JOURNALOP

Vol. 39, No.

APPLIED PHYSIOLOGY 3, September 1975.

Printed

in U.S.A.

Effect of increased bronchial

dimensions

static lung

recoil

on

of excised lungs

ROBERT E. HYATT, JOSEPH R. RODARTE, AND T. A. WILSON Division of Thoracic Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester 5590-l; and Department of Aerospace Engineering and Mechanics, University of Minnesota, Minneapolis, Minnesota 55455

On the other hand, there are data indicating that lung volume may play a major independent role in determining airway size. Klingele and Staub (8) found that terminal bronchi in excised cat lung changed diameter in proportion to changes in lung volume. More pertinent to the present work was the study by Hughes et al. (4) in which bronchi of excised dog lungs were measured during static inflationdeflation pressure-volume (PV) maneuvers. They found that, at the same lung volume, when Pst(L) might differ by l-7 cmH,O due to the prior volume history, bronchial diameters were essentially the same. They concluded that volume history and lung volume had a significant effect on the PD relationships of intrapulmonary bronchi and suggested that “lung tissue exerts an influence on airways which tends to make them conform to the surrounding parenchvma. ” Although the conditions of chest restriction studies differ considerably from the approach of Hughes et al. (4), it seemed appropriate to explore further the relative roles of lung volume and Pst(L) in determining airway size. We utilized a technique suggested by Faridy and Permutt (‘2). These workers noted that, if one refrigerated an excised lung for several days and then ventilated it, there was a striking, stable increase in Pst(L) at all lung volumes. We made roentgenologic measurements of airways before and after changing the static PV curve of dog lobes by this technique with the aim of elucidating the relative roles of lung volume and Pst(L) in determining airway dimensions.

HYATT, ROBERT E., JOSEPH R. RODARTE, AND T. A. WILSON. Effect of increased static lung recoil on bronchial dimensions of excised lungs. J. Appl. Physiol. 39(3) : 429-433. 1975.-We measured bronchial diameters and lengths during static deflation and inflation in eight excised dog lobes before and after static lung recoil (Pst(L)) had b een significantly increased by cooling the lobe for 48 h at 4OC and ventilating it for 3 h. In control lobes, bronchial diameters were the same at’ any volume even though Pst(L) was different during inflation and deflation. These results agree with those of Hughes et al. (J. Ap~l. Physiol. 32 : 25-35, 1972). However, when Pst(L) was increased, diameters at a given volume were significantly increased over control values; diameters at a given pressure were nearly the same as the controls. Therefore, under these conditions, bronchial diameter did not conform to lung volume. The ventilation process appeared to alter the circumferential elastic properties of the bronchi because diameters at all pressures were slightly larger after ventilation. Bronchial lengthvolume relationships were the same in both control and ventilated lobes. Thus, when Pst(L) was markedly increased, diameter corresponded best to lung recoil and length to lung volume. mechanical behavior;

properties bronchial

recoil; determinants

of bronchi; pressure-length

of bronchial

bronchial behavior;

pressure-diameter increased lung

dimensions

COMMON PRACTICE to quantify the dimensions of intraparenchymal bronchi by relating diameter or length to static lung recoil pressure (Pst(L)) (7, 9, 12-14). The validity of this approach is supported by the finding that the transpulmonary pressure-diameter (PD) behavior of bronchi within the parenchyma is very similar to that when the bronchi are excised and subjected to equal transmural distending pressures (7). Indirect support for equating Pst(L) to transmural pressure has come from studies, in man, in which chest-cage restriction was used to increase Pst(L) acutely. Caro and associates (1) found that airway conductance, as a function Of lung volume, increased with restriction whereas the relationship between conductance and Pst(L) was not altered. Stubbs and Hyatt (15) confirmed these findings and also found that, although maximal expiratory flow (V,,,) as a function of volume was increased with restriction, the relationship between V,,, and Pst(L) was not changed. These studies suggested that airway diameter was more dependent on Pst(L) than on lung volume, but bronchial diameter was not measured directly. IT HAS BEEN

METHODS

We performed complete studies on seven upper lobes and one lower lobe from eight dogs killed by an intravenous overdose of pentobarbital. The vessels supplying a lobe were ligated after the blood drained from them, and the lobar bronchus was cannulated. In preliminary studies we measured PV curves immediately after the animal was killed and again after 48 h of refrigeration and found no difference; this agrees with the finding of Faridy and Permutt (2). Therefore, the lobe was bathed in saline and placed in a refrigerator at 4°C for 48 h. It was then warmed to room temperature (approx 23°C) and the airways were outlined with finely powdered tantalum. The lobe was degassed in a vacuum jar and slowly inflated to a static pressure of 20 cm&O, with care taken that all regions were uniformly 429

Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.

430

HYATT,

inflated. Air was removed in stepwise fashion with pressure and volume measurements being made after 1 min at pressures of 16, 12, 8, 4, and 2 cmHzO. All volumes were corrected for gas compression. The lobe was reinflated in stepwise fashion to 10-l 5 cmHaO except for one lobe for which no inflation points were obtained. At each deflation or inflation step, roentgenograms were made (14). After the second inflation, air was removed until a pressure of 2-4 cmH,O was achieved; then, the cannula was clamped, the lobe was weighed, and its displacement in water was recorded. We corrected all volumes for tissue volume by assuming a tissue density of 1.065. The lobe was again degassed, reinflated to a state of uniform expansion, and ventilated with a piston pump for 3 h with a tidal volume equal to 30 % of total lobe capacity (TLC) and a frequency of 12 cycles/min. TLC was the volume contained at an inflation pressure of 20 cmH20. During the ventilation procedure, the lobe was kept moist and end-expiratory pressure was atmospheric. After 3 h of ventilation, the lobe was degassed and the pressure-volume sequence with roentgenograms, described above, was repeated. In four additional lobes that had been refrigerated for 48 h, we compared PV curves obtained with air to those obtained with saline filling. The procedure was to obtain a control air PV curve, ventilate the lobe for 3 h as described above, repeat the air PV curve, and then obtain a PV curve using saline to inflate the lobe (11). All PV curves were begun from the degassed state. Saline curves were accepted only if leakage was less than 10 % of the total volume added. To determine if the 3 h of ventilation altered bronchial tone, we introduced 7 ml of a 5 % solution of isoproterenol into the bronchial tree of four of the eight collapsed lobes prior to obtaining the control PV curve. After 10 min, as much of the solution as possible was removed, the lobe was degassed, and the PV and roentgenographic studies were performed. We attempted to assess whether the ventilation process per se altered intrinsic bronchial elasticity exclusive of changes in bronchial tone. We used two approaches. 1) In a series of six lobes, we increased lung recoil of cooled lobes by the 3-h ventilation procedure. Airways were outlined with tantalum, and deflation PD data were ob100

r-

RODARTE,

AND WILSON

Diameter % control maximum

100

80

Volume

60

40

(%

control

20

TLC)

0

4

8

Psttkl,

12

16

20

cm Hz0

FIG. 2. Mean & SE for pooled data of all bronchi studied before (control) and after (ventilated) cooling and 3 h of ventilation. Diameter (as percentage of control maximal diameter) is plotted against volume (left) and against static lung recoil pressure (Pst (L)) (right). In left panel, control curve is discontinuous because of the one lobe for which no inflation data were obtained. For ease of comparison, the ventilated curve is presented as discontinuous over the same volume range. Maximal diameters of ventilated bronchi in left panel are slightly higher than in right panel due to unequal numbers of data points.

tamed at pressures of 20, 8, 4, and 2 cmH20. The major portion of the bronchial tree was dissected free of the parenchyma and rendered airtight, and then the PD run was repeated with the specimen hanging free (7). The PD behavior at various sites in the bronchial tree of each lobe was compared before and after removal of the bronchi from the parenchyma; 18 such comparisons were obtained. Airways in this series were not pretreated with isoproterenol. 2) In another set of experiments we obtained control PD and PV curves on three lobes immediately after the animal was killed. The lobes were then ventilated for 3 h to produce an increase in elastic recoil (3). Next, air was added to the lobes to achieve an inflation pressure of 20 cmH20 and the lobe was held at this volume for 3 h (Faridy et al. (3) showed that this procedure would return Pst(L) to control levels). PD and PV curves were then repeated. Isoproterenol was introduced into the bronchial tree before the first PV run and again before the 3 h of inflation to ensure that bronchial smooth muscle was relaxed. Because seven of the lobes studied were upper lobes, we thought it valid to estimate bronchial length changes from the roentgenograms (14). Length changes of 32 bronchial segments were studied. Lengths at a Pst(L) of 20 cmHzO varied from 1 to 9 cm. RESULTS

. ......... ...

0

IIll

0

II

4

8

Pst(kl

Ve

n t

I

12

i 1 Q t e

I

16

I

d

]

20

, cm Hz0

FIG. 1. Mean (rf= SE) pressure-volume curves for eight lobes studied before (control) and after (ventilated) cooling and 3 h of ventilation. Static lung recoil (Pst(L)) is plotted against volume as percentage of control total lobe volume (TLC).

Static PV curves. After ventilation, Pst(L) was increased at all lung volumes during deflation and inflation in each lobe (Fig. 1); for example, during deflation at 50 % of control TLC, mean Pst(L) was increased 8.6 cmHzO after ventilation. To protect against the possibility of air leaks, lobes were not routinely inflated above 20 cmH,O pressure, so the maximal volumes were less in the ventilated lobes than in the control. However, in preliminary studies we inflated several ventilated lobes to pressures of 32-40 cmHzO, at which point they contained the same volume as control lobes at 20 cmHaO. Pressure-diameter-volume interrelationships. The four lobes

Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.

INCREASED

LUNG

RECOIL

AND BRONCHIAL

SIZE

TABLE 1. Comparison of bronchial diameters at equal volumes during decflation Mean Volume,

% of Control

TLC

30 75 * For difference

from

control,

Diameter,

mm

Control

Ventilated

3.10 3.55

3.76* 3.88”

P < 0.001

(paired

t-test).

TABLE 2. Comparison of bronchial diameters at equal pressures during deflation Mean

Pst (L), cmH20

20 4 * For

difference

from

control,

Diameter,

mm

Control

Ventilated

3.76 3.44

3.90” 3.64*

P < 0.001.

with isoproterenol instilled into the bronchial tree prior to study did not differ statistically from the four untreated lobes in PD behavior or -degree of hysteresis; hence, data from all eight studies were pooled. A total of 48 intraparenchymal bronchi were suitable for analysis in the control state and after ventilation. At a pressure of 20 cmHzO, bronchi ranged in diameter from 1.1 to 9.0 mm (mean, 3.8 mm). Figure 2 presents pooled data for all bronchi during deflation and inflation. At a given lobe volume, bronchial diameter after ventilation was considerably increased. This pattern was seen in each of the 48 bronchi studied (see Fig. 4 for a typical example). Table 1 summarizes the absolute deflation diameter-volume (DV) data at 30 and 75 % of control TLC. The mean diameter increase was 21 % at 30% TLC and 9% at 75 % TLC. The inflation DV behavior showed similar changes (Fig. 2, left). The PD plots before and after ventilation are more nearly the same (Fig. 2, right). However, the bronchial diameter after ventilation was slightly increased at any given Pst(L). This pattern was seen in 35 of the 48 bronchi studied; PD plots were identical in the remaining 13 bronchi. The increase in diameter after ventilation was statistically significant at all pressures. The increase was 4 % at a Pst(L) of 20 cmH,O and 6 % at 4 cmHzO (Table 2). PD behavior during inflation showed similar changes (Fig. 2, right). Observations relative to the effect of hysteresis on bronchial diameter are summarized in Table 3, where diameters during deflation and inflation are compared at 50 % of control TLC. In the control lobes there was no significant difference in the 41 available comparisons, even though mean Pst(L) was 2.0 cmH,O greater during inflation (range, 0.8-5.3 cmH,O). In the ventilated lobes we had only 23 comparisons and, although the diameters on inflation were only slightly larger, the difference was statistically significant. This difference is not reflected in Fig. 2 where 48 data points were available for the deflation run and only 23 for inflation. It was only on the paired t-test analyses that the difference emerged. Mean Pst(L) at 50 % of control TLC was 2.8 cmH,O greater during inflation after ventilation (range, 2-4 cmHzO).

431 Pressure-length behavior. Figure 3 depicts the relationship of bronchial length to pressure and volume for one segment. The figure is typical for all segments studied. At any Pst(L), bronchial length was less after ventilation; control and ventilated lengths were identical at similar lobe volumes. Air and saline pressure-volume curves. Ventilation of the refrigerated lobes produced the anticipated increase in Pst(L). Pressure-volume curves after saline filling were found to overlap the deflation limb in the control, air-filled state. This is similar to the behavior described in normal, nonventilated lobes (11). Intact-excised diameter comparisons. PD behavior of bronchi during deflation at 18 sites was compared before and after removal of the lung parenchyma of lobes whose recoil was increased by cooling and ventilation. Mean intact diameters at pressures of 20, 8, 4, and 2 cmH,O were 7.6, 7.4, 6.9, and 6.2 mm, respectively. Mean excised diameters at the same pressures were 7.4, 7.3, 7.0, and 6.4 mm, respectively. Paired t-test analysis at each of the pressures studied revealed no significant difference between the diameters in the intact and excised states (P > 0.1). Eect of ventilation on PD behavior. In the three fresh lobes that were studied under control conditions and then after 3 h of ventilation plus 3 h of static inflation, we confirmed that ventilation of a fresh lobe increased recoil and that a period of inflation returned the PV curve to that observed prior to ventilation (3). Thus we could compare the effect of 3 h of ventilation on PD behavior in a lobe whose PV curve was unchanged. Twenty-four bronchi were compared during deflation. At a Pst(L) of 20 cmH,O, mean bronchial diameter was 5.1 mm in the control state and increased to 5.3 mm after ventilation and static inflation; at Pst(L) of 4 cmH,O, the mean diameter increased from 4.7 to 4.9 mm. By paired t-test analysis, these increases of 4 % were both significant (P < 0.001). TABLE 3. Comparison of bronchial diameters during deflation and injation at 50% control TLC Mean

Condition

Diameter,

mm

Deflation

Control Ventilated * For

Inflat ion

3.34 3.55

difference

from

3.37 3.59”

P < 0.05.

control, Length,

cm T2

-CCdntrol .............. V e n t i 10 t e d I

20

I

16

12 P$)

I

I

I

8

I

4

1 c m Hz0

FIG. 3. Interrelationships bronchial length, and lobe lated) cooling and ventilation

1

I

0

100

Volume, among static lung recoil volume before (control) for one segment.

200

ml pressure (Pst (L)), and after (venti-

Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.

432

HYATT,

DISCUSSION

Ventilation of an excised lobe after it h.as been kept at low temperature for 48 h leads to a significant stable increase in lung recoil. Because we and others (3) found that ventilation did not alter the PV curve obtained during saline filling, the increased Pst(L) appears to be due to changes in the surface film lining the lung (17) and not to alterations of tissue elements. The ability to produce acute increases in Pst(L) in the excised lobe has allowed us to examine in greater detail the relative influence of volume and static transpulmonary pressure on bronchial dimensions. Lobe volume clearly was the major determinant of bronchial length. Ventilation did not alter the control volumelength relationships. In control lobes, our data agree with those of Hughes et al. (4). Bronchial diameter at a given volume was unchanged even though Pst(L) differed during inflation and deflation In the ventilated lobe, however, the small difference between deflation and inflation diameters at the same volume reached the level of statistical significance. We have no in behavior in the explanation for this slight difference ventilated lobes. On the other hand, when Pst(L) was acutely increased by ventilation, our data suggest that changes in bronchial diameters were best correlated with changes in lung recoil pressure, in accord with the conclusion reached from the chest restriction studies (1, 15). The PD plots before and after ventilation were more nearly alike than were the DV plots (Fig. 2; Tables 1 and 2). Let us first examine our data with the assumption that the ventilation process did not alter the intrinsic mechanical behavior of bronchi. Then, if diameter followed volume exactly, the PD plot after ventilation would be considerably below the control plot because volume was less at all pressures. This behavior, represented by the dashed line in Fig. 4A, was never seen; indeed, diameters at a given pressure tended to be slightly larger. Conversely, if diameter followed pressure exactly, one would predict that the DV plot after ventilation would be shifted to the right (dashed line in Fig. 4@, as was found. However, the above analysis should be viewed with cau-

300

-

8

I

I

I

I

I

4

8

12

16

Pst(,) -

Control

I

20

, cm H,O ------

Ve n t i I a t e d

Diameter, --es-

mm

Predicted

FIG. 4. A: observed pressure-diameter (PD) data of a typical bronchus with predicted PD behavior if the original DV behavior had not been altered and if volume were the sole determinant of diameter. B: observed diameter-volume (DV) data of the same bronchus with predicted line if the original PD behavior had not changed and if pressure were the sole determinant of diameter. See text for further details.

RODARTE,

AND WILSON

tion until further information is available on the magnitude of parenchymal-bronchial interdependence. For example, Hughes and associates (5) have recently reported that interdependence is relative. They found that diameter changes of 15-20 % could occur without appreciable changes of tension in surrounding tissue. Table 1 and Fig. 2 indicate that, at a given lung volume, we rarely exceeded diameter changes of 20 %. In light of these findings, it might not be surprising if diameter did not conform to volume change but rather to lung recoil. Although PD plots before and after ventilation were similar, there nevertheless was a slight but significant increase in diameter at any pressure that is difficult to explain. One would predict theoretically that, if there had been no change in bronchial mechanics due to ventilation and if Pst(L) were the major determinant of diameter, the diameters at a given pressure should have been slightly smaller after ventilation. This follows from considerations of regional parenchymal stress. In the ventilated case, bronchi are larger at a given volume than under control conditions. The increased diameter should have distorted surrounding tissue elements and decreased to some extent the local tissue recoil pressure and hence the transpleural pressure applied to their walls (I 0, 16). However, here again one must recall the results of Hughes et al. (5) and the possibility that the inhomogeneities produced in our study were not sufficient to cause appreciable changes in local tissue tension. Clearly we were not able to demonstrate a stressdecreasing effect from studies comparing the PD behavior of intact and excised bronchi in the ventilated lung. In 18 comparisons there was no significant difference between bronchial diameter at various pressures whether the bronchus was surrounded by parenchyma or dissected free of the lung. Therefore, the effect of regional stress relief must have been small. It appears that ventilation increased circumferential distensibility of the bronchi. Changes in smooth muscle tone appear to be ruled out because prior treatment of bronchi with isoproterenol did not alter the results. Indeed, this result suggests that there was little or no tone in the lobes prior to ventilation. Bronchi after ventilation were shorter at any given pressure because volume was less. Could this have rendered them more distensible? We think not because previous work from this laboratory (6) failed to show changes in PD behavior in excised bronchi when they were lengthened or shortened by amounts comparable to those encountered in this study. The probable explanation is that the ventilation process distensiper se caused an increase in the ci .rcumferential bility of the bronchi. This is suggested by our studies of fresh noncooled lobes before and after ventilation, in which the postventilation PV curve was returned to control values by static inflation. This study revealed increases in diameter of 4 % after ventilation at pressures of 20 and 4 cmH20. These increases are quite close to those encountered in the ventilated cooled lobe. Furthermore, bronchial lengths were the same before and after the ventilation-static inflation procedure, yet diameters were larger. This further argues against bronchial shortening as a cause of the increased circumferential distensibility (see above).

Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.

INCREASED

LUNG

RECOIL

AND

BRONCHIAL

433

SIZE

The effect of correcting our data for the apparent change in intrinsic bronchial PD behavior has been illustrated in Fig. 4. For example, if the control and ventilated PD curves of Fig. 4A are made to coincide and the DV curves are appropriately corrected, one still finds a wide separation of the DV plots between control and ventilated studies (Fig. 4B). This reinforces our conclusion that, under the conditions of this study, diameter followed distending pressure and not lobe volume. In a previous study (14) it was shown that circumferential and longitudinal elasticities of bronchi differed. In addition, in the present study we have shown that, when lung recoil the factors controlling circumis markedly increased,

ferential and longitudinal extensions of bronchi differ, the diameter being predominately governed by lung recoil and the length by lung volume. The authors acknowledge the valuable technical assistance rendered by Grace Brown and Mark A. Schroeder. This investigation was supported in part by Research Grants HL12229 and HL-16726 and a contract from the National Institute of Occupational Safety and Health (HSM 99-72-133). J. R. Rodarte is the recipient of a Pulmonary Academic Award (HL-70816) from the National Heart and Lung Institute. Address reprint requests to R. E. Hyatt, Mayo Clinic. Received

for publication

24 October

1974.

REFERENCES 1. CARO, C. G., J. BUTLER, AND A. B. DUBOIS. Some effects of restriction of chest cage expansion on pulmonary function in man: an experimental study. J. Clin. Invest. 39 : 573-583, 1960. ob2. FARIDY, E. E., AND S. PERMUTT. Surface forces and airway struction. J. AppZ. Fhysiol. 30 : 319-32 1, 1971. 3. FARIDY, E. E., S. PERMUTT, AND R. L. RILEY. Effect of ventilation on surface forces in excised dogs’ lungs. J. AppZ. Physiol. 2 1: 14531462, 1966. 4. HUGHES, J. M. B., F. G. HOPPIN, JR., AND J. MEAD. Effect of lung inflation on bronchial length and diameter in excised lungs. J. AppZ. Physiol. 32 : 25-35, 1972. 5. HUGHES, J. M. B., H. A. JONES, A. G. WILSON, B. J. B. GRANT, AND N. B. PRIDE. Stability of intrapulmonary bronchial dimensions during expiratory flow in excised lungs. J. AppZ. Physiol. 37: 684694, 1974. 6. HYATT, R. E. Bronchial mechanics. In : Current Research in Chronic Airways Obstruction (Ninth Aspen Emphysema Conference, 1966). Washington, D.C. : US Govt. Printing Office, 1968, p. 239-255. 7. HYATT, R. E., AND R. E. FLATH. Influence of lung parenchyma on pressure-diameter behavior of dog bronchi. J. AppZ. Physiol. 21: 1448-1452, 1966. 8. KLINGELE, T. G., AND N. C. STAUB. Terminal bronchiole diameter changes with volume in isolated, air-filled lobes of cat lung. J. ApeI. Physiol. 30 : 224-227, 1971. 9C. MARSHALL, R. Effect of lung inflation on bronchial dimensions in the dog. J. A/$1. Physiol. 17 : 596-600, 1962.

AND D. LEITH. Stress distribution in 10. MEAD, J., T. TAKISHIMA, lungs: a model of pulmonary elasticity. J. AppZ. Physiol. 28: 596-608, 1970. AND E. P. RADFORD, 11. MEAD, J., J. L. WHITTENBERGER, JR. Surface tension as a factor in pulmonary volume-pressure hysteresis. J. APPZ. Physiol. 10 : 19 l-l 96, 1957. 12. MURTAGH, P. S., D. F. PROCTOR, S. PERMUTT, B. KELLY, AND S, EVERING. Bronchial mechanics in excised dog lobes. J. APPZ. Physiol. 31: 403-408, 197 1. l3 . MURTAGH, P. S., D. F. PROCTOR, S. PERMUTT, B. KELLY, AND S. EVERING. Bronchial closure with Mecholyl in excised dog lobes. J. APPZ. PhysioZ. 31: 409-415, 1971. R., AND R. E. HYATT. Static mechanical behavior of 14. SITTIPONG, bronchi in excised dog lung. J. APPZ. Physiol. 37 : 201-206, 1974. 15. STUBBS, S. E., AND R. E. HYATT. Effect of increased lung recoil pressure on maximal expiratory flow in normal subjects. J. Af$Z. 16

Physiol.

32 : 325-331,

1972.

WILSON, T. A. A continuum analysis of a two-dimensional me’ chanical model of the lung parenchyma. J. APPZ. Physiol. 33: 472478, 1972. I., H. W. TAEUSCH, K. KYEI-ABOAGYE, AND 17* WYSZOGRODSKI, M. E. AVERY. Prevention of pulmonary surfactant inactivation during hyperventilation by added end-expiratory pressure. J. AMZ. Phvsiol. 38: 461466. 1975.

Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.

Effect of increased static lung recoil on bronchial dimesions of excised lungs.

We measured bronchial diameters and lengths during static deflation and inflation in eight excised dog lobes before and after static lung recoil (Pst(...
1MB Sizes 0 Downloads 0 Views