blood in the field of view. These effects are addressed
below. They are opposite in sign (i.e., they tend to cancel each other)
and probably result in a small net underestimation of the magnitude of
the changes in Cc and Vc with changes in . Other minor technical
limitations of light-scattering measurements with changes in are
discussed in detail in the companion paper (6).
. The
volume of siloxane deposited, if spread uniformly, would result in a
siloxane film layer ~0.01 µm thick at TLC and about twice that at
FRC. This thickness is a negligible fraction of alveolar diameter and
on the order of magnitude of the 0.1-µm thickness of the normal
surfactant layer (15); thus it is thin enough to avoid
changes in acinar architecture simply because of its volume. There is,
however, significant uncertainty regarding the nature and degree of
spreading (which is discussed in detail in the companion paper; see
Ref. 6).
As discussed extensively by Wilson (32), an increase in
is expected to cause a decrease in septal area at a given
VL, but the magnitude of the change is uncertain. The
change in area has been quantified morphometrically by Bachofen et al.
(3) in rabbit lungs fixed after rinsing with a detergent
and by us in unfixed rabbit lungs (6) after siloxane
nebulization. Decreasing septal area at a given VL would
change the optical properties of the lung, and diffuse light scattering
would then overestimate the actual change in Vc (25). If
septal area at FRC fell by 17% after siloxane treatment
(6), then the corrected Vc postsiloxane would be ~50%,
rather than 30%, of control. This technical issue does not affect our
estimates of Cc, because these are based on measurements made at a
single VL and (either pre- or postsiloxane).
We are primarily interested in septal capillaries, but some of the
blood in the volume sampled by diffuse light scattering is in larger
extra-alveolar vessels. Our estimates of Cc and Vc postsiloxane with
changes in are an average of all the blood in the sampled volume.
More than two-thirds of the blood in lung parenchyma is in pulmonary
capillaries (8, 13), and the contribution of capillary
blood to our measurements is likely to be larger because we are
sampling far from the hilum, in a region where large and moderately
sized vessels are scarce. Further, the effective pressure outside
extra-alveolar vessels is pleural pressure. In our experimental model,
pleural pressure equals ambient pressure, and the effect of increasing
was an increased PL at all VL up to ~90%
TLC. Because we controlled vascular Ptm, the intravascular pressure
also increased as increased. Therefore, the extra-alveolar vessels
would be expected to increase, not decrease, their volume with
increased . Our finding of a net decrease in Vc (an average for all
the vessels in the sampled volume) with increasing is therefore an
underestimate of the true fall in capillary volume.
Change in lung P-V curve and .
The magnitude of the change in postsiloxane varies with
VL and is manifested by the difference in PL.
This effect is large at low VL and falls to zero at high
VL (Fig. 3) for reasons explained below. The change in
PL at 50% TLC was similar in all animals, ~5
cmH2O, similar to the lavage preparation of Smith and
Stamenovi
(22). The lavage preparation is thought
to result in a lung with an approximately constant , independent of
lung volume (14, 33), and to the degree that this is so
our preparation is likely to be nearly the same. At the VL
at which the deflation pre- and postsiloxane P-V curves meet, there is
no change in lung configuration (6, 22); thus in the
siloxane-exposed lungs is equal to its value in normal lungs at this
VL. The deflation P-V curves met at ~90% TLC, a result
similar to those of (22), and near the volume at which
Schürch et al. (21) found in normal rat lungs
during deflation of 20 dyn/cm. These findings suggest that the in
our preparation after siloxane is probably near 21 dyn/cm (6,
22).
Change in Vc and Cc.
Increased resulted in decreased Vc and Cc at VL from
~40 to 90% TLC. That is, at VL at which the siloxane
exposed lungs had increased (an isovolume increase in
PL), both Cc and Vc postsiloxane were decreased. The
changes in capillary volume and compliance were greatest at the lung
volumes at which the change was greatest. At VL at
which the normal and postsiloxane were probably unchanged so were
pre- and postsiloxane Cc and Vc. This last finding suggests that our
treatment with nebulized siloxane resulted in a change in without
injury to the lung parenchyma or pulmonary vasculature. We are unable
to measure the absolute capillary compliance; however, at most
VL, the reference Vc is smaller after treatment (Fig. 5),
therefore the fall in absolute capillary compliance is greater than
that for specific compliance, Cc (Fig. 6).
suggests that the direct effect
of on capillaries dominates any indirect effect of decreased septal
tissue stress associated with modest septal retraction (which would
have increased Cc and Vc). This further suggests that most capillaries
have a positive radius of curvature (i.e., they bulge out into the
alveolus). [The photomicrographs Figs. 1, 11, 12, and 19 in Ref.
28 show this feature. By contrast, cryo-scanning electron
microscopy studies (4) report relatively smooth alveolar
surfaces with little capillary bulging, but these were done at 15 cmH2O transpulmonary pressure with the lung in zone
1 or 2 and so are not directly comparable.]
Alternatively, decreased Cc and Vc in the presence of increased could be caused by extreme septal retraction (see, e.g., Fig. 16 in
Ref. 28) such that the capillaries become physically
compressed. On the basis of our estimates of the change in surface area
after siloxane (6), we feel that this is unlikely. On the
other hand, because our primary data are a measure of blood volume per
unit volume, they do not allow us to distinguish between these possible
mechanisms for the change in Cc and Vc with , but they also are not
dependent on any specific morphometric model for their fundamental interpretation.
Our findings compared with others'.
We have demonstrated a decrease in capillary size and compliance with
increased , which is in agreement with work suggesting that exerts a compressive force on capillaries (28, 29, 31).
Although we did not measure resistance directly, smaller and stiffer
capillaries should have increased resistance. This conclusion is
opposite to that previously drawn by others on the basis of vascular
pressure-flow data during inflation compared with deflation (5,
18, 23) or on video microscopy of subpleural alveoli
(17).
.] They concluded that, at fixed
VL, increased decreases capillary resistance, but an
alternative interpretation of their data suggests otherwise.
Specifically, at ~50% TLC (the only lung volume at which they
present data during both inflation and deflation), they found a smaller
pressure drop across the middle segment, 5.0 mmHg, during deflation
(when is lower) than during inflation, 10.2 mmHg (when is
higher). The lower pressure drop during deflation is consistent with a lower, not higher, resistance when is lower and is in agreement with our data.
Pain and West (18) and Bruderman et al. (5)
found pulmonary vascular pressure-flow relationships consistent with
lower resistance during inflation (when is higher) than during
deflation. Their findings were dependent on the entire pulmonary
circulation, not just the microvasculature; nonetheless their data
suggest that increased decreased microvascular resistance. We
cannot explain the apparent inconsistency between our volume findings and their flow findings.
Nieman et al. (17) report that capillary (middle segment)
resistance decreased after surfactant depletion with detergent, which
they report increased the minimum to 24 dyn/cm. This change in should have increased the PL near 50% TLC (where normal
is much lower than 24 dyn/cm), while causing only small changes in
the lung P-V curve at high VL (where normal is somewhat
higher than 24 dyn/cm) (21). However, they report (Fig. 1 in Ref. 17) that control and treated P-V curves are
indistinguishable at 50% TLC; the posttreatment P-V curve diverges
only at high VL. These P-V data are not consistent with
increased , and it is difficult to characterize the changes in
surface properties that occurred in these experiments. Nieman et al.
(17) also report that, as observed by video microscopy,
subpleural capillaries become distended and recruited in areas that
were atelectatic, but not in areas with "normal appearance" after
Tween lavage. Capillaries were also unchanged after saline lavage
(which should also have increased ). There are no data to indicate
the magnitude of the change in , and they found changes in capillary
behavior only in areas that were grossly atelectatic. By contrast, we
studied lungs with increased and at VL at which they
were still inflated with no evidence of atelectasis.
Speculations on consequences to gas exchange.
In lungs with a heterogeneous distribution of , there are separate
effects on ventilation and perfusion that could combine to cause a
deterioration in gas exchange. We emphasize that the mechanism we are
about to discuss is independent of pure shunt through gas-free
(atelectatic or edema-filled) lung regions. For given end-inspiratory
and end-expiratory pressures, lung regions with high will have a
lower (regional) FRC as a result of increased recoil but a higher
(regional) tidal volume due to increased local lung compliance compared
with lung regions with lower . Local perfusion will also be
systematically altered by variations in because of changes in
capillary mechanics. Compared with regions with lower , regions with
higher will have smaller, stiffer capillaries, which may result in
increased local resistance. Given common upstream (PA) and downstream
(PV) pressures, an increased local resistance would result in lower
local blood flow to regions with higher . Together, these effects
would result in increased ventilation (
)-to-perfusion (
)
ratios (/) in areas with high (increased
combined with decreased ), and, for a given total and
, low / in areas with normal . These effects would produce an overall decline in gas exchange efficiency via increased / heterogeneity. Unlike pure shunt through gas
free lung regions, the / mismatch secondary to the
effects of changes in may not be substantially reduced by
increasing end-expiratory VL with increased positive
end-expiratory pressure unless end-expiratory VL is raised
to unacceptably high levels (80-90% TLC or higher; see Figs. 3,
5, and 6). In addition, as Vc falls so does red cell transit time,
which could also impair gas exchange. Changes in Ptm and regional blood
flow would likely be associated with the changes in Vc and would
somewhat mitigate the fall in transit time. (For a detailed discussion
of changes in red cell transit time with changes in capillary mechanics
and their consequences for gas exchange, see Refs. 19 and
25.)
Speculations on consequences for neutrophil sequestration.
Neutrophils are larger in diameter than many pulmonary capillaries
(7). Their transit times are determined by a combination of the deformability of neutrophils and the diameter and distensibility of the capillaries. Because the sizes of capillaries and neutrophils are so closely matched, even small changes in capillary mechanics can
have substantial effects on neutrophil sequestration. If, in the
presence of increased , the capillaries are both smaller and
stiffer, then a larger number of capillaries would be smaller than
neutrophils and this could result in slowing of neutrophil transit, or
increased neutrophil sequestration in the lung. These effects may be
especially important in disease when neutrophil deformability is also
decreased (9).
. Importantly, these are changes
that are directly attributable to and are independent of the many
other factors associated with diseases which may also influence
capillary mechanics. Furthermore, the findings in this study are
underestimates of the magnitude of changes directly associated with
altered seen in diseases such as acute respiratory distress
syndrome, if in those cases is significantly higher than in our
experiments. We conclude that alterations in in a variety of
pulmonary diseases have direct effects on capillary mechanics and may
play a significant role in the pathophysiology of gas-exchange
deterioration and increased leukocyte sequestration in the lung.
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ACKNOWLEDGEMENTS |
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We are grateful to Dr. Krishna Gazula of the Harvard School of Public Health, who determined the size distribution of the nebulized siloxane aerosol, and to Shasta Kielbasa, John P. Morris, and Lydia S. Stickney for technical assistance.
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FOOTNOTES |
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This work was supported by National Heart, Lung, and Blood Institute Grant HL-55569.
Address for reprint requests and other correspondence: G. P. Topulos, Dept. of Anesthesiology, Perioperative and Pain Medicine, Brigham & Women's Hospital, 75 Francis St., Boston, MA 02115 (E-mail: topulos{at}zeus.bwh.harvard.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
April 15, 2002;10.1152/japplphysiol.00779.2001
Received 25 July 2001; accepted in final form 8 April 2002.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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  J. P. Butler, R. E. Brown, D. Stamenovic, J. P. Morris, and G. P. Topulos Effect of surface tension on alveolar surface area J Appl Physiol, September 1, 2002; 93(3): 1015 - 1022. [Abstract] [Full Text] [PDF]
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) and postsiloxane exposure (
)
for all 4 dog lobes. Lung volumes (VL) are normalized to
control total lung capacity (TLC), i.e., VL at
PL = 30 cmH2O presiloxane. After siloxane,
lobes have increased recoil below ~90% TLC due to increased 
) and Vc
(
