scholarly journals The mechanics of the lung parenchyma and airway responsiveness to metacholine

2004 ◽  
Vol 61 (4) ◽  
Author(s):  
F.G. Salerno ◽  
O. Resta ◽  
M.P. Foschino-Barbaro ◽  
A. Spanevello
Keyword(s):  
Mechanical Properties ◽  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Muscle Activation ◽  
Mechanical Load ◽  
Lung Parenchyma ◽  
Smooth Muscle Contraction ◽  
Airway Narrowing

The lung parenchyma is anatomically and mechanically connected to the intraparenchymal airways. Due to forces of interdependence the lung parenchyma represents a mechanical load that opposes bronchial narrowing during airway smooth muscle activation. The mechanical load caused by the parenchyma is a function of the number of the alveolar attachments to the airways, and of the mechanical properties of the parenchyma. The extracellular matrix is a major component of the lung parenchyma responsible of most of its mechanical properties. The excessive airway narrowing observed in the asthmatic population may be the consequence of the altered mechanical properties of the extracellular matrix reducing the mechanical load that opposes airway smooth muscle contraction.

scholarly journals The extracellular matrix of the lung and airway responsiveness in asthma

2016 ◽  
Vol 71 (1) ◽  
Author(s):  
F.G. Salerno ◽  
M.P. Foschino Barbaro ◽  
O. Toungoussova ◽  
E. Carpagnano ◽  
P. Guido ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Mechanical Load ◽  
Bronchial Hyperresponsiveness ◽  
Lung Parenchyma ◽  
Smooth Muscle Contraction ◽  
Airway Remodelling ◽  
Airway Narrowing ◽  
Matrix Deposition ◽  
Airways Smooth Muscle

The extracellular matrix is the main determinant of the structure and of mechanical behaviour of the lung. The extracellular matrix is also responsible for the mechanical interdependence between airway and parenchyma due to the alveolar attachments to the airways. Asthma is characterized by bronchial hyperresponsiveness, airway remodelling and inflammation, and an altered extracellular matrix may play a role in all these functional and structural abnormalities. The excessive airway narrowing observed in asthma may be related to the altered viscoelastic properties of lung parenchyma and airway wall, determining a decrease in the mechanical load opposing the airways’ smooth muscle contraction. Indeed, an altered extracellular matrix deposition in asthma in humans, has been demonstrated. In addition, in the asthmatic lung, the matrix seems to contribute to airway inflammation, airway remodelling, and to those alterations of the smooth muscle function of the airway and morphology typical of asthma.

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.

Blockade of eosinophil migration by 5-lipoxygenase and cyclooxygenase inhibition in explanted guinea pig trachealis

1995 ◽  
Vol 268 (3) ◽  
pp. L446-L454 ◽  
Author(s):  
N. M. Munoz ◽  
A. R. Leff
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Cyclooxygenase Inhibition ◽  
Airway Narrowing ◽  
Eosinophil Migration ◽  
Eosinophil Chemotaxis ◽  
Physical Consequences

We studied the effects of 5-lipoxygenase inhibition with A63162 and cyclooxygenase inhibition with indomethacin (INDO) on 1) eosinophil chemotaxis and 2) airway narrowing caused by 10(-6) M formyl-Met-Leu-Phe (fMLP) in tracheal explants from guinea pigs. Airway narrowing was assessed by calibrated micrometry, and eosinophil migration from the lamina propria was expressed as number of eosinophils contained per 1 cm tracheal segment. After 120 min, treatment with fMLP caused an increase in luminal eosinophils from 6,804 +/- 1,786 to 303,347 +/- 75,609 cells (P < 0.001); airway diameter narrowed by 20.4 +/- 1.4%. In six preparations, A63162 inhibited airway narrowing caused by fMLP by 54.9 +/- 6.1%; INDO had a similar effect on airway diameter. However, maximal inhibition of eosinophil migration was greater after 10(-6) M A63162 (38,393 +/- 7,434 cells; P < 0.001 vs. fMLP alone) than after treatment with 10(-5) M INDO (123,547 +/- 19,499 cells; P < 0.05). We demonstrate a method that permits simultaneous measurements of eosinophil migration and airway smooth muscle contraction in a guinea pig tracheal explant preparation. Our data suggest that eosinophil chemotaxis and changes in internal airway diameter are caused by activation of both 5-lipoxygenase and cyclooxygenase pathways and that cell migration is independent of the physical consequences of airway smooth muscle contraction.

Lower airway smooth muscle contraction induced by (red tide) toxin

1987 ◽  
Vol 79 (6) ◽  
pp. 899-908 ◽  
Author(s):  
T SHIMODA ◽  
J KRZANOWSKI ◽  
R LOCKEY ◽  
D MARTIN ◽  
M PEREZCRUET ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Red Tide ◽  
Smooth Muscle Contraction ◽  
Lower Airway

scholarly journals Allergic sensitization enhances the contribution of Rho-kinase to airway smooth muscle contraction

2004 ◽  
Vol 143 (4) ◽  
pp. 477-484 ◽  
Author(s):  
Dedmer Schaafsma ◽  
Reinoud Gosens ◽  
I Sophie T Bos ◽  
Herman Meurs ◽  
Johan Zaagsma ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Allergic Sensitization ◽  
Rho Kinase ◽  
Smooth Muscle Contraction
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