scholarly journals Effect of severe calorie restriction on the lung in two strains of mice

2008 ◽  
Vol 295 (2) ◽  
pp. L356-L362 ◽  
Author(s):  
John M. Bishai ◽  
Wayne Mitzner
Keyword(s):  
Calorie Restriction ◽  
Normal Diet ◽  
Lung Mechanics ◽  
Histological Changes ◽  
Lung Capacity ◽  
Volume Curve ◽  
Copd Patients ◽  
Pressure Volume Curve ◽  
Lung Structure ◽  
Genetically Determined

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.

Changes in lung mechanics induced by acute isocapnic hypoxia

1977 ◽  
Vol 42 (3) ◽  
pp. 413-419 ◽  
Author(s):  
N. A. Saunders ◽  
M. F. Betts ◽  
L. D. Pengelly ◽  
A. S. Rebuck
Keyword(s):  
Total Lung Capacity ◽  
Lung Compliance ◽  
Specific Conductance ◽  
Lung Mechanics ◽  
Recoil Pressure ◽  
Lung Capacity ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Residual Capacity ◽  
Dynamic Lung Compliance

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.

Lung volume and pleural pressure in the anesthetized hamster

1979 ◽  
Vol 46 (5) ◽  
pp. 927-931 ◽  
Author(s):  
Y. L. Lai
Keyword(s):  
Lung Volume ◽  
Esophageal Pressure ◽  
Lung Compliance ◽  
Pleural Pressure ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Residual Capacity ◽  
Wall Compliance

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.

Effects of airway versus arterial CO2 changes on lung mechanics in dogs

1975 ◽  
Vol 38 (4) ◽  
pp. 603-607 ◽  
Author(s):  
R. H. Ingram
Keyword(s):  
Partial Pressure ◽  
Normal Level ◽  
Static Pressure ◽  
Artery Occlusion ◽  
Lung Mechanics ◽  
Small Airways ◽  
Co2 Partial Pressure ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Unilateral Pulmonary Artery Occlusion

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.

Alveolar volume-surface area relation in air- and saline-filled lungs fixed by vascular perfusion

1979 ◽  
Vol 47 (5) ◽  
pp. 990-1001 ◽  
Author(s):  
J. Gil ◽  
H. Bachofen ◽  
P. Gehr ◽  
E. R. Weibel
Keyword(s):  
Mathematical Function ◽  
Vascular Perfusion ◽  
Alveolar Volume ◽  
Entire Volume ◽  
Lung Capacity ◽  
Surface Areas ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Best Fit ◽  
Volume Range

The influence of volume changes and interfacial forces on the geometry of peripheral air spaces was studied in excised rabbit lungs inflated with either air or saline and fixed by vascular perfusion at four points of the deflation limb of the pressure-volume curve corresponding to 100, 80, 60, and 40% of the total lung capacity (TLC). In air-filled lungs pleating and folding of alveolar septa were observed, especially in alveolar corners. However, the alveolar surfaces were smooth, except at low lung volumes where some surface crumpling occurred. In saline-filled lungs pleats were absent; the alveolar surface was irregular at all inflation levels due to undulating walls and bulging capillaries. Morphometry indicated that at all alveolar volumes (VA) the surface areas (SA) were larger in saline- than air-filled lungs. No simple mathematical function was found to characterize the relation between SA and VA over the entire volume range studied. Within the range of normal breaths (80 to 40% TLC) the best fit for n in the function SA = k.VnA was 0.58 for saline-filled lungs (r = 0.93) and 0.33 for air-filled lungs (r = 0.68), suggesting different and complex deflation patterns.

Breathing He-O2 shifts the lung pressure-volume curve of the dog

1983 ◽  
Vol 54 (2) ◽  
pp. 576-581 ◽  
Author(s):  
N. Berend ◽  
K. L. Christopher ◽  
N. F. Voelkel
Keyword(s):  
Total Lung Capacity ◽  
High Viscosity ◽  
Cyclooxygenase Inhibitors ◽  
Gas Mixture ◽  
Lung Capacity ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Lung Expansion ◽  
Alveolar Duct ◽  
Curve Shift

To determine whether breathing a mixture of 80% He-20% O2 affects the lung pressure-volume (PV) curve, eight anesthetized paralyzed dogs were studied in a volume-displacement plethysmograph. Static PV curves on air were compared with PV curves obtained after equilibration with He-O2. The He-O2 PV curves were significantly shifted upward by an average of 5% total lung capacity. There was no change in compliance, indicating that the shift was due to lung expansion rather than a change in elasticity. Pretreatment of the dogs with cyclooxygenase inhibitors abolished the PV shift with He-O2. Four dogs had PV curves recorded on air and a mixture of O2, SF6, and Ne, a gas mixture with the same density as air but with 45% greater viscosity. The PV curve shift was even greater than observed with He-O2 and could again be virtually abolished with a cyclooxygenase inhibitor. These results suggest that breathing a high-viscosity gas mixture results in alveolar duct dilatation due to the release of a prostaglandin bronchodilator. This may need to be taken into account in the analysis of flow augmentation with He-O2.

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 ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Lung Volume ◽  
Lung Surfactant ◽  
Control Level ◽  
Surface Force ◽  
Lung Mechanics ◽  
Tissue Elasticity ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Alveolar Surface

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.

Measurement of lung expansion with computed tomography and comparison with quantitative histology

1995 ◽  
Vol 79 (5) ◽  
pp. 1525-1530 ◽  
Author(s):  
H. O. Coxson ◽  
J. R. Mayo ◽  
H. Behzad ◽  
B. J. Moore ◽  
L. M. Verburgt ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Pressure Gradient ◽  
Pleural Pressure ◽  
Lung Volumes ◽  
Quantitative Histology ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Lung Structure ◽  
Lung Expansion ◽  
Regional Lung

The total and regional lung volumes were estimated from computed tomography (CT), and the pleural pressure gradient was determined by using the milliliters of gas per gram of tissue estimated from the X-ray attenuation values and the pressure-volume curve of the lung. The data show that CT accurately estimated the volume of the resected lobe but overestimated its weight by 24 +/- 19%. The volume of gas per gram of tissue was less in the gravity-dependent regions due to a pleural pressure gradient of 0.24 +/- 0.08 cmH2O/cm of descent in the thorax. The proportion of tissue to air obtained with CT was similar to that obtained by quantitative histology. We conclude that the CT scan can be used to estimate total and regional lung volumes and that measurements of the proportions of tissue and air within the thorax by CT can be used in conjunction with quantitative histology to evaluate lung structure.

Alterations of mechanical properties and morphology in excised rabbit lungs rinsed with a detergent

1979 ◽  
Vol 47 (5) ◽  
pp. 1002-1010 ◽  
Author(s):  
H. Bachofen ◽  
P. Gehr ◽  
E. R. Weibel
Keyword(s):  
Surface Area ◽  
Lung Volume ◽  
Progressive Collapse ◽  
Lung Surfactant ◽  
Volume Ratio ◽  
Vascular Perfusion ◽  
Lung Capacity ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Volume Range

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.

RELATION OF THE MARKERS OF MYOCARDIAL DYSFUNCTION AND SYSTEMIC INFLAMMATION WITH STRUCTURAL AND FUNCTIONAL PARAMETERS OF THE LUNGS IN MYOCARDIAL INFARCTION PATIENTS

2018 ◽  
Vol 17 (2) ◽  
pp. 24-28
Author(s):  
O. M. Polikutina ◽  
Y. S. Slepynina ◽  
E. D. Bazdyrev ◽  
V. N. Karetnikova ◽  
O. L. Barbarach
Keyword(s):  
Myocardial Infarction ◽  
Systemic Inflammation ◽  
Myocardial Dysfunction ◽  
Control Group ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Functional Changes ◽  
Functional Parameters ◽  
Lung Capacity ◽  
Copd Patients

Aim. To evaluate the structural and functional changes in the lungs of ST elevation myocardial infarction (STEMI) patients with absence or presence of chronic obstructive lung disease (COPD), and the relation with myocardial dysfunction and systemic inflammation.Material and methods. Totally, 189 STEMI patients included: group 1 — STEMI with COPD of moderate and mild grade, 2 — STEMI with no lung pathology. Groups were comparable by clinical and anamnestic parameters. Assessment of lung function and blood collection were done at 10­12 day of STEMI. For comparison of the parameters representing structural and functional changes in the lungs and comparison of C­reactive protein (CRP), N­terminal pro­brain natriuretic peptide (NT­proBNP) concentration, a control group was formed with no pulmonary pathology, comparable by age and sex with the STEMI patients.Results. In COPD patients, higher values revealed of the parameters representing the part of residual volumes in pulmonary structure. Higher residual volume (RV) was found also in STEMI and no COPD comparing to controls, however the relation RV/TLC (total lung capacity) was not higher than normal range. In both groups there were lower values of diffusion lung capacity (DLCO) comparing to controls. The lowest DLCO found in COPD patients. Concentration of NT­proBNP (H=41,6; p<0,001) and CRP (H=38,6; p<0,001) in COPD was significantly higher in STEMI with no COPD patients than in controls. The negative correlations found for NT­proBNP and CRP with forced expiratory volume 1 sec, FEV/FVC1, DLCO, and positive — with the values of thoracic volume, RV/TLC.Conclusion. In STEMI patients the increase revealed of residual lung volumes. Mostly the level of residual volumes is high in STEMI and COPD patients. There are associations of NT­proBNP and CRP with structural and functional parameters of the lungs regardless of COPD.

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