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Biomedical subjects

R A Meiss

Publications and source records attributed to R A Meiss.

At least 19 recordsLinked to original sources
PubMed2003

Anisotropic properties of tracheal smooth muscle tissue.

The anisotropic (directional-dependent) properties of contracting tracheal smooth muscle tissue are estimated from a computational model based on the experimental data of length-dependent stiffness. The area changes are obtained at different muscle lengths from experiments in which stimulated muscle undergoes unrestricted shortening. Then, through an interative process, the anisotropic properties are estimated by matching the area changes obtained from the finite element analysis to those derived from the experiments. The results obtained indicate that the anisotropy ratio (longitudinal stiffness to transverse stiffness) is about 4 when the smooth muscle undergoes 70% strain shortening, indicating that the transverse stiffness reduces as the longitudinal stiffness increases. It was found through a sensitivity analysis from the simulation model that the longitudinal stiffness and the in-plane shear modulus are not very sensitive as compared to major Poisson's ratio to the area changes of the muscle tissue.

Algorithms↗
PubMed2003

Non-linear material models for tracheal smooth muscle tissue.

The aim of this study is to investigate the hyperelastic material models to describe the non-linear stress-strain behavior of tracheal smooth muscle tissue. Specifically, the goal is to validate the material model with experimental data using different finite element models and discuss the trends in stress-strain behavior of smooth muscle tissue. Both 2D and 3D finite element analyses were carried out to estimate the stress-strain behavior of the smooth muscle tissue. The results obtained indicate that the developed Ogden material model is valid and useful in explaining the stress strain behavior of tracheal smooth muscle tissue under different conditions. Finite element simulation results of the stress-strain behavior in the transverse direction are presented.

Animals↗
PubMed2000

H(2)O(2) mediates Ca(2+)- and MLC(20) phosphorylation-independent contraction in intact and permeabilized vascular muscle.

One purpose of the current study was to establish whether vasoconstriction occurs in all vessel types in response to H(2)O(2). Isometric force was measured in pulmonary venous and arterial rings, and isobaric contractions were measured in mesenteric arteries and veins in response to H(2)O(2). A second purpose was to determine whether H(2)O(2)-induced contraction is calcium independent. The addition of H(2)O(2) to calcium-depleted (using the Ca(2+) ionophore ionomycin in zero calcium EGTA buffer) muscle caused contraction. Furthermore, permeabilized muscle contracted in response to H(2)O(2) even in zero Ca(2+). The final purpose was to determine whether the 20-kDa regulatory myosin light chain (MLC(20)) phosphorylation plays a role in H(2)O(2)-induced contraction. Pulmonary arterial strips were freeze-clamped at various time points during H(2)O(2)-induced contractions, and the relative amounts of phosphorylated MLC(20) were measured. H(2)O(2) caused dose-dependent contractions that were independent of MLC(20) phosphorylation. ML-9, a myosin light chain kinase inhibitor, had no effect on the H(2)O(2) contractile response. In conclusion, H(2)O(2) induces Ca(2+)- and MLC(20) phosphorylation-independent contraction in pulmonary and systemic arterial and venous smooth muscle.

Animals↗
PubMed1999

Influence of intercellular tissue connections on airway muscle mechanics.

Contraction of smooth muscle in visceral organs is modified by structures external to the muscle. Within muscle tissue itself, connective tissue plays an important role in force transference among the contractile cells. Connections arranged radially can affect contractile mechanics by limiting tissue expansion at short lengths. Previous work suggests that increased stiffness at extreme shortening is due to such radial constraints. Two approaches to further study of these effects are reported. To increase radial constraints, very thin Silastic bands were placed loosely about strips of canine trachealis muscle at rest length. The strips were allowed to shorten under light afterloads, expanding until restrained by the bands. Subsequent removal of the bands allowed increased shortening, with less increase in stiffness at short lengths. Related isometric effects were observed. To reduce constraints, muscle strips were partially digested with collagenase. Compared with control conditions, this treatment permitted further shortening, with less increase in stiffness at short lengths. These results emphasize the role of extracellular structures in determining mechanical function of smooth muscle.

Animals↗
PubMed1997

A viscoelastic material model to represent smooth muscle shortening.

The mechanical properties of a contracting smooth muscle can be changed by changing its length. A viscoelastic material model was developed to predict the length-dependent stiffness changes when a constrained muscle is allowed to shorten under a constant external force. Three-dimensional finite element simulations were carried out to estimate the stiffness changes and compared to available experimental data. A good agreement was found indicating that the viscoelastic material model developed gives a valid representation of the length dependent stiffness changes of a smooth muscle. Sensitivity analysis was carried out to determine the relative effects of material constants in the model on the length dependent stiffness.

Computer Simulation↗
PubMed1996

Potentiation of smooth muscle contractility after rapid changes in isotonic force.

The sudden application of step increases in afterload (0.4-3.0 s in duration) arrested the isotonic shortening of electrically stimulated ovarian ligament smooth muscle strips from rabbits. Force steps were chosen to produce, after initial rapid yielding, a quasi-steady state in which muscle length and force remained constant. Removal of the extra afterload allowed renewed shortening that began with a velocity transiently greater than that measured before the force step (at same muscle length). The rate of force redevelopment was also transiently potentiated under isometric conditions after the removal of the extra load. Both types of potentiation depended on force-step duration, and the transients decayed exponentially with a time constant of approximately 0.25 s. The stiffness of the muscle during the force step was initially depressed but then increased along an exponential time course while force and length remained constant. These observations are consistent with an initial detachment of a portion of the cross-bridge array, which then reattached during the course of the force step, with potentiation being due to either a transient increase in cycling rate or a time-dependent reconfiguration of cytoskeletal elements supporting the contractile system.

Animals↗
PubMed1995

Mechanisms for the mechanical plasticity of tracheal smooth muscle.

In smooth muscle tissues, the relationship between muscle or cell length and active force can be modulated by altering the cell or tissue length during stimulation. Mechanisms for this mechanical plasticity were investigated by measuring muscle stiffness during isometric contractions in which contractile force was graded by changing stimulus intensity or muscle length. Stiffness was significantly higher in contracted than in resting muscles at comparable forces; however, the relationship between stiffness and force during force development was curvilinear and independent of muscle length and stimulus intensity. This suggests that muscle stiffness during force development reflects properties of cellular components other than cross bridges which contribute to the series elasticity only during activation. During the tonic phase of isometric contraction, muscle stiffness increased while force remained constant. A step decrease in the length of a contracted muscle resulted in a high level of stiffness relative to force during isometric force redevelopment following the length step. We propose that the arrangement of the cytoskeleton can adjust to changes in the conformation of resting smooth muscle cells but that the organization of the cytoskeleton becomes more fixed upon contractile activation and is modulated very slowly during a sustained contraction. This may provide a mechanism for optimizing force development to the physical conformation of the cell at the time of activation.

Animals↗
PubMed1994

Contractility and myosin heavy chain isoform patterns in developing tracheal muscle.

Changes in airway smooth muscle reactivity with development may be caused by either modification of the excitation-contraction coupling system or alteration of the contractile apparatus. The mechanism responsible for the reported changes in reactivity was addressed in this study by examining airway smooth muscle contractility and myosin heavy chain isoform patterns as a function of post-neonatal development. Changes in length and force, in response to supramaximal electrical stimulation, were recorded simultaneously as functions of time for tracheal smooth muscle (TSM) strips from 8-week-old and 25-week-old male rabbits. Both the passive and active length-tension (L-T) curves as well as the force-velocity (F-V) curves for the two age groups of rabbit TSM were not significantly different indicating no changes in contractility during post-neonatal development in rabbits. This conclusion is surprising in light of reports of myosin heavy chain (MHC) isoform shifts in porcine trachealis during comparable periods of development. Therefore, MHC isoform ratios were compared by sodium dodecyl sulfate-polyacrylimide gel electrophoresis for tracheal smooth muscle from male rabbits of 8 and 25 weeks of age. Unlike the reported MHC isoform shifts in the pig tracheal muscle, the rabbit trachealis showed no difference in MHC isoform ratios between the two age groups compared in this study. In conclusion, no changes occur in contractility or MHC isoform patterns during post-neonatal development of rabbit tracheal smooth muscle. Therefore, reported changes in airway muscle reactivity are likely due to changes in receptors or in second messenger systems rather than to changes in the contractile apparatus.

Animals↗
PubMed1994

Transient length-related mechanical states in smooth muscle.

The isotonic shortening of electrically stimulated ovarian ligament smooth muscle strips from rabbits was studied by briefly applying sudden increases in afterload (force steps, 0.6 to 3.0 s long) just sufficient to halt the shortening. Upon removal of the extra afterload, the isotonic shortening velocity significantly increased compared with prestep velocities measured at the same muscle lengths. The degree of potentiation depended upon the duration of the force step. Muscles yielded initially when the step was applied, and their stiffness decreased. During the zero-velocity portion of the force step there was a steady increase in stiffness back to levels appropriate to that force. Complete force-velocity curves were made following short (0.6 s) and long (3.0 s) force steps. The values for Vmax (and all intermediate velocities) were significantly greater following a long force step. In a final experimental series, muscles were held isometric immediately after removal of the force step. Force rose monotonically, with a more rapid redevelopment following a long force step. A mathematical model is presented, according to which the effect of the duration of the force step on the poststep mechanical properties may be due to either the alteration of an internal resistance to shortening or a change in the kinetic properties of the cross-bridge array. A hypothesis is proposed relating the steady decline in isotonic shortening velocity to a partial local depletion of energy-yielding substrates.

Animals↗
PubMed1993

Persistent mechanical effects of decreasing length during isometric contraction of ovarian ligament smooth muscle.

When isometrically-contracting strips of ovarian ligament smooth muscle were suddenly shortened by 10-20% of their length, force fell rapidly and then redeveloped along an exponential time course. The amount of force recovered fell short of that expected in an isometric contraction at the new length, and this force deficit was proportional to the magnitude of the length step (approximately 80% of force was recovered after a 10% shortening). A sudden imposed decrease in length was more effective in reducing subsequent force than was isotonic shortening. Early in the recovery phase the stiffness of the muscle was decreased to less than its expected value; stiffness recovered to expected levels on an exponential time course approximately three to four times faster than force recovery itself. Force-velocity curves made during the redevelopment phase showed a reduced maximal force (Fmax) and an increased maximal shortening velocity (Vmax) when compared with control contractions matched in force, time and length. The curves crossed at approximately 10% of Fmax. During isometric relaxation the muscles showed an increase in their expected stiffness; prior imposed shortening (as above) reduced the relaxation stiffness increase in proportion to the prior force deficit. The persistent effects of early events on the later phases of the contraction, as well as the increase in shortening velocity with very light loads, are consistent with the hypothesis that the sudden shortening detaches crossbridges and that same fail to reattach during force recovery. During isotonic shortening of unperturbed muscle some slowly-cycling crossbridges may act as an internal load and reduce shortening velocity.

Animals↗
PubMed1992

Limits to shortening in smooth muscle tissues.

The extent of shortening in smooth muscle tissues is limited by a number of internal and external factors. In this study, continuous measurements of the stiffness of active muscle were made to characterize the mechanical forces acting to limit shortening. Rabbit ovarian ligament and mesotubarium superius muscles were allowed to shorten as far as possible under light afterloads; under these conditions a stiffness increase was observed that was closely related to the instantaneous muscle length and that was unaffected by other factors influencing the degree of shortening (afterload, time and intensity of activation, temperature, etc.). The results are considered in terms of a hypothesis relating the tissue-based constraints on radial expansion at short lengths to an additional load on the contractile apparatus, an internal force that is externally manifested as an increase in axial stiffness. Changing the cellular volume by varying the tonicity of the bathing medium provided tentative confirmation of the hypothesis.

Animals↗
PubMed1990

Reactive oxygen species alter contractile properties of pulmonary arterial smooth muscle.

Reactive oxygen species alter pulmonary arterial vascular tone and cause changes in pulmonary vascular resistance. The objective of this investigation was to determine direct effects of oxygen radicals on the contractile properties of pulmonary arterial smooth muscle. Isolated pulmonary arterial rings from Sprague-Dawley rats were placed in tissue baths containing Earle's balanced salt solution (gassed with 95% O2 - 5% CO2, 37 degrees C, pH 7.4). Vessels were contracted with 80 mM KCl to establish maximum active force production (Po). All other responses were normalized as percentages of Po for comparative purposes. Reactive oxygen metabolites were generated enzymatically with either the xanthine oxidase (XO) reaction or the glucose oxidase (GO) reaction, or hydrogen peroxide (H2O2) was added directly to the muscle bath. Exposure to XO, GO, or to H2O2 resulted in a contractile response that was sustained during the 30-min exposure period. The muscle fully relaxed following removal of the reactive oxygen species. Resting tension remained unchanged throughout the experimental period, suggesting no functional change in membrane potential. The contractile response was dose dependent and was not prevented by either cyclooxygenase or lipoxygenase inhibition, or by removal of the endothelium. Pretreatment of vessels with superoxide dismutase (SOD) partially blocked the XO-induced contraction, while mannitol or deferoxamine had no effect on the response to XO. However, pretreatment with catalase (CAT) completely blocked the XO-induced contraction. These data suggest that superoxide ions and hydrogen peroxide are the major causative agents. Following O2-radical exposure, vessels showed a decrease in contractile responsiveness to 80 mM KCl (recovery response), suggesting damage to the smooth muscle cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Studies of arterial smooth muscle relaxation in younger (16-18 week) and older (28-31 week) spontaneously hypertensive rats.

Both isometric and isotonic relaxation rates have previously been reported to be decreased in caudal arterial and mesenteric resistance arterial smooth muscle from 16- to 21-week-old spontaneously hypertensive rats (SHR) compared with muscle from age-matched normotensive Wistar-Kyoto rats (WKY). An increased maximum velocity of shortening (Vmax) and an increased shortening ability (delta Lmax) have also been reported for arterial smooth muscle from 16- to 21-week-old SHR. It has been suggested that both increased narrowing and prolonged narrowing of arteries contribute to the development of hypertension. However, SHR Vmax is not different from WKY Vmax when studying arterial muscle from older (28- to 31-week-old) rats. Thus increased arterial narrowing ability cannot be a contributing factor to the maintenance of hypertension. In this study the role of relaxation rate in the maintenance of hypertension was examined by comparing the relaxation rates of isometric and isotonic contractions of caudal arterial strips from 16- to 21-week-old SHR (n = 9) and WKY (n = 8) and from 28- to 31-week-old SHR (n = 7) and WKY (n = 5). While relaxation rates were lower for 16- to 21-week-old SHR compared with age-matched WKY preparations for both isometric and isotonic contractions, only isometric relaxation rates were found to be different in 28- to 31-week-old SHR compared with 28- to 31-week-old caudal arterial muscle (p less than 0.05). Vmax tended to normalize from a once-elevated velocity, while isometric relaxation rate remained decreased in SHR with ageing and (or) with progression of the hypertensive condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Regulation of glycerinated smooth muscle contraction and relaxation by myosin phosphorylation.

Regulation of isometric force maintenance, isotonic shortening velocity, and muscle stiffness by myosin phosphorylation was examined during both contraction and relaxation of chemically permeabilized (glycerinated) rat uterine smooth muscle. Phosphorylation of the 20,000-Da light chain of myosin (LC20) was manipulated by varying the calcium activity of the bathing solution or by thiophosphorylation of LC20 in the presence of ATP gamma S. With saturating calcium and calmodulin, LC20 phosphorylation was 0.43 mol PO4/mol LC20. This increased to 0.92-0.96 mol PO4/mol LC20 on addition of ATP gamma S. Over the entire range of phosphorylation, there was a significant (P less than 0.001) linear correlation between force and phosphorylation. Stiffness increased monotonically with increasing force; however, the relationship was nonlinear, with stiffness increasing faster at lower levels of activation. Force, stiffness, shortening velocity, and LC20 phosphorylation were compared at identical calcium activities during steady-state conditions of partial contraction and partial relaxation. The ratio of the value of each parameter measured during relaxation to that measured during contraction was 1.11 for force, 1.09 for stiffness, 1.01 for shortening velocity, and 0.83 for LC20 phosphorylation. These results support the hypothesis that contraction and relaxation in glycerinated rat uterine muscle are regulated primarily by phosphorylation and dephosphorylation of LC20.

Adenosine Triphosphate↗