Effect of posture on airway length and diameter in the dog

Respiration Physio~~y (1974) 22,381-397;

~orth-Ho~~~d P~~ish~~g Company, Amsterdam

EFFECT OF POSTURE ON AIRWAY LENGTH AND DIAMETER IN THE DOG

A. G. WILSON, HAZEL A. JONES and J. M. B. HUGHES ~epart~~ts

of Radiology and Medicine, Royal Postgraduate Medical School, Ha~rsmith

Hospitals

Du Cane Road, London WI2 OHS, United Kingdom

Postural changes in regional airway length and diameter, before and after atropine, were studied bronchographically in anaesthetixed and recently killed dogs at end expiration. FRC was allowed to change with posture in the anaesthetized dog but was held constant in the dead dog. Systematic regional differences in airway length and diameter have been demonstrated; they vary with posture. When compared with the horizontal posture apical airways in the anaesthetized dog were longer and wider when the dog was erect and shorter and narrower when inverted. Changes in basal airways were small or absent. After atropine ail airways increased in diameter and apex-base differences on going from the horizontal to upright posture were more marked; airway length was unaffected. Comparabie findings were made in exsanguinated dogs turned prone to supine under isovolume conditions. Estimates of regional transpulmonary pressure, bronchial compliance and regional airways resistance have been made in the live dog from airway dimensions in various postures.

Abstract.

Airway compliance Atropine Bronchography

Bronchomotor tone Pleural surface pressure Regional differences

Previous work in man and animals has demonstrated the impor~nt influence of posture on alveolar size. Milic-Emili et al. (1966), using ‘33Xe in man, showed that at normal lung volumes the regional volume of ventilated units expressed as a y0 TLC was greater in the upper than in the lower lung zones. In dogs Glazier et al. (1967) showed, by direct measurement of alveolar size in sections of lung frozen in the chest, that in the head-up position apical alveoli at end expiration were about four times the volume of basal ones. Hogg and Nepszy (1969), also in the dog frozen in the head-up posture, demonstrated from density measurements that the upper zone of the lung was more expanded (8040% TLC) than the lower (30440% TLC). These findings of different regional expansions of alveoli have been explained on the basis of the known ~avi~tionally induced gradient of pleural surface pressure. Accepted for publication 6 August 1974.

381

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A. G. WILSON. H. A. JONES AND J. M. B. HUGHES

Similar forces might be expected to influence airway size. One attempt has been made to measure directly airway diameter in different regions (Gayard and Mourlot, 1971) but these studies in erect man failed to show any regional difference in the behaviour of airway calibre between apex and base. The purpose of the present investigation was to see if regional differences in airway length and diameter were demonstrable by direct measurement of bronchograms of anaesthetized dogs in various postures. Materials and methods LIVE DOGS

Eight greyhounds (22-33 kg) were used. Anaesthesia was induced with 25 mg/kg thiopentone sodium and maintained with 1% chloralose and 20% urethane, Tracheostomy was performed and a femoral artery cannulated to allow arterial blood pressure monitoring and blood gas sampling. Using a steerable catheter (Medi-Tech. Inc. Mass., U.S.A.) airways in the left apical and left diaphragmatic lobes were dusted with tantalum powder (nominal particle size 5 p) to obtain a bronchogram. The dogs lay right side down in a V-shaped trough attached to a tilting table and were immobilized by their forelimbs and pelvis. Chest radiographs (lig. 1) were taken by a tube shift method-method A (Hughes et al., 1972) which allows true length and diameter of various bronchial segments to be calculated. The radiographs were exposed at end expiration after a constant volume history (inflation to an airway pressure of 25-30 cm Hz0 followed by three tidal breaths). In two experiments transpulmonary pressure was monitored with an intraoesophageal balloon connected to a 268B (Sanborn) pressure transducer. Exposure times were kept short (0.003 set) to eliminate movement blurr, but to achieve this it was necessary to use a broad focal spot (2 mm) and screen films (Kodak R.P. 54 and fast tungstate screens). The focus-film distance was 120 cm, the tube shift 30 cm and exposures were made at an approximate kVp of 87. Airways studied varied between 1 and 5 mm in diameter, the majority lying between 2 and 4 mm. From the radiographs the position of the various measured segments along the long axis of the lung was derived and expressed as a percentage of lung height (100% being apex and 0% costophreni~ recess). Radiographs were taken with the dog horizontal (lying on its right side), head up and head down. Exposures were delayed for at least 5 min after reaching any one position to allow stabilization. After a series of control observations and posture changes, the dogs were given 1.2 to 1.8 mg atropine intravenously and the observations repeated. At the end of the in vivo observations the dogs were heparinised and killed by exsanguination. The left lung was removed intact and weighed. The left main stem bronchus was cannulated and using a positive inflating pressure the static pressurevolume deflation curve was determined (mean of 3 runs) with a maximum transpulmonary pressure (Ptp) of 30 cm HzO, Lung gas volume at Ptp 0 cm Ii,0

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Fig. 1. Tube shift tantalum bronchogram in anaesthetized dog; airways in left upper and left diaphragmatic lobes are outlined.

was determined by displacement and weighing. Tube shift radiographs were taken at various known Ptp’s after a constant volume history with inflation to 30 cm Hz0 and deflation to the pressure required. Non-screen film (Kodak, Crystallex), a tine focal spot (0.28 x 0.40 mm) and a lower kVp (47.5) were used. Airway lengths and diameters including those in uiuo were expressed as a percentage of the length and diameter in the excised lung at a Ptp of 30 cm H,O. DEAD DOGS

Four greyhounds (weight 24-35 kg) were anaesthetized with thiopentone and pentobarbitone sodium. Tracheostomy was performed and two of the four dogs were given 1.2 mg of atropine intravenously. Three animals were killed with intravenous potassium chloride and one by exsanguination. Airways ventrally (near

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A. G. WILSON, H. A. JONES AND J. M. B. HUGHES

the sternum) and dorsally (near the spine) were dusted with tantalum powder (nominal particle size 5 p) to obtain a bronchogram. Lateral tube shift radiographs were taken with the dog supine after a constant volume history that involved inflation to a Ptp of 30 cm Hz0 and deflation to FRC. The trachea was then clamped and the animal turned prone. Airway pressure was noted and radiographs taken before turning the dog supine again. Measurements were made of the diameter and length of various airway segments as well as the position of the segments on the anterior-posterior axis extending from the sternum to the paravertebral recess. Finally, the chest was opened on both sides to atmosphere, the lungs inflated to 30 cm Hz0 and a final radiograph taken. All lengths and diameters were expressed as a percentage of those at Ptp 30 cm H,O in the open-chested animal. Results INTACT DOGS

Control observations and atropine administration. At the beginning of each experiment segmental lengths and diameters were measured in the horizontal posture on three occasions each separated by about 20 min. Mean airway length and diameter data are plotted in fig. 2. Airway length remained unchanged in the period of observation and though there was a tendency for diameter to increase with time the change was small and not statistically significant. After atropine airway length in the horizontal posture did not change (fig. 2), but airway diameter showed a large increase from a mean of 48.8 to 73S’dmax. Airway length Live dogs horizontal to head-up posture. The mean change in length (i.e. airway length vertical as %max minus airway length horizontal as %max) on going from

ATROPINE

Fig. 2. Anaesthetized dog, horizontal. Change in airway length (0) and diameter (0) as %max, with time and after intravenous atropine. Each of the first 3 points represents mean data from 8 experiments ( fSEM) separated approximately by 20&n periods.

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385

-ire-------q o br

l

APEX

BASE 0

I

I

50

100

PERCENT OF LUNG HEIGHT

Fig. 3. Mean change in airway length on going from horizontal to head-up posture. Symbols identify the experiments and each point is the mean change of segmental length (length erect as %max minus length horizontal as %max) plotted against mean height for the upper or lower half of the lung. Positive values on ordinate indicate that airways were longer in the head-up posture.

the horizontal to head-up posture for all eight experiments is plotted against the mean height of the upper and lower zone segments in fig. 3. Airways in the upper half of the lung were longer in the upright position, the mean difference from horizontal length being + 10.7%. Bronchi in the lower half showed either no change or a small increase or decrease in the head-up position, the mean change being - 1.8%. Only one of the eight experiments failed to show any difference in regional behaviour between upper and lower zones. If the results are looked at in terms of absolute length (fig. 4), in the horizontal posture upper zone airways were 76%max A I RWAY

BEFOREATROPINE

n v

LENGTH AFTER ATROP INE

88

82

a 76

82

74

70

a 78

82

79

0 72

Fig. 4. Absolute airway length as %max in various postures before and after atropine. Numbers represent mean dam for upper and lower zone airways from 8 experiments (horizontal and head up) and 3 experiments (he& down).

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A. G. WILSON, H. A. JONES AND J. M. B. HUGHES

( kO.8 SEM) length and lower zone ones 82%max ( *0.9 SEM) length. In the upright posture the former increased to 88%max (+ 1.2 SEM) whilst the latter did not change. Small inconsistencies between the results expressed in absolute terms and as differences occur because the mean values calculated and used in fig. 3 give each experiment equal weight, while each individual airway is given equal weight in calculating values used in fig. 4. The number of airways measured per zone varied between 3 and 6. The regional difference in behaviour between the head-up and horizontal posture was identical before and after atropine. Absolute results (fig:4) are very similar to those before atropine with basal segments being slightly longer 83%max (kO.8 SEM) than apical ones 78%max (f0.8 SEM) in the horizontal and much shorter 80% max (f 1.3 SEM) than apical ones 90%max (+ 1.2 SEM) when head up. Diameter The mean changes on going from the horizontal

to head-up posture for each experiment are plotted against mean height in fig. 5. In general, airways in both the upper and lower zones became wider but in live experiments there was a definite regional difference in behaviour in that upper zone airways showed a much larger increase than ones in the lower zone. In two experiments there was no regional difference in behaviour and in one a large difference in the opposite direction. This last atypical change was thought to be due to relaxation of bronchospasm which was observed during manipulation of the catheter at broncho-

.

.

.A

00

t

t 0

.-o-__---_~ 0

BASE

-10 0

APEX _ 50

100

PERCENT OF LUNG HEIGHT

Fig. 5. Mean change in airway diameter on going from the horizontal to head-up posture. Symbols identify the experiments and each point is the mean change in airway diameter (diameter erect as %max minus diameter horizontal as %max) plotted against mean height for the upper or lower half of the lung. Positive values on ordinate mean that airways were wider in the head-up posture.

POSTURAL CHANGES IN AIRWAY DIMENSIONS

387

graphy. If this experiment is excluded, upper zone airways showed a mean change of percentage diameter on going into the head-up posture of + 15.9% and lower zone ones of +6.3%. In absolute terms (fig. 6) diameters are relatively smaller expressed as %max than are lengths. In the horizontal posture apical [46%max (_+ 1.5 SEM)] and basal [46%max (_+ 1.9 SEM)] diameters were the same and in the upright posture apical airways were wider [59%max ( f 2.7 SEM) as opposed to Sl%max ( f 2.8 SEM)]. AIRWAY BEFORE ATROPINE

a 46

DIAMETER AFTER ATROPINE

46

v 76

59

Fig. 6. Absolute airway diameter as %max in various postures before and after atropine. Numbers represent the mean data as in fig. 4.

The mean change in diameter

on assuming the head-up posture for all eight experiments is compared before and after atropine in fig. 7. Atropine did not alter the behaviour of upper zone airways which as before became much wider in the upright posture (+ 15.4%) but it did make a difference to lower zone ones which showed no significant change in diameter from the horizontal values. These results are almost identical with the length results both before and after atropine. The absolute values (fig. 6) show that apical airways are slightly narrower than basal [7l%max ( f 1.9 SEM) vs 77%max (k2.3 SEM)] when horizontal and much wider when head up [apical 86%max (k2.4 SEM), basal 76%max (f2.1 SEM)]. Live dogs horizontal to head-down posture. In three experiments

the dogs were tipped head down from the horizontal position both before and after atropine. In the inverted position (figs. 4 and 6) after atropine basal airways were both longer than apical ones [79%max (+ 1.8 SEM) vs 72%max (+ 1.9 SEM)] and wider [76%max (& 5.3 SEM) vs 59’Amax ( f 5.0 SEM)]. Fiudings before atropine were similar but the differences were smaller and did not reach statistical significance. Thus basal airway length [74%max ( f 2.6 SEM)] was greater than apical [irO/dnax (,1.5 SEM)] an d airways at the base were wider [43%max (+ 2.6 SEM)] than those at the apex [4l%max (+2.5 SEM)].

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A. G. WILSON, H. A. JONES AND J. M. B. HUGHES

APEX

BASE

I 50

-10 * 0 PERCENT

OF

I 100 LUNG

HEIGHT

Fig. 7. Mean change in airway diameter on going from horizontal to head-up posture before (-) and after (------) atropine. Each point is the mean change in diameter (diameter erect as %max minus diameter horizontal as %max) plotted against mean height for the upper and lower half of the lung for all 8 experiments. Bars indicate SEM.

Blood pressure and blood gases. The mean systolic blood pressure was at its lowest

when the dogs were horizontal (mean 158 mm Hg) and at its highest with head up tilt (mean 184 mm Hg). There was always a 15-20 mm Hg rise in mean systolic blood pressure on tilting either head-up or head-down. The largest differences in gas tensions occurred before atropine in supine animals (Po, 85 mm Hg, Pco2 37 mm Hg) and in the vertical posture also before atropine (PO, 60 mm Hg, Pco2 51 mm Hg). Intermediate values were obtained in other postures before and after atropine. COMBINED EXCISED/LIVE

DATA

Figure 8 relates in viva to excised airway dimensions. For three upper lobes, the in uiuo mean airway length (‘Amax) has been plotted against diameter (“/omax) in the horizontal, head-up and head-down posture both before and after atropine (interrupted lines). In addition on the same graph the airway length/diameter relationship in the excised lung (continuous line) is shown for various degrees of lung inflation with the corresponding Ptp’s on the top abscissa. In uiuo three tidal breaths were allowed following deflation from TLC before the radiograph was exposed, therefore the volume history differed from that in the excised lung. Measurements of oesophageal pressure however, did not show any increase in Ptp after tidal breathing.

POSTUFCAI_ CHANGES IN AIRWAY DIMENSIONS

TRI?

0

too4oQ

Before Af

EXCISED

LUNG

510

25

389

(cmti,O) 30

atropinc

ttr atropine

Excised

lung

/ / ’

/

/

/

9’ 0'

40I

I

I

I

40

60

80

AIRWAY

LENGTH

1

100

%

Fig. 8. Combined excised and in uiuo data obtained from 3 upper lobes. Length as Qnax plotted against diameter as %max for excised (-) and in oioo ( ------) upper lobes. 0, horizontal; V, inverted; A, head up; open symbols, before a&opine; closed, after a&opine. Airway lengths in the excised lung have been plotted against Ptp on the upper abscissa.

Except at low lung volumes and transpulmonary pressure (less than 35% of maximum volume or less than Ptp 2.5 cm HzO) changes of airway length were closely related to changes in the cube root of lung volume. In eight excised lungs at Ptp’s of 10, 5, 2.5 and 0 cm H,O airway length (as percent maximum) was 91.1,84.5, 73.0 and 67.5 while the cube root of lung-volume (as percent maximum) at the same Ptp’s was 90.3, 81.8, 73.1 and 56.5, respectively. This confirms earlier work (Hughes et al., 1972) and suggests that regional airway length will reflect the volume of the surrounding parenchyma. Since the relationship between lung volume and Ptp is very similar in uiuo and in freshly excised lungs, it is likely that airway length and Ptp will show a similar correlation. Several points emerge from this graph. Firstly, whilst airway length in any given position is identical before and after atropine, airway diameter is bigger in all postures after atropine. Secondly, airways are at their shortest and narrowest when the dog is head down, intermediate in the horizontal position and longest when the animal is head up. Thirdly, the slope of the in z&o curves (interrupted lines), which is related to airway compliance, increases after atropine. Finally, on the assumption that the lung volume-Ptp and length-Ptp behaviour of in viuo and excised lungs is similar, transpulmonary pressure surrounding the upper zone can be estimated by relating in uivo airway length to the Ptp in the excised lung at the corresponding airway length (see Discussion).

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A. G. WILSON, H. A. JONES AND J. M. B. HUGHES

EXSANGUINATED DOGS

Unlike the anaesthetized dogs in which FRC was allowed to change with posture, lung volume was kept constant. In the supine position the tracheostomy was open to atmosphere; after closure the animal was turned prone. The mean change of airway pressure on turning prone was - 5 cm H20. STERNUM

-10

0

+10

+20

PRON - SUP& AIRWAYlENGTH DIFFERENCE R Fig. 9. Dead dog turned supine to prone. Each point is the plot of % height of segment in supine position against change in length (length prone %max minus length supine %max). The line drawn is the regression of x on y (r = -0.86).

In fig. 9 the change in length (i.e. prone length o/,max minus supine length %max) of each segment on going from the supine to the prone posture is plotted against the position of the segment in terms of lung height %. Airways near the sternum become shorter in the prone position and dorsal airways longer. The line through the points is a regression of x on y (r= -0.86). Figure 10 shows a similar plot of diameter change against % height. The line through the points is the regression of x on y (r= -0.65). Diameter changes resembled length changes and airways near the steal in the supine position became narrower when in the prone position. Dorsal airways showed the reverse change.

391

POSTURAL CHANGES IN AIRWAY D~NSIONS

0

DORSUM

1 -3D

1 -20

1 -10

I 0

I +10

1 *xl

+M

PROW - SUPlhE AIRWAY OhMETER DIFAENCE %

Fig. lO.Dead dog turned supine to prone. Each point is the plot of % height of segment in supine position against change in diameter (diameter prone %max minus diameter supine %max). The line drawn is the regression of x on y (r = -0.65).

Discussion AIRWAY LENGTH

On changing posture at end expiration from the horizontal to the head-up posture three types of volume change occur. Firstly, total gas volume in the lungs increases (Hurtado and Fray, 1933: Craig, 1960). This increase in FRC results from an overall increase in Ptp since in the head-up posture the abdomen exerts an inspiratory effect on the lung, whilst in the horizon& posture it has an expiratory effect. Secondly, there is a regional redistribution of gas volume with the upper zones expanding relative to the lower (Milic-E~li et al., 1966; Sutherland et at., 1968; Glazier et al., 1967; Hogg and Nepszy, 1969). Finally, there may be regional changes in shape due to redistribution of gas within a zone at a given volume. The regional differences in expansion are thought to be related to the known gradient of pleural surface pressure (Agostoni, 1972). In the horizontal posture the anaesthetized dog lay right side down; using the data of D’Angelo et al. (1970) Ptp might be expected to be 0 cm H,O at the most dependent region and 5 cm H,O in the uppermost region. In our preparation the left (upper) lung was dusted, thus airways would be exposed to a Ptp in excess of that at the transition point between hemithoraces (2 cm H,O) of the order of 3 to 3.5 cm H,O. In the erect posture the mean surface pressure surroun~g the upper zone would be about -6.5 cm Hz0 and surrounding the lower zone -3.5 cm H,O. On tilting from horizontal to head-up the upper zone would be exposed to more negative pressure and will increase in

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A. G. WILSON. H. A. JONES AND J. M. B. HUGHES

volume but the lower zone remaining essentially isobaric will change volume little. Hyatt et al. (1970) and Hughes et al. (1972) have shown in isolated dog lobes that above FRC airway length follows the cube root of lung volume; if the same relationship held in viva segmental bronchial length would reflect local lung volume. The changes in regional airway length on tilting head up from the horizontal posture were consistent with the expected local alterations of volume predicted from changes in the pleural surface pressure gradient. This relationship was unaltered by atropine suggesting that either the alteration of bronchomotor tone does not change longitudinal elastance or that, if it does, interdependence between airway length and local lung volume obscures any change. Evidence is conflicting on the effects of bronchomotor tone on longitudinal tension in airways (Radford and Lefcoe, 1955; Olsen et al., 1967). On inversion all airways became shorter and there was no significant difference in regional behaviour [mean change upper zone - 5.2% ( f 1.1 SEM), lower zone -6.8% (t_ 2.3 SEM)]. Th ese changes are consistent with the known decrease in FRC on inversion (Agostoni and Mead, 1964) and might suggest an absent pleural surface pressure gradient when head down. But if the absolute values of airway length are considered apical airways are shorter than basal ones when inverted (fig. 4); the similarity of change from the horizontal to the head-down posture is due to the fact that in the lateral decubitus position basal airways are longer than apical ones. This suggests that in the horizontal posture the apical zone is less expanded than the basal, reflecting either differences in compliance or differences in the mean pleural surface pressure surrounding the zones. Although differences in compliance between apex and base in excised dog lungs have been demonstrated (Faridy et al., 1967) they are in the wrong direction to explain our findings. Regional differences in airway length when inverted suggest that there is a gradient of pleural surface pressure in this posture. Estimation of pleural surface pressure In fig. 4 the mean difference between apical and basal length before and after atropine when erect is about + 8%max and when inverted - 5.5%max. By assuming that the lung volume-Ptp and length-Ptp relationships are the same in uiuo as in excised lungs the mean Ptp of zones in the intact animal can be estimated by relating in uiuo airway length to the Ptp in the excised lung at the corresponding length (see fig. 8). We have calculated that the mean Ptp of the apical zone is 1 cm Hz0 head down, 3 cm H,O when horizontal and 11 cm H,O in the head-up posture. Similarly the gradient of pleural surface pressure between the upper and lower zones in all experiments when head up is 0.28 cm Hz0 *cm- ’ and when head down 0.09 cm HzO. cm -I. Although these estimates are derived indirectly they are of the same order as more directly obtained measurements of pleural surface pressure (Agostoni, 1972). As discussed, changes in expansion or airway length with alterations of posture can be brought about by (1) total volume changes, (2) regional volume changes

POSTURAL CHANGES IN AIRWAY DIMENSIONS

393

Fig. 11. Tracings from lateral chest *radiographs in two dogs showing lung shape in the horizontal (-), head-up (------) and head-down (. . . . .) posture.

and (3) change in shape at a given volume. We are unable to assess very accurately the contribution of lung shape to length changes since we could not hold regional volume constant during postural alterations. Qualitatively as shown by the tracings of thoracic shape in the lateral position (rig. 11) there was little change in overall shape between the horizontal and inverted postures; in the vertical posture some bowing of the vertebral column generally caused a change in lung configuration. On the other hand, assuming that when horizontal the volumes of the zones are approximately the same and that the cube root of regional volume (%max) equals mean airway length (“/omax) the relative contributions of total and regional volume changes can be estimated. Total volume change can be related to (basal airway length %max + apical airway length %max)/2 and regional changes to the difference between horizontal and vertical airway length (%max). On changing from the horizontal to the head-up posture FRC increases by 7% TLC entirely due to increased expansion of the upper zone whereas on inversion FRC decreases by 7% TLC, 57% of the change occurring at the base and 43% at the apex. DIAMETER

The diameter of an airway is a function of its compliance and the transbronchial pressure (Ptb). Bronchial compliance in turn depends on the properties of the elastic and smooth muscle tissue of the airway wall so that alterations in smooth muscle tone by, for example, atropine or bronchoconstricting drugs will change airway compliance. In addition, smooth muscle tension at a given fibre length is affected by its previous stretch history (Bulbring, 1955) and this gives rise to an intrinsic airway hysteresis (Martin and Proctor, 1958). The extrabronchial pressure in the thin connective tissue space surrounding intrapulmonary airways and thus transmural pressure (Ptb) in these airways is not known, though it will be related to transpulmonary pressure.

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A. G. WILSON, H. A. JONES AND J. M. B. HUGHES

Our results show that there is a relationship between airway diameter and local bronchial length (or local Ptp). In other words, when airways become longer they also become wider and vice versa (figs. 4 and 6). This behaviour is further illustrated in fig. 8 which relates in uivo and excised airway dimensions in the upper zones of three lungs studied both head-up and head-down. The upper zones were chosen as the changes are larger and easier to illustrate than in the basal zones. The in vim mean airway length (‘Amax) has been plotted against diameter (%max), as interrupted lines, in the horizontal, head-up and head-down posture both before and after atropine. The airway length/diameter relationship in the excised lung (fig. 8, continuous line) is shown for various degrees of lung inflation with the corresponding Ptp’s on the top abscissa. In oiuo three tidal breaths were allowed following deflation from TLC before the radiograph was exposed at FRC and thus the volume history differed from that in the excised lung. Measurements of oesophageal pressure did not show any increase in Ptp after tidal breathing. Nevertheless, the volume history in the in uiuo situation probably allowed some recovery of airway tone. It is not clear why the airway length-diameter plot in the excised lung and in uiuo after atropine are different. Possibly the atropine dose was inadequate, allowing some bronchomotor tone to remain in uiuo or otherwise the empty vessels in the excised lung, which share a common sheath with the airways, reduced the constraints on the bronchi in that situation. Lung shape in uivo may have differed from that excised. The slope of the in uivo curves, which is a function of airway compliance, increased after atropine. This is consistent with the increased slope of conductance-transpulmonary pressure (or lung volume) plots in man after atropine (Butler et al., 1960; Vincent et al., 1970). Purely mechanical factors (local variation in lung expansion) can account for regional airway length changes, but other factors may play a part in the changes of bronchial diameter. Blood flow (West and Dollery, 1960) ventilation (Bryan et al., 1966) alveolar gas tensions (Anthonisen et al., 1966) and the amount of interstitial fluid (Levine and Mellins, 1972) are all know to vary in a systematic way with posture. In addition, tipping is accompanied by reflex activity to maintain homeostasis. We think it is unlikely that any of these factors are important determinants of bronchial calibre as similar changes occurred not only after atropine, but also in the exsanguinated animal turned prone to supine. Distribution of airway resistance With alterations in posture length and diameter change in the same direction. These changes will have opposite effects on flow resistance but diameter will dominate because conductance for laminar flow is proportional to r4/ 1. For laminar flow conditions the change in resistance in the upper and lower zones with posture can be estimated. Going to the head-up position from the horizontal apical zone resistance decreases by 57% and basal by 34”/,; on inversion, apical resistance increases by 46% and basal by 18%. As the distribution of resistance in the horizontal posture between zones is not known it is strictly only possible

POSTURAL CHANGES IN AIRWAY DIMENSIONS

395

to compare changes of resistance within any one zone. But if it is assumed that the number and length of pathways in both zones is approximately the same the distribution of resistance in the horizontal posture can be calculated from the average dimensions of the airways. On this basis, airway resistance (Raw) in apical and basal zones was approximately equal (Raw apical/Raw basal= l/1.08) in the horizontal posture. Taking into account the postural changes in percent resistance within each zone, apical resistance in the head-up posture would be less than basal and in the head-down posture basal resistance would be less than apical. The distribution of resistance in series along the length of the bronchial tree has been measured using retrograde catheters (Macklem and Mead, 1967) but information on the partitioning of parallel resistance in relation to gravity is lacking apart from indirect observations on the distribution of ventilation. At slow flow rates ventilation is distributed according to regional lung compliance (Milic-Emili et al., 1966) but at high flow rates resistance may assume more importance. At high flow rates in the upright posture the distribution of ventilation becomes more uniform (Robertson et al., 1969) and in later studies reversal was found (Hughes et al., 1972) with the apical distribution of a ‘33Xe bolus exceeding that to the base. Our results provide measurements of bronchial dimensions consistent with these findings but whether they fully explain them is still not proven since the pleural surface pressure gradient measured under static conditions may change during rapid inspiration and expiration. DISTRIBUTION OF STRESS BETWEEN AIRWAYS AND PARBNCHYMA

In the excised lung airway length closely followed the cube root of lung volume. In the intact animal we have no estimate of absolute regional volumes, but from Glazier et al. (1967) the calculated ratios [alveolar volume (headup)]*: [alveolar volume (horizontal)]* for apical zones in greyhounds are 1: 1.12 and for basal zones 1:0.99 (10 cm above and below the mid-height point). Corresponding ratios of airway length derived from our study [mean airway length (head up)]: [mean airway length (horizontal)] for apical zones are 1: 1.16 and for basal zones 1: 1.0. These findings suggest that both in the excised lung and in uiuo airway length and local lung expansion are well matched and that sheer stresses between airway wall and parenchyma are kept to a minimum. This situation does not hold for airway diameter. At a given airway length and lung expansion airway diameter varied from animal to animal and in a given individual from time to time. Thus the mean horizontal airway diameter in the upper zone in these experiments varied from 35%max to 65%rnax, despite the fact that the dogs were of a similar size and presumably had similar pleural surface pressure gradients as suggested by similar mean airway lengths. In addition, with the administration of atropine the airway diameter increased for a given mean airway length (fig. 8). Th ese observations suggest that local radial stresses between airways and parenchyma vary at the same airway length and lung expansion.

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A. G. WILSON, H. A. JONES AND J. M. B. HUGHES

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