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.

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.

In vivo dimensional response of airways of different size to transpulmonary pressure

1975 ◽  
Vol 39 (1) ◽  
pp. 23-29 ◽  
Author(s):  
G. M. Tisi ◽  
V. D. Minh ◽  
P. J. Friedman
Keyword(s):  
Tidal Volume ◽  
Total Lung Capacity ◽  
Transpulmonary Pressure ◽  
Main Stem ◽  
Peripheral Airways ◽  
Lung Capacity ◽  
Linear Plot ◽  
The Difference ◽  
Lateral Roentgenograms

We studied four supine dogs that were anesthetized with pentobarbital, intubated, and ventilated with a piston pump. The dimensional response of central (CAW) (greater than 2 mm diam) and peripheral airways (PAW) (smaller than 2 mm diam) to changes in transpulmonary pressure (Ptp) was determined by progressive increments in tidal volume (VT). A specially designed electronics relay circuit permitted this relationship to be obtained for points of no flow during tidal volume breathing: i.e., preinspiration (FRC); end inspiration (FRC + VT). The airways were dusted with powdered tantalum. Six airway divisions were identified: four CAW: trachea, main stem, lobar, segmental; and two PAW: subsegmental, and lobular. AP and lateral roentgenograms were obtained by standard technics and primary magnification (mag factor 2). Airway diameters were plotted as a function of transpulmonary pressure between 3 and 26 cmH2O with the diameter at total lung capacity expressed as 100%. The data show that: 1) there is significant distensibility above 5 cmH2O for all airways from the trachea to the lobular airways; 2) that the pressure-diameter plot is a linear plot for each airway from 3 to 26 cmH2O with R values between 0.846 and 0.957; 3) the peripheral lobular airways are more distensible than the central airways (P smaller than 0.05). We attribute the difference in distensibility of the peripheral lobular airways to their lack of cartilaginous support, and their decreased muscular support when compared to the CAW.

Pressure-volume characteristics of excised human lungs: effects of sex, age, and emphysema

1980 ◽  
Vol 49 (4) ◽  
pp. 558-565 ◽  
Author(s):  
N. Berend ◽  
C. Skoog ◽  
W. M. Thurlbeck
Keyword(s):  
Body Length ◽  
Total Lung Capacity ◽  
Transpulmonary Pressure ◽  
Lung Volumes ◽  
Lung Capacity ◽  
Human Lungs ◽  
Males And Females ◽  
Group 2 ◽  
Volume Characteristics

Static deflationary pressure-volume curves were obtained in 28 emphysema-free (18 male and 10 female) and 39 emphysematous excised human lungs inflated to a maximum transpulmonary pressure (Pl) of 30 cmH2O. In emphysema-free lungs, the lung volumes at Pl 30 cmH2O (V30) were significantly related to body length in males and were significantly larger than predicated total lung capacity in vivo. However, corrected for stature (V30/body length), there was no significant age correlation. In both males and females, highly significant correlations between the PL at 50--90% V30 and age were obtained. There were no significant differences in these regressions between males and females. The emphysematous lungs were divided into three groups with increasing emphysema grades. Progressive decreases in the PL at 50--90% V30 and increases in the V30 were seen in the groups with increasing degrees of emphysema. Significant changes occurred in these measurements even in group 2 with mild emphysema, suggesting that the lesions of emphysema are not directly responsible for these changes.

Alveolar liquid pressure measured by micropipettes in isolated dog lung

1982 ◽  
Vol 53 (3) ◽  
pp. 737-743 ◽  
Author(s):  
S. J. Lai-Fook ◽  
K. C. Beck
Keyword(s):  
Interstitial Fluid ◽  
Total Lung Capacity ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Initial Weight ◽  
Liquid Pressure ◽  
Lung Inflation ◽  
Main Determinant ◽  
Lung Capacity ◽  
Alveolar Surface

Micropipettes (2–5 microns), in conjunction with a servo-nulling system, were used to measure liquid pressure (Pliq) in subpleural alveoli of lobes of dog lungs made edematous by perfusing with plasma to a constant extravascular weight gain (W). Pliq was measured at fixed transpulmonary pressure (Ptp) in lungs whose W was more than 0.5 that of the initial weight (Wi). In six lobes at W/Wi = 0.6, Pliq, relative to alveolar pressure (Palv), was -2.6 +/- 0.4 cmH2O (mean +/- SE), -11.8 +/- 0.6, and -17.5 +/- 1.7 at deflation Ptp values of 5, 15, and 25 cmH2O, respectively. The Pliq increased to -2, -7, and -13.7, respectively, at W/Wi = 2.8. Based on a mean alveolar radius of 50 micron at Ptp at 25 cmH2O and values of Palv - Pliq, values for alveolar surface tension (tau) at W/Wi = 0.6 were 6, 30, and 44 dyn/cm at Ptp of 5, 15, and 25 cmH2O, respectively. In five other lobes at W/Wi = 0.5 and at 65 and 84% total lung capacity, tau was much higher on lung inflation than on deflation. If pericapillary interstitial fluid pressure (Pi) and Pliq were identical under edematous conditions, tau would be the main determinant of Pi.

Effect of lung inflation in vivo on airways with smooth muscle tone or edema

1997 ◽  
Vol 82 (2) ◽  
pp. 491-499 ◽  
Author(s):  
Robert H. Brown ◽  
Wayne Mitzner ◽  
Yonca Bulut ◽  
Elizabeth M. Wagner
Keyword(s):  
Smooth Muscle ◽  
Total Lung Capacity ◽  
Muscle Tone ◽  
Transpulmonary Pressure ◽  
Airway Wall ◽  
Lung Inflation ◽  
Airway Narrowing ◽  
Lung Capacity ◽  
Luminal Area

Brown, Robert H., Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner. Effect of lung inflation in vivo on airways with smooth muscle tone or edema. J. Appl. Physiol. 82(2): 491–499, 1997.—Fibrous attachments to the airway wall and a subpleural surrounding pressure can create an external load against which airway smooth muscle must contract. A decrease in this load has been proposed as a possible cause of increased airway narrowing in asthmatic individuals. To study the interaction between the airways and the surrounding lung parenchyma, we investigated the effect of lung inflation on relaxed airways, airways contracted with methacholine, and airways made edematous by infusion of bradykinin into the bronchial artery. Measurements were made in anesthetized sheep by using high-resolution computed tomography to visualize changes in individual airways. During methacholine infusion, airway area was decreased but increased minimally with increases in transpulmonary pressure. Bradykinin infusion caused a 50% increase in airway wall area and a small decrease in airway luminal area. In contrast to airways contracted with methacholine, the luminal area after bradykinin increased substantially with increases in transpulmonary pressure, reaching 99% of the relaxed area at total lung capacity. Thus airway edema by itself did not prevent full distension of the airway at lung volumes approaching total lung capacity. Therefore, we speculate that if a deep inspiration fails to relieve airway narrowing in vivo, this must be a manifestation of airway smooth muscle contraction and not airway wall edema.

Alveolar surface tension, lung inflation, and hydration affect interstitial pressure [Px(f)]

1984 ◽  
Vol 57 (1) ◽  
pp. 262-270 ◽  
Author(s):  
W. Hida ◽  
J. Hildebrandt
Keyword(s):  
Interstitial Fluid ◽  
Total Lung Capacity ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Mineral Oil ◽  
Interstitial Pressure ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Alveolar Surface

Peribronchoarterial interstitial fluid pressure [Px(f)] was measured by wicks inserted between bronchus and artery of dog lobes filled with air, saline, 6% dextran in saline, or mineral oil. Five inflations were made to total lung capacity, with one min stops at eight selected volume levels in each cycle. Deflation recoil (measured as transpulmonary pressure, Ptp) was largest for air and least for saline and dextran, and it fell between these extremes for mineral oil. Correspondingly, Px(f) was most negative for air, slightly less negative for mineral oil, and least for saline and dextran. On the first cycle, the Px(f) for saline and dextran were nearly equal, but in later cycles Px(f) with saline drifted fairly rapidly toward alveolar pressure. By plotting Px(f) vs. Ptp, all first-cycle curves were brought toward a single line. During later cycles, Ptp and Px(f) always changed together along this line, except for saline. We conclude that 1) at fixed vascular pressure, Px(f) depends mainly on Ptp and less on lung volume; 2) large changes in Px(f) with saline suggest that at least some fluid can enter this interstitial space quite rapidly; and 3) peripheral tissue swelling with saline causes some reduction in Ptp, and both swelling and lower recoil contribute to increased trapping of saline.

scholarly journals The Strain on Airway Smooth Muscle During a Deep Inspiration to Total Lung Capacity

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Ynuk Bossé
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Total Lung Capacity ◽  
In Vitro Studies ◽  
Deep Inspiration ◽  
Bronchodilator Effect ◽  
Lung Capacity ◽  
Residual Capacity

The deep inspiration (DI) maneuver entices a great deal of interest because of its ability to temporarily ease the flow of air into the lungs. This salutary effect of a DI is proposed to be mediated, at least partially, by momentarily increasing the operating length of airway smooth muscle (ASM). Concerningly, this premise is largely derived from a growing body of in vitro studies investigating the effect of stretching ASM by different magnitudes on its contractility. The relevance of these in vitro findings remains uncertain, as the real range of strains ASM undergoes in vivo during a DI is somewhat elusive. In order to understand the regulation of ASM contractility by a DI and to infer on its putative contribution to the bronchodilator effect of a DI, it is imperative that in vitro studies incorporate levels of strains that are physiologically relevant. This review summarizes the methods that may be used in vivo in humans to estimate the strain experienced by ASM during a DI from functional residual capacity (FRC) to total lung capacity (TLC). The strengths and limitations of each method, as well as the potential confounders, are also discussed. A rough estimated range of ASM strains is provided for the purpose of guiding future in vitro studies that aim at quantifying the regulatory effect of DI on ASM contractility. However, it is emphasized that, owing to the many limitations and confounders, more studies will be needed to reach conclusive statements.

Effect of volume and volume history of the lungs on pulmonary shunt flow

1964 ◽  
Vol 207 (1) ◽  
pp. 235-238 ◽  
Author(s):  
Nicholas R. Anthonisen
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Full Range ◽  
Transpulmonary Pressure ◽  
Pulmonary Shunt ◽  
Shunt Flow ◽  
Lung Capacity ◽  
Surface Active Properties ◽  
History Of ◽  
Surface Active

Relative pulmonary shunt flow (Qs/Qt), was measured in denitrogenated open-chested cats during apnea over the full range of lung volumes. The particular lung volume and transpulmonary pressure were also measured. When completely collapsed lungs were inflated, Qs/Qt decreased sharply to 3% at total lung capacity (TLC). During deflation from TLC Qs/Qt was insensitive to changes in lung volume. Qs/Qt remained low during reinflation after deflation from TLC. These changes in shunt flow can be interpreted as due to either recruitment or collapse of gas exchange units during lung volume change. It appears that completely collapsed lungs inflate very unevenly but that deflation from TLC proceeds remarkably evenly. Reinflation after deflation from TLC also seems to proceed evenly, and the manifest pressure-volume hysteresis is most likely due to hysteresis of the surface-active properties of the alveolar lining material.

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.

Lung volumes after antigen infusion in the guinea pig in vivo: effects of vagal section

1978 ◽  
Vol 45 (6) ◽  
pp. 957-961 ◽  
Author(s):  
J. M. Drazen ◽  
S. H. Loring ◽  
C. Venugopalan
Keyword(s):  
Total Lung Capacity ◽  
Hypersensitivity Reactions ◽  
Immediate Hypersensitivity ◽  
Similar Extent ◽  
Static Compliance ◽  
Lung Volumes ◽  
Lung Capacity ◽  
In Vivo Effects ◽  
Gas Volume

The effects of intravenous antigen infusion on lung volumes and quasi-static deflationary pulmonary compliance in guinea pigs previously sensitized to ovalbumin were studied in vivo. Ovalbumin infusion significantly increased minimal gas volume to a similar extent in animals with intact or cut vagi. Total lung capacity fell only in animals with intact vagi. Quasi-static compliance fell in both groups of animals, but the fall was significantly greater in animals with intact vagi. These data demonstrate that immediate hypersensitivity reactions alter lung volumes and the elastic properties of the lung by both vagal dependent and vagal independent mechanisms.

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