Tissue elastance influences airway smooth muscle shortening: comparison of mechanical properties among different species

2002 ◽  
Vol 80 (9) ◽  
pp. 865-871 ◽  
Author(s):  
Anabelle M. Opazo Saez ◽  
R Robert Schellenberg ◽  
Mara S Ludwig ◽  
Richard A Meiss ◽  
Peter D Paré
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Isometric Force ◽  
Published Data ◽  
Passive Tension ◽  
Active Force ◽  
Muscle Shortening ◽  
Human Airways ◽  
Tissue Elastance

We have observed striking differences in the mechanical properties of airway smooth muscle preparations among different species. In this study, we provide a novel analysis on the influence of tissue elastance on smooth muscle shortening using previously published data from our laboratory. We have found that isolated human airways exhibit substantial passive tension in contrast to airways from the dog and pig, which exhibit little passive tension (<5% of maximal active force versus ~60% for human bronchi). In the dog and pig, airway preparations shorten up to 70% from Lmax (the length at which maximal active force occurs), whereas human airways shorten by only ~12% from Lmax. Isolated airways from the rabbit exhibit relatively low passive tension (~22% Fmax) and shorten by 60% from Lmax. Morphologic evaluation of airway cross sections revealed that 25-35% of the airway wall is muscle in canine, porcine, and rabbit airways in contrast to ~9% in human airway preparations. We postulate that the large passive tension needed to stretch the muscle to Lmax reflects the high connective tissue content surrounding the smooth muscle, which limits shortening during smooth muscle contraction by imposing an elastic load, as well as by causing radial constraint.Key words: isometric force, isotonic shortening, elastance.

Mechanisms for the mechanical response of airway smooth muscle to length oscillation

1997 ◽  
Vol 83 (3) ◽  
pp. 731-738 ◽  
Author(s):  
X. Shen ◽  
M. F. Wu ◽  
R. S. Tepper ◽  
S. J. Gunst
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Mechanical Response ◽  
Muscle Tone ◽  
Isometric Force ◽  
Muscle Length ◽  
Contractile Element ◽  
Active Force ◽  
Cross Bridge

Shen, X., M. F. Wu, R. S. Tepper, and S. J. Gunst. Mechanisms for the mechanical response of airway smooth muscle to length oscillation. J. Appl. Physiol. 83(3): 731–738, 1997.—Airway smooth muscle tone in vitro is profoundly affected by oscillations in muscle length, suggesting that the effects of lung volume changes on airway tone result from direct effects of stretch on the airway smooth muscle. We analyzed the effect of length oscillation on active force and length-force hysteresis in canine tracheal smooth muscle at different oscillation rates and amplitudes during contraction with acetylcholine. During the shortening phase of the length oscillation cycle, the active force generated by the smooth muscle decreased markedly below the isometric force but returned to isometric force as the muscle was lengthened. Results indicate that at rates comparable to those during tidal breathing, active shortening and yielding of contractile elements contributes to the modulation of force during length oscillation; however, the depression of force during shortening cannot be accounted for by cross-bridge properties, shortening-induced cross-bridge deactivation, or active relaxation. We conclude that the depression of contractility may be a function of the plasticity of the cellular organization of contractile filaments, which enables contractile element length to be reset in relation to smooth muscle cell length as a result of smooth muscle stretch.

Cardiotrophin-1 alters airway smooth muscle structure and mechanical properties in airway explants

2004 ◽  
Vol 287 (6) ◽  
pp. L1165-L1171 ◽  
Author(s):  
Xueyan Zheng ◽  
Danyi Zhou ◽  
Chun Y. Seow ◽  
Tony R Bai
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Structural Changes ◽  
Treated Group ◽  
Structural Features ◽  
Passive Tension ◽  
Airway Wall ◽  
Optimal Length ◽  
Functional Changes

Induction of hypertrophy and inhibition of apoptosis may be important mechanisms contributing to increased airway smooth muscle (ASM) mass in asthma. Data from our laboratory indicate that cardiotrophin-1 (CT-1) induces hypertrophy and inhibits apoptosis in isolated human ASM cells. To determine whether these novel effects of CT-1 also occur in the airway tissue milieu and to determine whether structural changes are accompanied by functional changes, matched pairs of guinea pig airway explants were treated with or without CT-1 for 7 days, and structural features as well as isometric and isotonic contractile and relaxant mechanical properties were measured. CT-1 (0.2–5 ng/ml) increased both myocyte mass and extracellular matrix in a concentration-dependent fashion. CT-1 (10 ng/ml)-treated tissues exhibited a significant increase in passive tension at all lengths on day 7; at optimal length, passive tension generated by CT-1-treated tissues was 1.72 ± 0.12 vs. 1.0 ± 0.1 g for control. Maximal isometric stress was decreased in the CT-1-treated group on day 7 (0.39 ± 0.10 kg/cm2) vs. control (0.77 ± 0.15 kg/cm2, P < 0.05). Isoproterenol-induced relaxant potency was reduced in CT-1-treated tissues, log EC50 being −7.28 ± 0.34 vs. −8.12 ± 0.25 M in control, P < 0.05. These data indicate that CT-1 alters ASM structural and mechanical properties in the tissue environment and suggest that structural changes found in the airway wall in asthma are not necessarily associated with increased responsiveness.

Myosin thick filament lability induced by mechanical strain in airway smooth muscle

2001 ◽  
Vol 90 (5) ◽  
pp. 1811-1816 ◽  
Author(s):  
Kuo-Hsing Kuo ◽  
Lu Wang ◽  
Peter D. Paré ◽  
Lincoln E. Ford ◽  
Chun Y. Seow
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Cross Sections ◽  
Structural Changes ◽  
Isometric Force ◽  
Mechanical Strain ◽  
Thick Filament ◽  
Functional Changes ◽  
Thick Filaments ◽  
Length Changes

Airway smooth muscle adapts to different lengths with functional changes that suggest plastic alterations in the filament lattice. To look for structural changes that might be associated with this plasticity, we studied the relationship between isometric force generation and myosin thick filament density in cell cross sections, measured by electron microscope, after length oscillations applied to the relaxed porcine trachealis muscle. Muscles were stimulated regularly for 12 s every 5 min. Between two stimulations, the muscles were submitted to repeated passive ±30% length changes. This caused tetanic force and thick-filament density to fall by 21 and 27%, respectively. However, in subsequent tetani, both force and filament density recovered to preoscillation levels. These findings indicate that thick filaments in airway smooth muscle are labile, depolymerization of the myosin filaments can be induced by mechanical strain, and repolymerization of the thick filaments underlies force recovery after the oscillation. This thick-filament lability would greatly facilitate plastic changes of lattice length and explain why airway smooth muscle is able to function over a large length range.

Mechanical properties of human bronchial smooth muscle in vitro

1992 ◽  
Vol 73 (4) ◽  
pp. 1481-1485 ◽  
Author(s):  
K. Ishida ◽  
P. D. Pare ◽  
J. Hards ◽  
R. R. Schellenberg
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Electrical Field Stimulation ◽  
Tracheal Smooth Muscle ◽  
Cross Sectional ◽  
Velocity Of Shortening ◽  
Muscle Shortening ◽  
Tension Generation ◽  
Very High

The in vitro mechanical properties of smooth muscle strips from 10 human main stem bronchi obtained immediately after pneumonectomy were evaluated. Maximal active isometric and isotonic responses were obtained at varying lengths by use of electrical field stimulation (EFS). At the length (Lmax) producing maximal force (Pmax), resting tension was very high (60.0 +/- 8.8% Pmax). Maximal fractional muscle shortening was 25.0 +/- 9.0% at a length of 75% Lmax, whereas less shortening occurred at Lmax (12.2 +/- 2.7%). The addition of increasing elastic loads produced an exponential decrease in the shortening and velocity of shortening but increased tension generation of muscle strips stimulated by EFS. Morphometric analysis revealed that muscle accounted for 8.7 +/- 1.5% of the total cross-sectional tissue area. Evaluation of two human tracheal smooth muscle preparations revealed mechanics similar to the bronchial preparations. Passive tension at Lmax was 10-fold greater and maximal active shortening was threefold less than that previously demonstrated for porcine trachealis by us of the same apparatus. We attribute the limited shortening of human bronchial and tracheal smooth muscle to the larger load presumably provided by a connective tissue parallel elastic component within the evaluated tissues, which must be overcome for shortening to occur. We suggest that a decrease in airway wall elastance could increase smooth muscle shortening, leading to excessive responses to contractile agonists, as seen in airway hyperresponsiveness.

Airway basement membrane perimeter in human airways is not a constant; potential implications for airway remodeling in asthma

2004 ◽  
Vol 97 (2) ◽  
pp. 556-563 ◽  
Author(s):  
Brent E. McParland ◽  
Peter D. Paré ◽  
Peter R. A. Johnson ◽  
Carol L. Armour ◽  
Judith L. Black
Keyword(s):  
Smooth Muscle ◽  
Basement Membrane ◽  
Airway Smooth Muscle ◽  
Muscle Tone ◽  
Airway Remodeling ◽  
Organ Bath ◽  
Smooth Muscle Tone ◽  
Asthmatic Patients ◽  
Constant Potential ◽  
Human Airways

Many studies that demonstrate an increase in airway smooth muscle in asthmatic patients rely on the assumption that bronchial internal perimeter ( Pi) or basement membrane perimeter ( Pbm) is a constant, i.e., not affected by fixation pressure or the degree of smooth muscle shortening. Because it is the basement membrane that has been purported to be the indistensible structure, this study examines the assumption that Pbm is not affected by fixation pressure. Pbm was determined for the same human airway segment ( n = 12) fixed at distending pressures of 0 cmH2O and 21 cmH2O in the absence of smooth muscle tone. Pbm for the segment fixed at 0 cmH2O was determined morphometrically, and the Pbm for the same segment, had the segment been fixed at 21 cmH2O, was predicted from knowing the luminal volume and length of the airway when distended to 21 cmH2O (organ bath-derived Pi). To ensure an accurate transformation of the organ bath-derived Pi value to a morphometry-derived Pbm value, had the segment been fixed at 21 cmH2O, the relationship between organ bath-derived Pi and morphometry-derived Pbm was determined for five different bronchial segments distended to 21 cmH2O and fixed at 21 cmH2O ( r2 = 0.99, P < 0.0001). Mean Pbm for bronchial segments fixed at 0 cmH2O was 9.4 ± 0.4 mm, whereas mean predicted Pbm, had the segments been fixed at 21 cmH2O, was 14.1 ± 0.5 mm ( P < 0.0001). This indicates that Pbm is not a constant when isolated airway segments without smooth muscle tone are fixed distended to 21 cmH2O. The implication of these results is that the increase in smooth muscle mass in asthma may have been overestimated in some previous studies. Therefore, further studies are required to examine the potential artifact using whole lungs with and without abolition of airway smooth muscle tone and/or inflation.

Relation between length, isometric force, and O2 consumption rate in vascular smooth muscle

1975 ◽  
Vol 228 (3) ◽  
pp. 915-922 ◽  
Author(s):  
RJ Paul ◽  
JW Peterson
Keyword(s):  
Smooth Muscle ◽  
Oxygen Consumption ◽  
Oxygen Consumption Rate ◽  
Consumption Rate ◽  
Isometric Force ◽  
Chemical Energy ◽  
Energy Utilization ◽  
Passive Tension ◽  
Basal Rate ◽  
Length Dependence

The length-tension and length-oxygen consumption rate relationships were studied in bovine mesenteric vein at 37 degrees C. The absence of spontaneous mechanical activity permits straightforward interpretation in terms of active (smooth muscle) and passive components of the vein wall. Longitudinal loops, the predominant smooth muscle component being oriented in the longitudinal (axial) direction, were maximally stimulated using epinephrine (2-5 mug-ml-1). An optimum length for isometric tension development was exhibited at which the passive tension was 25% of the total tension. The population regression indicated that tension was developed at lengths which ranged from 0.33 to 1.41 times the length at which maximum tension was developed. Oxygen consumption was measured using a Clark-type polarographic electrode. Basal oxygen consumption was 0.432 plus or minus 0.014 (n equal to 121) mumol-min-1 (g dry wt)-1. The basal rate was found to be independent of the passive tension. Under conditions of maximal stimulation, the oxygen consumption rate at L-o, the resting length at which the tissue maintained 1 g-wt passive tension, was approximately twice the basal rate. The length dependence of the suprabasal oxygen consumption was parallel to that of the active isometric force. This parallel relation reflected a linear relation between active isometric force (deltaP-o) and suprabasal oxygen consumption rate (deltaJ-o2). The slope of the deltaJ-o2-deltaP-o linear regression was 0.142 plus or minus 0.013 nmol O2-MIN-1 (G-WT-CM)-1. DeltaJ-o2 at the minimum contracted length, at which no active force was developed, was 15-20% of the deltaJ-o2 measured when maximum isometric force was developed. This provides an upper bound to the rate of chemical energy utilization required for activation processes. The length dependence of active isometric force and chemical energy utilization is most simply interpreted in terms of a sliding-filament model.

Specific reaginic antibody IgG1-induced changes of airway smooth muscle cells

1988 ◽  
Vol 65 (2) ◽  
pp. 767-775 ◽  
Author(s):  
M. Souhrada ◽  
J. F. Souhrada
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Isometric Force ◽  
Airway Smooth Muscle Cells ◽  
Base Line ◽  
Dependent Relationship ◽  
Reaginic Antibody ◽  
Induced Changes ◽  
Igg1 Concentration

It was found that 1) an administration of both immunoglobulin G1 (IgG1) or immunized serum caused an immediate depolarization and an increase in the isometric force of airway smooth muscle (ASM) cells, followed by a sustained hyperpolarization and a return of the tone to the base-line values; 2) an IgG1 concentration-dependent relationship was found between a peak depolarization, a peak hyperpolarization, and a peak isometric force; for these events 50% effective dose (ED50) was found to be 0.17, 0.14, and 0.25 microgram/ml of IgG1, respectively; 3) both electrical and contractile responses to ovalbumin of ASM cells sensitized with IgG1 were also dependent on the concentration of IgG1; the ED50 values of this relationship were 0.27 and 0.25 micrograms/ml of IgG1, respectively; 4) amiloride (10(-8) to 10(-5) M) pretreatment and a sodium-deficient environment attenuated sensitized-induced electrical and contractile changes as well as the response of ASM to ovalbumin (0.1%); and 5) pretreatment of ASM with diphenhydramine (10(-5) M) or FPL 55712 (10(-6) M) had no effect on sensitization-induced changes in membrane potential but attenuated electrical and contractile response of ASM to ovalbumin (0.1%).

In vivo loads on airway smooth muscle: the role of noncontractile airway structures

1992 ◽  
Vol 70 (4) ◽  
pp. 602-606 ◽  
Author(s):  
Philip Robinson ◽  
Mitsushi Okazawa ◽  
Tony Bai ◽  
Peter Paré
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Activation ◽  
Muscle Length ◽  
Tracheal Cartilage ◽  
Elastic Load ◽  
Muscle Shortening ◽  
Trachealis Muscle

The degree of airway smooth muscle contraction and shortening that occurs in vivo is modified by many factors, including those that influence the degree of muscle activation, the resting muscle length, and the loads against which the muscle contracts. Canine trachealis muscle will shorten up to 70% of starting length from optimal length in vitro but will only shorten by around 30% in vivo. This limitation of shortening may be a result of the muscle shortening against an elastic load such as could be applied by tracheal cartilage. Limitation of airway smooth muscle shortening in smaller airways may be the result of contraction against an elastic load, such as could be applied by lung parenchymal recoil. Measurement of the elastic loads applied by the tracheal cartilage to the trachealis muscle and by lung parenchymal recoil to smooth muscle of smaller airways were performed in canine preparations. In both experiments the calculated elastic loads applied by the cartilage and the parenchymal recoil explained in part the limitation of maximal active shortening and airway narrowing observed. We conclude that the elastic loads provided by surrounding structures are important in determining the degree of airway smooth muscle shortening and the resultant airway narrowing.Key words: elastic loads, tracheal cartilage, airway smooth muscle shortening.

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