Changes of lung surfactant and pressure-volume curve in bleomycin-induced pulmonary fibrosis

1991 ◽  
Vol 70 (3) ◽  
pp. 1300-1308 ◽  
Author(s):  
K. Osanai ◽  
K. Takahashi ◽  
S. Sato ◽  
K. Iwabuchi ◽  
K. Ohtake ◽  
...  

We investigated whether alveolar surface force increased and participated in the lung pressure-volume relationship in bleomycin-induced pulmonary fibrosis in hamsters and, if so, whether lung surfactant was hampered in the lungs. On the air-filled pressure-volume curve, decreases of lung volume from control level were significantly higher at 3-8 cmH2O pressure on day 10 than on day 30. Because the change of lung tissue elasticity evaluated from the saline-filled pressure-volume curve was equal for the 2 days, the higher decrease of air volume on day 10 was due primarily to contribution of alveolar surface force. Pressure differences between deflation limbs of air-filled and saline-filled pressure-volume curves, which represented net alveolar surface force, were significantly higher at any lung volume between 50 and 90% total lung capacity on day 10, but almost no significance was observed on day 30. Phospholipid concentration in bronchoalveolar lavage fluid significantly decreased on day 10 but had improved by day 30. Analysis of phospholipid species in purified lung surfactant showed decreased fractions of disaturated phosphatidylcholine and phosphatidylglycerol on day 10. Surface-active properties of the surfactant, measured by a modified Wilhelmy balance, were remarkably hampered on day 10, but most of them had improved by day 30. We consider that the quantitative and functional abnormalities of lung surfactant have a part in the aggravation of lung mechanics in the acute phase of pulmonary fibrosis.

1979 ◽  
Vol 47 (5) ◽  
pp. 1002-1010 ◽  
Author(s):  
H. Bachofen ◽  
P. Gehr ◽  
E. R. Weibel

To assess the influence of alterations of lung surfactant on the geometry of peripheral air spaces, the morphology of detergent-rinsed rabbit lungs was studied. In comparison to normal excised rabbit lungs, fixed in the same manner by vascular perfusion at different points on the deflation pressure-volume curve, the most important differences are as follows. 1) With decreasing lung volume there is a progressive collapse of alveoli; at low lung volume (40% of total lung capacity (TLC) (most alveoli are collapsed, and the air is contained in overextended ducts. 2) Accordingly, the alveolar surface area-to-volume ratio is considerably smaller in particular at medium and low lung volumes. 3) There is only a slight change of mean air-space curvature between 80 and 40% TLC. Hence, the results indicate that in detergent-rinsed lungs volume changes are brought about predominantly by recruitment and derecruitment of alveoli. It appears that both a normal surfactant and the mechanical interdependence within the fibrous continuum are required to maintain a normal respiratory surface area within the lung volume range of normal breathing.


1977 ◽  
Vol 42 (3) ◽  
pp. 413-419 ◽  
Author(s):  
N. A. Saunders ◽  
M. F. Betts ◽  
L. D. Pengelly ◽  
A. S. Rebuck

We measured lung mechanics in seven healthy males during acute isocapnic hypoxia (PAO2 = 40–50 Torr; PACO2 = 38–42 Torr). Hypoxia was accompanied by increases in total lung capacity (mean increase +/- SD; 0.40 +/- 0.24 liters; P less than 0.005) functional residual capacity (0.34 +/- 0.25 liters; P less than 0.01) and residual volume (0.56 +/- 0.44 liters; P less than 0.02) in all subjects. Specific conductance of the lung decreased during hypoxia (P less than 0.02). The static deflation pressure-volume curve of the lung was shifted upward during hypoxia in all subjects. Resting end-expiratory recoil pressure of the lung was slightly, but not significantly lower during hypoxtic expiratory lung compliance was greater during hypoxia (0.39 +/- 0.04 l/cmH2O) than control measurements (0.31 +/- 0.05 l/cmH2O; P less than 0.005). No change was noted in dynamic lung compliance. All changes in lung mechanics were reversed within three minutes of reoxygenation. We conclude that acute isocapnic hypoxia increases total lung capacity in man and suggest that this may be due to the effect of hypoxia on the airways and pulmonary circulation.


1979 ◽  
Vol 46 (5) ◽  
pp. 927-931 ◽  
Author(s):  
Y. L. Lai

Lung volumes and respiratory pressures were measured in anesthetized male hamsters weighing an average 117 g. In 16 supine animals functional residual capacity (FRC) determined by body plethysmograph was 1.12 +/- 0.23 (SD) ml (about 20% total lung capacity, TLC) slightly and significantly larger than the FRC measured by saline displacement, 1.01 +/- 0.15 ml. Similar results were found in six prone animals. Paralysis did not significantly alter supine FRC. Contrary to published reports, pleural pressure (Ppl) estimated from esophageal pressure was negative at FRC. The fact that lung volume decreased by 0.2 ml (about 4% TLC) when the chest was opened at FRC provided additional evidence of negative Ppl at FRC. No consistent changes in the lung pressure-volume curve were found after the chest was opened. Deflation chest wall compliance just above FRC was about twice lung compliance. The vital capacity and reserve volumes in this study agreed with values reported in the literature. However, absolute lung volumes (TLC, FRC, and residual volume) were lower by about 1.4 ml, possibly because of earlier overestimates of box FRC.


1975 ◽  
Vol 38 (4) ◽  
pp. 603-607 ◽  
Author(s):  
R. H. Ingram

The effects of changes in airway CO2 partial pressure (PAco2) and arterial CO2 partial pressure (Paco2) on lung mechanics were studied in dogs by utilizing unilateral pulmonary artery occlusion and a tracheal divider which allowed separate variation of PAco2 and Paco2. When Paco2 was held at a reasonably normal level, lower than normal PAco2 levels resulted in large compliance decreases, alteration of the complete static pressure-volume curves, and increases in resistance. Invreases in PAco2 to hypercapnic levels did not produce changes. When PAco2 was held at a reasonably normal level, changes in Paco2 levels were positively and directly related to resistance with small and inconsistent effects on compliance and on complete static pressure-volume curves. A combination of low PAco2 and high Paco2 produced large increases in resistance, alterations of the static pressure-volume curve, and decreases in compliance. Vagotomy during the combined stimulus resulted in only a decrease in resistance without change in lung elastic properties. The results suggest that the mechanical effects of airway hypocapnia and systemic hypercapnia are additive. However, small airways effects of low PAco2 appear to be maximal and uninfluenced by the vagally mediated response to Paco2 increases.


2008 ◽  
Vol 295 (2) ◽  
pp. L356-L362 ◽  
Author(s):  
John M. Bishai ◽  
Wayne Mitzner

There is a body of literature in animal models that has suggested the development of emphysema following severe calorie restriction. This has led to the notion of “nutritional emphysema” that might have relevance in COPD patients. There have been few studies, however, that have looked closely at both the mechanics and lung structure in the same animals. In the present work, we examined lung mechanics and histological changes in two strains of mice that have substantial differences in alveolar size, the C57BL/6 and C3H/HeJ strains. We quantified the dynamic elastance and resistance at 2.5 Hz, the quasistatic pressure volume curve, and the alveolar chord lengths in lungs inflated to a lung capacity at 25–30 cmH2O. We found that after 2 or 3 wk of calorie restriction to 1/3 their normal diet, the lungs became stiffer with increased resistance. In addition, the lung capacity was also decreased. These mechanical changes were reversed after 2 wk on a normal ad libitum diet. Histology of the postmortem fixed lungs showed no changes in the mean alveolar chord lengths with calorie restriction. Although the baseline mechanics and alveolar size were quantitatively different in the two strains, both strains showed similar qualitative changes during the starvation and refeeding periods. Thus, in two strains of mice with genetically determined differences in alveolar size, neither the mechanics nor the histology show any evidence of emphysema-like changes with this severe caloric insult.


1989 ◽  
Vol 257 (2) ◽  
pp. L1-L12 ◽  
Author(s):  
D. F. Tierney

By appreciating the influence of surface forces on lung mechanics, discovering pulmonary surfactant, and then recognizing its deficiency states a small number of investigators began the first 30 years of pulmonary surfactant research. These investigators had different backgrounds and took diverse approaches to understand surface forces in the lung. Their careers provide a fascinating study of the means by which new discoveries are made. After recognizing the critical importance of surfactant, investigators turned to a series of questions that obviously needed to be answered and they attempted to learn the following: 1) how to quantitate surfactant; 2) its biochemical and structural composition; 3) how it leaves the alveolar surface after secretion; and 4) its role in lung diseases. This research established the basis for pursuing the cellular and molecular biology of surfactant.


1987 ◽  
Vol 62 (6) ◽  
pp. 2220-2223 ◽  
Author(s):  
F. J. Cerny

Lung volumes in sex-, age-, height-, and weight-matched Black subjects are 10–15% lower than those in Caucasians. To determine whether this decreased lung volume affected the ventilatory adaptation to exercise, minute ventilation (VE), its components, frequency (f) and tidal volume (VT), and breathing pattern were observed during incremental cycle-ergometer exercise. Eighteen Caucasian (age 8–30 yr) and 14 Black (age 8–25 yr) subjects were studied. Vital capacity (VC) was lower (P less than 0.001) in the Black subjects [90.6 +/- 8.6 (SD) vs. 112.9 +/- 9.9% predicted], whereas functional residual capacity/total lung capacity was higher (P less than 0.05). VE, mixed expired O2 and CO2, VT, f, and inspiratory (TI), expiratory (TE), and total respiratory cycle (TT) duration were measured during the last 30 s of each 2-min load. Statistical comparisons with increasing power output were made at rest and from 0.6 to 2.4 W/kg in 0.3-W/kg increments. VE was higher in Blacks at all work loads and reached significance (P less than 0.05) at 0.6 and 1.5 W/kg. VE/VO2 was also higher throughout exercise, reaching significance (P less than 0.01) at 1.2, 1.5, and 1.8 W/kg. The Black subjects attained any given level of VE with a higher f (P less than 0.001) and lower VT. TI and TE were shortened proportionately so that TI/TT was not different. Differences in lung volume and the ventilatory response to exercise in these Black and Caucasian subjects suggest differences in the respiratory pressure-volume relationships or that the Black subjects may breathe higher on their pressure-volume curve.


2019 ◽  
Vol 126 (5) ◽  
pp. 1399-1408 ◽  
Author(s):  
Kris Nilsen ◽  
Francis Thien ◽  
Cindy Thamrin ◽  
Matt J. Ellis ◽  
G. Kim Prisk ◽  
...  

Derecruitment of air spaces in the lung occurs when airways close during exhalation and is related to ventilation heterogeneity and symptoms in asthma. The forced oscillation technique has been used to identify surrogate measures of airway closure via the reactance (Xrs) versus lung volume relationship. This study used a new algorithm to identify derecruitment from the Xrs versus lung volume relationship from a slow vital capacity maneuver. We aimed to compare two derecruitment markers on the Xrs versus volume curve, the onset reduction of Xrs (DR1vol) and the onset of more rapid reduction of Xrs (DR2vol), between control and asthmatic subjects. We hypothesized that the onset of DR1vol and DR2vol occurred at higher lung volume in asthmatic subjects. DR1vol and DR2vol were measured in 18 subjects with asthma and 18 healthy controls, and their relationships with age and height were examined using linear regression. In the control group, DR1vol and DR2vol increased with age ( r2 = 0.68, P < 0.001 and r2 = 0.71, P < 0.001, respectively). DR1vol and DR2vol in subjects with asthma [76.58% of total lung capacity (TLC) and 56.79%TLC, respectively] were at higher lung volume compared with control subjects (46.1 and 37.69%TLC, respectively) ( P < 0.001). DR2vol correlated with predicted values of closing capacity ( r = 0.94, P < 0.001). This study demonstrates that derecruitment occurs at two points along the Xrs-volume relationship. Both derecruitment points occurred at significantly higher lung volumes in subjects with asthma compared with healthy control subjects. This technique offers a novel way to measure the effects of changes in airways/lung mechanics. NEW & NOTEWORTHY This study demonstrates that the forced oscillation technique can be used to identify two lung volume points where lung derecruitment occurs: 1) where derecruitment is initiated and 2) where onset of rapid derecruitment commences. Measurements of derecruitment increase with age. The onset of rapid derecruitment was highly correlated with predicted closing capacity. Also, the initiation and rate of derecruitment are significantly altered in subjects with asthma.


Lung ◽  
1996 ◽  
Vol 174 (5) ◽  
Author(s):  
R.H. Sansores ◽  
A. Ramirez-Venegas ◽  
R. P�rez-Padilla ◽  
M. Monta�o ◽  
C. Ramos ◽  
...  

1982 ◽  
Vol 53 (6) ◽  
pp. 1512-1520 ◽  
Author(s):  
T. A. Wilson

An energy analysis and data from the literature on the relation among surface area, recoil pressure, and lung volume are used to calculate the surface tension-surface area curves corresponding to pressure-volume loops. The energy analysis has been described earlier (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 50: 921–926, 1981). It is based on the assumption that the tissue structure of the lung constitutes a conservative mechanical system and hence that pressure-volume hysteresis is primarily a result of surface tension-surface area hysteresis. Unlike previous methods of calculating surface tension from recoil pressure, this method does not rely on the assumption that the tissue component of recoil in the air-filled lung is the same as recoil pressure of the saline-filled lung at the same lung volume. The calculated values of surface tension decrease to less than 2 dyn/cm as surface area decreases along the deflation limb of the pressure-volume curve. Surface tension increases very steeply with surface area on the inflation limbs, reaching a limiting value of just under 30 dyn/cm. The shape of the surface tension-surface area curves, unlike the shape of the curves calculated by previous methods, is similar to the shape obtained on surface tension balances for fluid extracted from lungs.


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