Alveolar surface area-to-lung volume ratio in oleic acid-induced pulmonary edema

1996 ◽  
Vol 80 (3) ◽  
pp. 742-746 ◽  
Author(s):  
S. Suzuki ◽  
T. Akahori ◽  
N. Miyazawa ◽  
M. Numata ◽  
T. Okubo ◽  
...  
Keyword(s):  
Surface Tension ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Volume ◽  
Volume Ratio ◽  
Transpulmonary Pressure ◽  
Mean Free Path ◽  
Alveolar Surface Area ◽  
Alveolar Surface

It is unknown how the in vivo alveolar surface area-to-volume ratio (S/V) changes in low-pressure pulmonary edema. Here, the S/V is the area of the air-tissue interface per unit total volume (air plus tissue). We hypothesized that in oleic acid (OA)-induced edema inactivation of the pulmonary surfactant may increase surface tension and decrease the S/V at any given lung volume. OA (0.04 mg/kg) was intravenously injected into dogs. We measured the in vivo S/V (equivalent to the inverse of optical mean free path by light-scattering stereology and the pressure-volume (PV) curve 60-90 min after OA administration. OA administration decreased the lung volume at each transpulmonary pressure and increased the wet-to-dry weight ratio. The S/V decreased after OA administration (optical mean free path increased). The air-filled PV curves shifted downward after OA, but the saline-filled PV curves after OA administration did not differ significantly from control saline-filled curves. The difference in transpulmonary pressure between air- and saline-filled PV curves (an index of the magnitude of surface tension) was increased in OA-induced pulmonary edema. This study suggests that in OA-induced pulmonary edema the alveolar surface tension increases and the S/V decreases, presumably due to inactivation of surfactant by serum leakage to alveoli.

Effects of surfactant on the in vivo alveolar surface-to-volume ratio

1996 ◽  
Vol 80 (1) ◽  
pp. 86-90 ◽  
Author(s):  
N. Miyazawa ◽  
S. Suzuki ◽  
T. Akahori ◽  
T. Okubo
Keyword(s):  
Surface Tension ◽  
Pulmonary Surfactant ◽  
Total Lung Capacity ◽  
Volume Ratio ◽  
Transpulmonary Pressure ◽  
Mean Free Path ◽  
Lung Capacity ◽  
Alveolar Surface ◽  
Saline Lavage

To investigate how pulmonary surfactant influences alveolar structure in vivo, we examined the alveolar surface area-to-lung volume (S/V) ratio of the lung parenchyma of a live dog by light-scattering stereology before and after saline lavage. We measured the backscattered light pattern produced by applying a laser beam to the pleural surface of a ventilated animal and obtained the S/V [equivalent to the inverse of the optical mean free path (lambda)]. After saline lavage, V at transpulmonary pressure (P) of 30 cmH2O (defined as total lung capacity) decreased by 11.1 +/- 3.1% (SD) and the P-V curve shifted to a lower V. The lambda-V curve was shifted to a higher lambda and to a lower V after saline lavage. S/V decreased after saline lavage (lambda increased by 38 +/- 27% on the deflation limb at a V of 80% of control total lung capacity). The alveolar surface tension increased after saline lavage, and the increase in surface tension was greater on inflation than on deflation. We conclude that depletion of pulmonary surfactant increases the alveolar surface tension in vivo, resulting in a decrease in S/V.

High surface tension pulmonary edema induced by detergent aerosol

1985 ◽  
Vol 58 (1) ◽  
pp. 129-136 ◽  
Author(s):  
G. F. Nieman ◽  
C. E. Bredenberg
Keyword(s):  
Surface Tension ◽  
Pulmonary Edema ◽  
High Surface ◽  
Water Volume ◽  
Oncotic Pressure ◽  
Static Compliance ◽  
Surfactant Activity ◽  
Dioctyl Sodium Sulfosuccinate ◽  
Alveolar Surface

The effect of the detergent dioctyl sodium sulfosuccinate on pulmonary extravascular water volume (PEWV) was studied in adult anesthetized mongrel dogs. The detergent was dissolved as a 1% solution in a vehicle of equal volumes of 95% ethanol and normal saline and administered by ultrasonic nebulizer attached to the inspiratory tubing of a piston ventilator. Two hours following detergent aerosol PEWV measured gravimetrically was increased compared with either animals receiving no aerosol or those receiving an aerosol of vehicle alone. Loss of surfactant activity and increased alveolar surface tension were demonstrated by Wilhelmy balance studies of minced lung extracts, by a fall in static compliance, and by evidence of atelectasis and instability noted by gross observation and by in vivo microscopy. No significant changes in colloid oncotic pressure or pulmonary microvascular hydrostatic pressure were observed. These data suggest that pulmonary edema can be induced by increased alveolar surface tension and support the concept that one of the major roles of pulmonary surfactant is to prevent pulmonary edema.

Effect of vagal tone on airway diameters and on lung volume in anesthetized dogs

1976 ◽  
Vol 41 (4) ◽  
pp. 581-589 ◽  
Author(s):  
H. L. Hahn ◽  
P. D. Graf ◽  
J. A. Nadel
Keyword(s):  
Physical Properties ◽  
Lung Volume ◽  
Vagal Stimulation ◽  
Vagal Tone ◽  
Transpulmonary Pressure ◽  
Lung Parenchyma ◽  
Open Chest ◽  
Anesthetized Dogs

In 18 open-chest dogs we obtained pressure-diameter (P-D) curves from tantalum bronchograms and pressure-volume (P-V) curves by plethysmography. After vagotomy most of the decrease in diameter with decreasing transpulmonary pressure (Ptp) occured below 10 cmH2O and there was no P-D hysteresis. Smaller airways narrowed more with decreasing Ptp than larger ones. Bronchodilators did not increase diameters after vagotomy (P less than 0.2). With vagi intact, diameters were smaller at all Ptp (P less than 0.01) and exhibited hysteresis, but the lung P-V curve was unchanged. Vagal stimulation narrowed airways further at all Ptp and hysteresis was marked. Smaller airways narrowed more with vagal stimulation than larger ones. Vagal stimulation did not change the deflation limb of the P-V curve but decreased inflation volumes slightly at all Ptp (P less than 0.01). We conclude that in vivo toneis vagal and that it affects the physical properties of airways, but not oflungs, making the airways remarkably independent from lung parenchyma.

Comparison of postnatal lung growth and development between C3H/HeJ and C57BL/6J mice

2006 ◽  
Vol 100 (5) ◽  
pp. 1577-1583 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner
Keyword(s):  
Lung Volume ◽  
Lung Development ◽  
Inbred Mice ◽  
Left Lung ◽  
Transpulmonary Pressure ◽  
Mean Linear Intercept ◽  
Old Mice

Previous work by our group has demonstrated substantial differences in lung volume and morphometric parameters between inbred mice. Specifically, adult C3H/HeJ (C3) have a 50% larger lung volume and 30% greater mean linear intercept than C57BL/6J (B6) mice. Although much of lung development occurs postnatally in rodents, it is uncertain at what age the differences between these strains become manifest. In this study, we performed quasi-static pressure-volume curves and morphometric analysis on neonatal mice. Lungs from anesthetized mice were degassed in vivo using absorption of 100% O2. Pressure-volume curves were then recorded in situ. The lungs were then fixed by instillation of Zenker’s solution at a constant transpulmonary pressure. The left lung from each animal was used for morphometric determination of mean air space chord length ( Lma). We found that the lung volume of C3 mice was substantially greater than that of B6 mice at all ages. In contrast, there was no difference in Lma (62.7 μm in C3 and 58.5 μm in B6) of 3-day-old mice. With increasing age (8 days), there was a progressive decrease in the Lma of both strains, with the magnitude of the decrease in B6 Lma mice exceeding that of C3. C3 lung volume remained 50% larger. The combination of parenchymal architectural similarity with lung air volume differences and different rates of alveolar septation support the hypothesis that lung volume and alveolar dimensions are independently regulated.

Lung alveoli: endogenous programmed destruction and regeneration

2002 ◽  
Vol 283 (2) ◽  
pp. L305-L309 ◽  
Author(s):  
Gloria De Carlo Massaro ◽  
Svetlana Radaeva ◽  
Linda Biadasz Clerch ◽  
Donald Massaro
Keyword(s):  
Calorie Restriction ◽  
Lung Volume ◽  
Cell Apoptosis ◽  
Alveolar Wall ◽  
Cell Replication ◽  
Adult Mice ◽  
Alveolar Surface Area ◽  
Wall Cell ◽  
Ad Libitum ◽  
Alveolar Surface

Mammalian alveoli, complex architectural and cellular units with dimensions that are linked to the organism's O2consumption (V˙o2), are thought to be destroyed only by disease and not to spontaneously regenerate. Calorie restriction of adult mammals lowersV˙o2, and ad libitum refeeding returnsV˙o2to pre-calorie-restriction values. We took advantage of these relationships and tested the hypothesis in adult mice that calorie restriction (two-thirds reduction for 2 wk) followed by ad libitum refeeding (3 wk) would cause alveolar destruction and regeneration, respectively. Calorie restriction diminished alveolar number 55% and alveolar surface area 25%. Refeeding fully reversed these changes. Neither manipulation altered lung volume. Within 72 h, calorie restriction increased alveolar wall cell apoptosis and diminished lung DNA (∼20%). By 72 h of refeeding, alveolar wall cell replication increased and lung DNA rose to amounts in mice that were never calorie restricted. We conclude that adult mice have endogenous programs to destroy and regenerate alveoli, thereby raising the danger of inappropriate activation but the possibility of therapeutic induction, if similar programs exist in humans.

Surface tension influences cell shape and phagocytosis in alveolar macrophages

2006 ◽  
Vol 291 (4) ◽  
pp. L572-L579 ◽  
Author(s):  
Hiroko Akei ◽  
Jeffrey A. Whitsett ◽  
Michelle Buroker ◽  
Takafumi Ninomiya ◽  
Haruyuki Tatsumi ◽  
...  
Keyword(s):  
Surface Tension ◽  
Alveolar Macrophages ◽  
Surfactant Protein ◽  
Surfactant Film ◽  
Fluorescent Microbeads ◽  
Alveolar Surface ◽  
Mouse Macrophage Cell Line ◽  
Effect Of Surface

The effect of surface tension on alveolar macrophage shape and phagocytosis was assessed in vivo and in vitro. Surface tension was regulated in vivo by conditionally expressing surfactant protein (SP)-B in Sftpb−/−mice. Increased surface tension and respiratory distress were produced by depletion of SP-B and were readily reversed by repletion of SP-B in vivo. Electron microscopy was used to demonstrate that alveolar macrophages were usually located beneath the surfactant film on the alveolar surfaces. Reduction of SP-B increased surface tension and resulted in flattening of alveolar macrophages on epithelial surfaces in vivo. Phagocytosis of intratracheally injected fluorescent microbeads by alveolar macrophages was decreased during SP-B deficiency and was restored by repletion of SP-B in vivo. Incubation of MH-S cells, a mouse macrophage cell line, with inactive surfactant caused cell flattening and decreased phagocytosis in vitro, findings that were reversed by the addition of sheep surfactant or phospholipid containing SP-B. SP-B controls surface tension by forming a surfactant phospholipid film that regulates shape and nonspecific phagocytic activity of alveolar macrophages on the alveolar surface.

Quantitative lung morphology in Japanese waltzing mice

1978 ◽  
Vol 44 (3) ◽  
pp. 446-449 ◽  
Author(s):  
D. Bartlett ◽  
J. G. Areson
Keyword(s):  
Body Weight ◽  
Surface Area ◽  
Lung Volume ◽  
Lung Growth ◽  
Lung Morphology ◽  
Alveolar Surface Area ◽  
Albino Mice ◽  
Alveolar Surface

We have reinvestigated the question of whether exercise stimulates lung growth by determining body weight (BW), lung volume (LV), alveolar surface area (SA), and alveolar number (N) in Japanese waltzing mice, in their phenotypically normal littermates, and in normal albino mice. BW, LV, SA, and N were all less in waltzing mice than in their littermates; LV/BW, SA/BW, and N/BW were indistinguishable in the two groups. Age-matched albino mice had larger BW and smaller N/BW than the waltzers or their littermates. The results indicate that both waltzing mice and their nonwaltzing littermates have more highly compartmentalized lungs than albino mice of the same age. However, the data provide no support for the hypothesis that sustained exercise enhances lung growth.

Microvascular membrane permeability in high surface tension pulmonary edema

1986 ◽  
Vol 60 (1) ◽  
pp. 253-259 ◽  
Author(s):  
C. E. Bredenberg ◽  
G. F. Nieman ◽  
A. M. Paskanik ◽  
A. K. Hart
Keyword(s):  
Surface Tension ◽  
Pulmonary Edema ◽  
Protein Concentration ◽  
High Surface ◽  
Base Line ◽  
Total Protein Concentration ◽  
Airway Edema ◽  
Major Increase ◽  
Dioctyl Sodium Sulfosuccinate ◽  
Alveolar Surface

Pulmonary edema was induced in dogs by an aerosol of detergent dioctyl sodium sulfosuccinate. The permeability of the pulmonary microvascular membrane was assessed by cannulating an afferent tracheobronchial lymphatic and comparing the lymph-to-plasma total protein concentration (CL/CP) during high lymph flows induced by increasing left atrial (LA) pressure after detergent aerosol. Base-line CL/CP of 0.69 +/- 0.02 fell to 0.55 +/- 0.03 with increased LA pressure alone. CL/CP fell to 0.47 +/- 0.02 when LA pressure was increased following detergent, 0.51 +/- 0.04 following an aerosol of the vehicle in which the detergent was dissolved, and 0.73 +/- 0.10 following intravenous alloxan. In additional animals protein concentration of the airway edema fluid was compared with that of plasma. The ration of protein concentration of airway fluid to plasma was 0.63 +/- 0.08 following detergent aerosol, 0.64 +/- 0.10 following increased LA pressure, and 0.94 +/- 0.09 following administration of alloxan. These data indicate no major increase in pulmonary microvascular permeability following detergent aerosol and support the concept that pulmonary edema is the consequence of reduced interstitial perimicrovascular hydrostatic pressure caused by increased alveolar surface tension.

Functional assessment of pulmonary capillary surface area in the 2-mo-old lamb

1991 ◽  
Vol 70 (4) ◽  
pp. 1677-1685 ◽  
Author(s):  
B. R. Pitt ◽  
G. Lister ◽  
J. J. Perez Fontan ◽  
P. Davies
Keyword(s):  
Surface Area ◽  
Pulmonary Toxicity ◽  
Antineoplastic Agent ◽  
Maximal Velocity ◽  
Alveolar Surface Area ◽  
Pulmonary Capillary ◽  
Significant Difference ◽  
Normal Variability ◽  
Alveolar Surface

We recently reported that measurements of the maximal velocity of pulmonary endothelial angiotensin-converting enzyme (Vmax) in vivo provide information regarding microvascular surface area in the developing lamb. To obviate any subtle influences of development on Vmax aside from simple increases in surface area, we correlated Vmax with postmortem stereological assessments of alveolar surface area in the relatively mature lung of the 2-mo-old lamb (n = 14). We attempted to increase the range of surface area beyond its normal variability by injecting nine of the lambs with bleomycin, an antineoplastic agent with significant pulmonary toxicity in other species. Vmax, measured shortly after birth and then weekly, increased monotonically in all lambs. Despite their wide dispersion, Vmax and the stereological determinations correlated strongly at 2 mo of age, confirming that Vmax is a robust indicator of the surface area of the air-blood barrier. There was no significant difference in either measurement between the control lambs and those treated with bleomycin, suggesting that the newborn lamb is resistant to the effect of this agent.

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