The biomechanical properties of connective tissues are critical determinants of how mechanical forces acting on the body/organ produce physical changes at the cellular level. The Biomechanical properties of lung are discussed

1. TISSUE BIOMECHANICS IN LUNG
DISEASES
Dr. HINA VAISH(PT)
Assistant Professor
MMIPRM, MM(DU)
Mullana, Ambala

2. Biomechanical Properties of lung
Parenchyma
• The biomechanical properties of connective tissues
are critical determinants of how mechanical forces
acting on the body/organ produce physical changes
at the cellular level.
Biomechanical properties of lung are:
• Elastance and Resistance
• Viscoelasticity
• Stress-Strain Relationship
• Stress-Bearing Elements: Mechanical Contributions
of Elastin, Collagen, Fiber Network, and Interstitial
Cells

3. • The act of breathing entails the cyclic
application of physical stresses at the pleural
surface as well as the transmission of those
stresses throughout the lung tissue and its
adherent cells .
• The applied stresses result in length changes
of parenchymal structures (strain), yielding
volume variation.

4. • To support extreme strain variations, while
maintaining the minimal tissue diffusional
barrier necessary for adequate gas exchange,
lung parenchyma presents important stress-
bearing systems, including the gas-liquid
interface, the connective tissue matrix, and
the contractile apparatus .
• These stress-bearing elements can be
significantly changed during pathological
states, thus affecting lung mechanics

5. Lung Parenchyma Remodeling:
Micromechanics of Injured Lungs
• During disease states, small-scale heterogeneity in
mechanical properties (such as local shear moduli)
increases considerably, which contributes
importantly to local stress distributions (1).
• The determinants of the lung parenchymal stress and
strain distributions in the intact thorax depend
critically on the lung resistance to a shape change.
1.Pulmonary micromechanics of injured lungs. In: Lung Biology in Health and Disease. Ventilator-Induced Lung
Injury, edited by C. Lenfant. Bethesda, MD: Am. Physiol. Soc., 2006, vol. 215, chapt. 2, p. 21–44.

6. Several mechanisms have been suggested to
explain the larger shear modulus of injured
lungs, such as
• interfacial tensions associated with alveolar
exudates
• increased surface tension
• increased prestress of the axial elastin and
collagen network
• interstitial edema and matrix remodeling, and
scar formation and fibrosis .
1.Pulmonary micromechanics of injured lungs. In: Lung Biology in Health and Disease. Ventilator-Induced Lung
Injury, edited by C. Lenfant. Bethesda, MD: Am. Physiol. Soc., 2006, vol. 215, chapt. 2, p. 21–44.

7. • Damaged lungs present two attributes that
account for their increased risk of deformation
injury.
• First, the number of airspaces capable of
expanding during inspiration diminishes
(“baby lung”), increasing the risk of injury
from regional overexpansion, since units that
do not expand during breathing undergo a
stronger deforming stress (1).
1.Gattinoni L, Pesenti A, Avalli L, Rossi F, Bombino M. Pressure-volume curve of total respiratory system in
acute respiratory failure. Computed tomographic scan study. Am Rev Respir Dis 136: 730–736, 1987.

8. • Second, local impedance to lung expansion is
heterogeneous because of uneven distribution
of liquid and surface tension in distal
airspaces, which generates shear stress
between neighboring, interdependent units
that operate at different volumes (2).
2.MeadJ, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol 28: 596–608,
1970

9. • Subpleural alveoli of edematous isolated rat
lungs present wavy, flooded walls and contain
air pockets of different sizes and shapes (1).
The presence of differently sized air pockets
with diverse radii of curvature implies a
nonuniform alveolar gas pressure and/or
uneven surface tensions .
1.Hubmayr RD. Perspective on lung injury and recruitment: a skeptical look at the opening and collapse story. Am J
Respir Crit Care Med 165: 1647–1653, 2002.

10. • Bachofen and co-workers (1) suggested that
regional differences in the physicochemical
properties of the surfactant could be the
source of the nonuniform surface tension.
• A maintained nonuniform alveolar gas
pressure may suggest that the air pockets are
trapped by liquid and foam in conducting
airways (2).
1.Bachofen H, Schurch S, Michel RP, Weibel ER. Experimental hydrostatic pulmonary edema in rabbit lungs. Am Rev Respir Dis
147: 989–996, 1993.
2.Pulmonary micromechanics of injured lungs. In: Lung Biology in Health and Disease. Ventilator-Induced Lung Injury, edited by
C. Lenfant. Bethesda, MD: Am. Physiol. Soc., 2006, vol. 215, chapt. 2, p. 21–44.
↵

11. • The phenomenon of interdependence
between elements of the lung parenchyma
network, which promotes uniform expansion
of individual units.
• Stress increases whenever the sum of forces
of the surrounding tissue acts over a smaller
surface area.

12. • Consequently, when an obstructed unit (e.g.,
an alveolus, a lobule, or a lung segment)
resists expansion, the neighboring units exert
a large inflationary stress on it.
• Moreover, the tension and strain of individual
connective tissue elements onto the collapsed
segment increase out of proportion in relation
to those of more remote network structures.

13. • Indeed, the elastic system, a major
component of the extracellular matrix, that
plays an important role in maintaining the
patency of the airways and lung elastic recoil
is also altered, with elastic fiber deposition,
both in human lung fibrosis (1).
• On the other hand, increased elastin
destruction occurs in certain pathological
conditions owing to the release of powerful
elastolytic proteases by inflammatory cells .
1.Negri EM, Montes GS, Saldiva PHN, Capelozzi VL. Architectural remodelling in acute and chronic interstitial lung
disease: fibrosis or fibroelastosis? Histopathology 37: 393–401, 2000.
2.

14. • Analysis by histochemistry demonstrated that
lung collagen content augments in both acute
and chronic interstitial diseases, suggesting
that significant remodeling of alveolar tissue
occurs even in acute situations (1).
• The extracellular matrix remodeling process
occurs as a response to lung injury involving
all of its components in a kind of chain
reaction.
1.Saldiva PHN, Delmonte VC, Carvalho CRR, Kairalla RA, Auler JOC Jr. Histochemical evaluation of lung collagen
content in acute and chronic interstitial diseases. Chest 95: 953–957, 1989

15. • Reactivation of elastin synthesis occurs in
response to increased destruction, but in a
disordered manner.
• Thus elastosis could also partially respond for
the loss of the normal architecture of the
alveolar walls, contributing to the alveolar
mechanical dysfunction and remodeling
present in acute and chronic interstitial lung
diseases (1).
1.Negri EM, Montes GS, Saldiva PHN, Capelozzi VL. Architectural remodelling in acute and chronic interstitial lung
disease: fibrosis or fibroelastosis? Histopathology 37: 393–401, 2000

16. • The small leucine-rich proteoglycan decorin
regulates collagen fibril formation and spatial
arrangement in the matrix (1).
• Thus decorin may also play a role in the
remodeling associated with respiratory
diseases such as pulmonary fibrosis and
asthma .
• The alterations in tissue properties are likely
the result of abnormal collagen fibril
formation .
1.Iozzo RV. The family of the small leucine-rich proteoglycans: key regulators of matrix assembly and cellular
growth. Crit Rev Biochem Mol Biol 32: 141–174, 1997.

17. • Mechanical forces applied to normal lung
parenchyma, such as during mechanical ventilation,
can also induce structural and functional changes (1).
• Lung cells submitted to different types of force
produce proinflammatory mediators (2).
• In addition, mechanical forces induce expression of
extracellular matrix proteins by lung tissue (3,4).
1.Breen EC. Mechanical strain increases type I collagen expression in pulmonary fibroblasts in vitro. J Appl Physiol 88:
203–209, 2000.
2. Vlahovic G, Russel ML, Mercer RR, Crapo JD. Cellular and connective tissue changes in alveolar septal wall in
emphysema. Am J Respir Crit Care Med 160: 2086–2092, 1999.
3. Swartz MA, Tschumperlin DJ, Kamm RD, Drazen JM. Mechanical stress is communicated between different cell types to
elicit matrix remodelling. Proc Natl Acad Sci USA 22: 6180–6185, 2001.
4. Breen EC. Mechanical strain increases type I collagen expression in pulmonary fibroblasts in vitro. J Appl Physiol 88:
203–209, 2000.

18. • Tepper et al. (1) demonstrated, in isolated
rabbit intrapulmonary bronchial segments and
lung parenchymal tissue slices, that the
imposition of physiological levels of chronic
mechanical strain resulted in significant
changes in the passive and active physiological
responses of these tissues.
1.Tepper RS, Ramchandani R, Argay E, Zhang L, Xue Z, Liu Y, Gunst SJ. Chronic strain alters the passive and contractile
properties of rabbit airways. J Appl Physiol 98: 1949–1954, 2005

19. • The absence of chronic strain on
intraparenchymal airways resulted in smaller,
stiffer airways that generated greater
pressures and narrowed to a greater extent in
response to contractile stimulation than
airways that had been subjected to chronic
strain.
• In addition, the effects of strain were most
prominent in the smaller, more compliant
airways.

20. • Evidences gathered from lung parenchymal
strip oscillation disclosed that tissue elastance
and resistance augmented with increasing
operating force and decreased with increasing
amplitude.
• Additionally, a rise in force induced early
tissue remodeling (1). In this model, force and
amplitude variations simulate in vivo pressure
and volume changes, respectively ).
1.Garcia CSNB, Rocco PRM, Facchinetti LD, Lassance RM, Caruso P, Deheinzelin D, Morales MM, Romero PV, Faffe
DS, Zin WA. What increases type III procollagen mRNA levels in lung tissue: stress induced by changes in force or
amplitude? Respir Physiol Neurobiol 144: 59–70, 2004

21. • Moreover, pathophysiological conditions of
the lung may shift the balance of forces so as
to chronically alter the amount of strain
imposed on the airways (1,2).
1.Naghshin J, Wang L, Pare PD, Seow CY. Adaptation to chronic length change in explanted airway smooth muscle. J Appl
Physiol 95: 448–453, 2003.
2. Wang L, Pare PD, Seow CY. Effect of chronic passive length change on airway smooth muscle length-tension relationship. J
Appl Physiol 90: 734–740, 2001.

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