Biomedical subjects

D Stamenovic

Publications and source records attributed to D Stamenovic.

10 recordsLinked to original sources

PubMed1998

Is cytoskeletal tension a major determinant of cell deformability in adherent endothelial cells?

We tested the hypothesis that mechanical tension in the cytoskeleton (CSK) is a major determinant of cell deformability. To confirm that tension was present in adherent endothelial cells, we either cut or detached them from their basal surface by a microneedle. After cutting or detachment, the cells rapidly retracted. This retraction was prevented, however, if the CSK actin lattice was disrupted by cytochalasin D (Cyto D). These results confirmed that there was preexisting CSK tension in these cells and that the actin lattice was a primary stress-bearing component of the CSK. Second, to determine the extent to which that preexisting CSK tension could alter cell deformability, we developed a stretchable cell culture membrane system to impose a rapid mechanical distension (and presumably a rapid increase in CSK tension) on adherent endothelial cells. Altered cell deformability was quantitated as the shear stiffness measured by magnetic twisting cytometry. When membrane strain increased 2.5 or 5%, the cell stiffness increased 15 and 30%, respectively. Disruption of actin lattice with Cyto D abolished this stretch-induced increase in stiffness, demonstrating that the increased stiffness depended on the integrity of the actin CSK. Permeabilizing the cells with saponin and washing away ATP and Ca2+ did not inhibit the stretch-induced stiffening of the cell. These results suggest that the stretch-induced stiffening was primarily due to the direct mechanical changes in the forces distending the CSK but not to ATP- or Ca(2+)-dependent processes. Taken together, these results suggest preexisting CSK tension is a major determinant of cell deformability in adherent endothelial cells.

Cell Adhesion↗

PubMed1989

Chest wall impedance partitioned into rib cage and diaphragm-abdominal pathways.

We measured chest wall "pathway impedances" (ratios of pressure changes to rates of volume displacement at the surface) with esophageal and gastric balloons and inductance plethysmographic belts around the rib cage and abdomen during forced volume oscillations (5% vital capacity, 0.5-4 Hz) at the mouth of five relaxed, seated subjects. Volume displacements of the total chest wall surface, measured by summing the rib cage and abdominal signals, approximated measurements using volume-displacement, body plethysmography over the entire frequency range. Resistance (R) and elastance (E) of the diaphragm-abdomen pathway were several times greater than those of the rib cage pathway, except at the highest frequencies where diaphragm-abdominal E was small. R and E of the diaphragm-abdomen pathway and of the rib cage pathway showed the same frequency dependencies as that of the total chest wall: R decreased markedly as frequency increased, and E (especially in the diaphragm-abdomen) decreased at the highest frequencies. These results suggest that the chest wall can be reasonably modeled, over the frequency range studied, as a system with two major pathways for displacement. Each pathway seems to exhibit behavior that reflects nonlinear, rate-independent dissipation as well as viscoelastic properties. Impedances of these pathways are useful indexes of changes in chest wall mechanical behavior in different situations.

Abdomen↗

PubMed1989

On the imperfect elasticity of lung tissue.

This paper deals with a unifying hypothesis addressed at lung tissue resistance and its responses to neurohumoral and biophysical stimuli. The hypothesis holds that dissipative and elastic processes within lung tissue are coupled at the level of the stress-bearing element. Such a description leads naturally to consideration of a readily measured attribute of organ-level dissipative behavior called lung tissue hysteresivity, eta. On preliminary analysis this attribute is found to be nearly frequency independent and numerically conserved across species. To the degree that the numerical value of eta might be conserved during an intervention in which tissue dynamic elastance changes, such behavior would be consistent with the notion that elastic energy storage and dissipative energy loss reside within the very same stress-bearing element and, moreover, that those processes within the stress-bearing element bear an approximately fixed relationship. Tissue hysteresivity is closely related to the parameter K used by Bachofen and Hildebrandt (J. Appl. Physiol. 30: 493-497, 1971) to describe energy dissipation per cycle, and both lend themselves directly to interpretation based on processes ongoing at the levels of microstructure and molecule. Intraparenchymal connective tissues, surface film, and contractile elements appear to submit individually to this description and, in doing so, yield respective hysteresivities that are relatively well matched; this suggests that such hysteretic matching may be a necessary condition for synchronous expansion of the alveolar duct. The overriding simplicity with which this description organizes diverse observations implies that it may capture some unifying attribute of underlying mechanism.

Airway Resistance↗

PubMed1988

Elastic properties of air- and liquid-filled lung parenchyma.

Pressure-volume measurements and the punch indentation test are used to obtain the bulk modulus (kappa) and the shear modulus (mu) of lung parenchyma of air- and liquid-filled rabbit lungs. Plots of kappa and mu vs. transpulmonary pressure obtained from these measurements indicate that there is very little difference between the elastic behavior of the air- and liquid-filled lung, suggesting that the mechanism of resisting deformation in both cases is similar. On the other hand, from plots of kappa and mu vs. lung volume, it appears that the elastic moduli are higher in the air-filled lung than in the liquid-filled lung at the same volume. These differences, referred to as kappa gamma and mu gamma, as well as the difference in transpulmonary pressures (P gamma), are presumably due to the additional elastic recoil of the air-filled lung provided by alveolar surface tension (gamma). No conclusion could be reached about the shape of the kappa gamma vs. P gamma curve. However, the mu gamma vs. P gamma relationship appears to be approximately linear, with a slope of approximately 0.5. This result agrees qualitatively with the model (T. A. Wilson and H. Bachofen, J. Appl. Physiol. 52: 1064-1070, 1982) in which the part of the parenchyma that provides P gamma is pictured as mechanically analogous to an open cell liquid foam, having mu gamma = 0.4P gamma (J. Appl. Mech. Trans. ASME 51: 229-231, 1984), but it is statistically significant only at high lung volumes.

Air↗

PubMed1986

Surface forces in lungs. I. Alveolar surface tension-lung volume relationships.

Alveolar surface tension (gamma)-lung volume relationships were obtained for quasi-static and dynamic lung pressure-volume (PV) histories from measurements of PV curves of liquid- and air-filled excised rabbit lungs. PV relationships were measured at room temperature in lungs filled with test liquids with constant liquid-liquid interfacial tensions with alveolar surface-active materials; and air-filled lungs before and after the normal alveolar surface film was covered with test liquids with constant values of liquid- and air-liquid interfacial tensions. Interfacial tensions of test liquids were measured in a surface balance on monolayers of dipalmitoyl phosphatidylcholine. Values of gamma for the normal air-filled lung were obtained either from points of intersection between PV curves with the normal and test liquid interface or from a general relationship between gamma and the component of recoil pressure due to surface tension derived from the data. In contrast to previous analyses that have used PV measurements, this approach does not depend on assumptions about lung microstructural geometry. Surface tension-volume relationships for the normal air-filled lung show a prominent hysteresis with surface tension ranging from near 0 at low volumes during lung deflation to transiently high values near 40 dyn/cm during inflation; value of equilibrium surface tension (gamma EQ) near 28 dyn/cm; and characteristic transitions in surface film compressibility and associated transitions in film kinetic behavior in nonequilibrium film states where gamma deviates from gamma EQ. These features are consistent with the behavior predicted from current models of alveolar surface film behavior.

Animals↗

PubMed1986

Surface forces in lungs. II. Microstructural mechanics and lung stability.

Recent lung microstructural models describing interactions between alveolar surface tension (gamma) and forces in structural elements of the alveolar duct predict that the component of lung recoil pressure due to gamma (P gamma) is proportional to gamma/V1/3, where V is the total lung volume. This relation is tested against experimental data obtained from pressure-volume measurements of excised rabbit lungs with different constant values of gamma. It is found that for values of gamma less than approximately 18 dyn/cm the data generally agree with the model predictions. With higher values of gamma, a mismatch between the data and predictions first occurs at low and high volumes and then spreads over the entire volume range. The mismatch at the lower volumes coincides with the appearance of nonuniformities of lung expansion. The nonuniformities are characterized by a coexistence of under- and overexpanded regions of the parenchyma referred to as a mixture of phases. These nonuniformities, as well as a pressure-volume curve with a shape similar to the shape of measured curves, are predicted from an analysis of lung stability. Results of this work indicate that if the lung expands uniformly, P gamma proportional to gamma/V1/3 is a good approximation over a wide range of volumes. The stability analysis indicates that the equilibrium configurations of the lung parenchyma when gamma is independent of interfacial area and elevated above normal values are nonuniform states of expansion, characterizable as a mixture of phases. This result confirms that a dependence of gamma on surface area is normally required to achieve stable, uniform states of lung expansion.

Animals↗

PubMed1986

Surface forces in lungs. III. Alveolar surface tension and elastic properties of lung parenchyma.

The bulk modulus and the shear modulus describe the capacity of material to resist a change in volume and a change of shape, respectively. The values of these elastic coefficients for air-filled lung parenchyma suggest that there is a qualitative difference between the mechanisms by which the parenchyma resists expansion and shear deformation; the bulk modulus changes roughly exponentially with the transpulmonary pressure, whereas the shear modulus is nearly a constant fraction of the transpulmonary pressure for a wide range of volumes. The bulk modulus is approximately 6.5 times as large as the shear modulus. In recent microstructural modeling of lung parenchyma, these mechanisms have been pictured as being similar to the mechanisms by which an open cell liquid foam resists deformations. In this paper, we report values for the bulk moduli and the shear moduli of normal air-filled rabbit lungs and of air-filled lungs in which alveolar surface tension is maintained constant at 16 dyn/cm. Elevating surface tension above normal physiological values causes the bulk modulus to decrease and the shear modulus to increase. Furthermore, the bulk modulus is found to be sensitive to a dependence of surface tension on surface area, but the shear modulus is not. These results agree qualitatively with the predictions of the model, but there are quantitative differences between the data and the model.

Animals↗

PubMed1985

A strain energy function for lung parenchyma.

The strain energy for the air-filled lung is calculated from a model of the parenchymal microstructure. The energy is the sum of the surface energy and the elastic energies of two tissue components. The first of these is the peripheral tissue system that provides the recoil pressure of the saline-filled lung, and the second is the system of line elements that form the free edges of the alveolar walls bordering the alveolar ducts. The computed strain energy is consistent with the observed linear elastic behavior of parenchyma and the data on large deformations around blood vessels.

Air↗

PubMed1985

Regional lung strain in dogs during deflation from total lung capacity.

Regional lung distortion during deflation from total lung capacity to functional residual capacity (FRC) in intact supine and prone anesthetized dogs was determined from the displacement of multiple metallic markers embedded in the lung parenchyma. Distortion was expressed as strain (epsilon), which is related to fractional length changes. In the supine position, transverse strain (epsilon yy) was larger than vertical strain (epsilon xx) and cephalocaudal strain (epsilon zz) in the upper lobe. The FRC of the lower lobe was smaller than FRC of the upper lobe and all strains were larger, but epsilon zz increased most and became equal to epsilon yy. In the prone position, epsilon yy was largest in all upper lobes and in three of four lower lobes. Strains and volumes of the upper and lower lobes were similar. The upper and lower lobes rotated slightly around different axes, indicating that interpleural fissures allow additional degrees of freedom for the lungs to conform to the thoracic cavity. In the prone position, there were no consistent gradients of strain or volume. These results indicate that, in determining the regional distribution of FRC in the recumbent dog, in addition to the effect of gravity on the lung, there are important interactions between lung and thoracic cavity shapes.

Animals↗

PubMed1984

Mechanical properties of pleural membrane.

The pleural membrane is modeled as a planar collection of interconnected randomly oriented line elements. By assuming that the line elements follow the strain field of a continuum, a strain-energy function is formulated. From the strain-energy function, an explicit stress-strain equation for large deformations is derived. In the linear approximation of the stress-strain equation the shear modulus and the area modulus of the membrane are respectively found to be 2.4 and 2.8 times the tension at the reference state. The stress-strain equation for large deformations is used to predict the displacement field around a circular hole in pleura. Good agreement is found between these predictions and measurements made on ablated pleura from dog lungs. From these theoretical and experimental results the conclusion is drawn that the pleura has a significant role in carrying shear forces and maintaining the lung's shape.

Animals↗