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.

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.

scholarly journals Decreased airway narrowing and smooth muscle contraction in hyperresponsive pigs

2002 ◽  
Vol 93 (4) ◽  
pp. 1296-1300 ◽  
Author(s):  
Debra J. Turner ◽  
Peter B. Noble ◽  
Matthew P. Lucas ◽  
Howard W. Mitchell
Keyword(s):  
Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Porcine Model ◽  
Smooth Muscle Contraction ◽  
Airway Wall ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Airway Narrowing

Increased smooth muscle contractility or reduced smooth muscle mechanical loads could account for the excessive airway narrowing and hyperresponsiveness seen in asthma. These mechanisms were investigated by using an allergen-induced porcine model of airway hyperresponsiveness. Airway narrowing to electric field stimulation was measured in isolated bronchial segments, over a range of transmural pressures (0–20 cmH2O). Contractile responses to ACh were measured in bronchial segments and in isolated tracheal smooth muscle strips isolated from control and test (ovalbumin sensitized and challenged) pigs. Test airways narrowed less than controls ( P < 0.0001). Test pigs showed reduced contractility to ACh, both in isolated bronchi ( P < 0.01) and smooth muscle strips ( P < 0.01). Thus isolated airways from pigs exhibiting airway hyperresponsiveness in vivo are hyporesponsive in vitro. The decreased narrowing in bronchi from hyperresponsive pigs may be related to decreased smooth muscle contractility. These data suggest that mechanisms external to the airway wall may be important to the hyperresponsive nature of sensitized lungs.

Factors determining degree of inflation in intratracheally fixed rat lungs

1980 ◽  
Vol 48 (2) ◽  
pp. 389-393 ◽  
Author(s):  
G. Hayatdavoudi ◽  
J. D. Crapo ◽  
F. J. Miller ◽  
J. J. O'Neil
Keyword(s):  
Slow Rate ◽  
Total Lung Capacity ◽  
Formaldehyde Solution ◽  
Initial Flow ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Final Degree ◽  
Low Rate

The total lung capacity (TLC) of rats was measured in vivo and was compared to the displacement volume of the lungs following intratracheal fixation with glutaraldehyde or formaldehyde solution. When glutaraldehyde was used the speed of infusion of the fixative was an important factor in the final degree of lung inflation achieved. With a low rate of fixative infusion and a final pressure of 20 cm of fixative the glutaraldehyde-fixed lungs inflated to 55% TLC. With a high initial flow of glutaraldehyde and a final pressure of 20 cm of fixative the lungs inflated to 84% TLC. Fixation of lungs inside the intact chest wall was found to result in a higher degree of inflation. With a reservoir height of 20 cm and a low rate of fixative infusion lungs fixed in situ reached 74% TLC, whereas lungs fixed in situ, but from animals that have been exsanguinated prior to fixation, inflated to only 58% TLC. This suggests that the volume of the blood in the lungs prior to infusion of glutaraldehyde influences the degree of inflation achieved. Formaldehyde-fixed lungs required 72 h to be completely fixed and they were inflated to 90% TLC when a reservoir height of 20 cm was used. Because of the slow rate of fixation using with formaldehyde solution the rate of infusion was found not to limit the degree of inflation that could be achieved.

Effects of lung volume, bronchoconstriction, and cigarette smoke on morphometric airway dimensions

1988 ◽  
Vol 64 (3) ◽  
pp. 913-919 ◽  
Author(s):  
A. L. James ◽  
P. D. Pare ◽  
J. C. Hogg
Keyword(s):  
Smooth Muscle ◽  
Cigarette Smoke ◽  
Lung Volume ◽  
Muscle Tone ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Airway Wall ◽  
Lung Inflation ◽  
Wall Area ◽  
Airway Dimensions

To examine the role of airway wall thickening in the bronchial hyperresponsiveness observed after exposure to cigarette smoke, we compared the airway dimensions of guinea pigs exposed to smoke (n = 7) or air (n = 7). After exposure the animals were anesthetized with urethan, pulmonary resistance was measured, and the lungs were removed, distended with Formalin, and fixed near functional residual capacity. The effects of lung inflation and bronchoconstriction on airway dimensions were studied separately by distending and fixing lungs with Formalin at total lung capacity (TLC) (n = 3), 50% TLC (n = 3), and 25% TLC (n = 3) or near residual volume after bronchoconstriction (n = 3). On transverse sections of extraparenchymal and intraparenchymal airways the following dimensions were measured: the internal area (Ai) and internal perimeter (Pi), defined by the epithelium, and the external area (Ae) and external perimeter (Pe), defined by the outer border of smooth muscle. Airway wall area (WA) was then calculated, WA = Ae - Ai. Ai, Pe, and Ae decreased with decreasing lung volume and after bronchoconstriction. However, WA and Pi did not change significantly with lung volume or after bronchoconstriction. After cigarette smoke exposure airway resistance was increased (P less than 0.05); however, there was no difference in WA between the smoke- and air-exposed groups when the airways were matched by Pi. We conclude that Pi and WA are constant despite changes in lung volume and smooth muscle tone and that airway hyperresponsiveness induced by cigarette smoke is not mediated by increased airway wall thickness.

scholarly journals Dynamic equilibration of airway smooth muscle contraction during physiological loading

2002 ◽  
Vol 92 (2) ◽  
pp. 771-779 ◽  
Author(s):  
Jeanne Latourelle ◽  
Ben Fabry ◽  
Jeffrey J. Fredberg
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Experimental Method ◽  
Airway Smooth Muscle ◽  
Muscle Length ◽  
Transpulmonary Pressure ◽  
Smooth Muscle Contraction ◽  
Control Force ◽  
Airway Narrowing

Airway smooth muscle contraction is the central event in acute airway narrowing in asthma. Most studies of isolated muscle have focused on statically equilibrated contractile states that arise from isometric or isotonic contractions. It has recently been established, however, that muscle length is determined by a dynamically equilibrated state of the muscle in which small tidal stretches associated with the ongoing action of breathing act to perturb the binding of myosin to actin. To further investigate this phenomenon, we describe in this report an experimental method for subjecting isolated muscle to a dynamic microenvironment designed to closely approximate that experienced in vivo. Unlike previous methods that used either time-varying length control, force control, or time-invariant auxotonic loads, this method uses transpulmonary pressure as the controlled variable, with both muscle force and muscle length free to adjust as they would in vivo. The method was implemented by using a servo-controlled lever arm to load activated airway smooth muscle strips with transpulmonary pressure fluctuations of increasing amplitude, simulating the action of breathing. The results are not consistent with classical ideas of airway narrowing, which rest on the assumption of a statically equilibrated contractile state; they are consistent, however, with the theory of perturbed equilibria of myosin binding. This experimental method will allow for quantitative experimental evaluation of factors that were previously outside of experimental control, including sensitivity of muscle length to changes of tidal volume, changes of lung volume, shape of the load characteristic, loss of parenchymal support and inflammatory thickening of airway wall compartments.

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.

Differences in airway structure in immature and mature rabbits

2000 ◽  
Vol 89 (4) ◽  
pp. 1310-1316 ◽  
Author(s):  
R. Ramchandani ◽  
X. Shen ◽  
C. L. Elmsley ◽  
W. T. Ambrosius ◽  
S. J. Gunst ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Lower Percentage ◽  
Airway Wall ◽  
Airway Narrowing ◽  
Wall Area ◽  
Lung Capacity ◽  
Airway Wall Thickness ◽  
Structural Differences ◽  
Airway Walls ◽  
Formalin Fixed

Our laboratory has previously demonstrated that maximal bronchoconstriction produces a greater degree of airway narrowing in immature than in mature rabbit lungs (33). To determine whether these maturational differences could be related to airway structure, we compared the fraction of the airway wall occupied by airway smooth muscle (ASM) and cartilage, the proportion of wall area internal to ASM, and the number of alveolar attachments to the airways, from mature and immature (6-mo- and 4-wk-old, respectively) rabbit lungs that were formalin fixed at total lung capacity. The results demonstrate that the airway walls of immature rabbits had a greater percentage of smooth muscle, a lower percentage of cartilage, and fewer alveolar attachments compared with mature rabbit airways; however, we did not find maturational differences in the airway wall thickness relative to airway size. We conclude that structural differences in the airway wall may contribute to the greater airway narrowing observed in immature rabbits during bronchoconstriction.

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.

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