Effect of residual stress on transmural sarcomere length distributions in rat left ventricle

Rodriguez, Edward K.; Omens, Jeffrey H.; Waldman, Lewis K.; McCulloch, Andrew D.

doi:10.1152/ajpheart.1993.264.4.h1048

Cited by 79 publications

(73 citation statements)

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“…Residual stress and strain 32 might affect systolic stresses through a trans- mural variation of resting sarcomere length. 39 Such a variation affected myofiber strain and stress in systole in the LS0 simulation ͑Table 5͒, but did not affect the pattern of early shortening and prestretch, as observed in the NORM simulation.…”

Section: Modelmentioning

confidence: 85%

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Homogeneity of Cardiac Contraction Despite Physiological Asynchrony of Depolarization: A Model Study

Kerckhoffs

Bovendeerd

Kotte

et al. 2003

Annals of Biomedical Engineering

159

139

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Abstract-The use of mathematical models combining wave propagation and wall mechanics may provide new insights in the interpretation of cardiac deformation toward various forms of cardiac pathology. In the present study we investigated whether combining accepted mechanisms on propagation of the depolarization wave, time variant mechanical properties of cardiac tissue after depolarization, and hemodynamic load of the left ventricle ͑LV͒ by the aortic impedance in a threedimensional finite element model results in a physiological pattern of cardiac contraction. We assumed that the delay between depolarization for all myocytes and the onset of crossbridge formation was constant. Two simulations were performed, one in which contraction was initiated according to the regular depolarization pattern ͑NORM simulation͒, and another in which contraction was initiated after synchronous depolarization ͑SYNC simulation͒. In the NORM simulation propagation of depolarization was physiological, but wall strain was unphysiologically inhomogeneous. When simulating LV mechanics with unphysiological synchronous depolarization ͑SYNC͒ myofiber strain was more homogeneous and more physiologic. Apparently, the assumption of a constant delay between depolarization and onset of crossbridge formation results in an unrealistic contraction pattern. The present finding may indicate that electromechanical delay times are heterogeneously distributed, such that a contraction in a normal heart is more synchronous than depolarization.

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Section: Modelmentioning

confidence: 85%

“…͑11͔͒ varied linearly from 1.84 m at the endocardium to 1.96 m at the epicardium. 39 In the simulations BOUN, HETER, and LS0, myofiber contraction was initiated by the depolarization pattern, as calculated in the NORM simulation.…”

Section: ͑17͒mentioning

confidence: 99%

Homogeneity of Cardiac Contraction Despite Physiological Asynchrony of Depolarization: A Model Study

Kerckhoffs

Bovendeerd

Kotte

et al. 2003

Annals of Biomedical Engineering

159

139

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“…In the model, sarcomere length in the reference state l s,0 was set to 1.95 m for all sarcomeres in the LV wall, based on the average of measurements in the left ventricles of rats 15,34 and dogs. 36 Constitutive Behavior The active material parameter l x , the zero-force sarcomere length, was set to 1.62 m, based on experiments in rat cardiac trabeculae.…”

Section: Applied Parameter Values In Finite-element Modelmentioning

confidence: 99%

“…Measurements indicate that circumferential residual strain leads to a transmural gradient in sarcomere length in the unloaded left ventricle of the rat. 34 At positive filling pressure the transmural gradient in sarcomere length becomes less pronounced, indicating that residual strain may contribute to homogeneity of fiber strain at the beginning of ejection. 15 However, finite-element simulations of LV wall mechanics show that the effects of residual strain, represented by a transmural gradient in sarcomere length in the zero-pressure reference state, do not affect the end-systolic distribution of fiber strain.…”

Section: Figure 4 Distribution Of Fiber Strain Over the LV Wall Follmentioning

confidence: 99%

Optimization of Cardiac Fiber Orientation for Homogeneous Fiber Strain During Ejection

Rijcken

Bovendeerd

Schoofs

et al. 1999

Annals of Biomedical Engineering

103

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Abstract-The strain of muscle fibers in the heart is likely to be distributed uniformly over the cardiac walls during the ejection period of the cardiac cycle. Mathematical models of left ventricular ͑LV͒ wall mechanics have shown that the distribution of fiber strain during ejection is sensitive to the orientation of muscle fibers in the wall. In the present study, we tested the hypothesis that fiber orientation in the LV wall is such that fiber strain during ejection is as homogeneous as possible. A finite-element model of LV wall mechanics was set up to compute the distribution of fiber strain at the beginning ͑BE͒ and end ͑EE͒ of the ejection period of the cardiac cycle, with respect to a middiastolic reference state. The distribution of fiber orientation over the LV wall, quantified by three parameters, was systematically varied to minimize regional differences in fiber shortening during ejection and in the average of fiber strain at BE and EE. A well-defined optimum in the distribution of fiber orientation was found which was not significantly different from anatomical measurements. After optimization, the average of fiber strain at BE and EE was 0.025 Ϯ0.011 (meanϮstandard deviation) and the difference in fiber strain during ejection was 0.214Ϯ0.018. The results indicate that the LV structure is designed for maximum homogeneity of fiber strain during ejection.

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“…27,28 Compressive residual stresses shorten endocardial sarcomeres in the unloaded ventricle and are balanced by tensile residual stresses that prestretch epicardial fibers. 29 This provides a mechanism for maintaining transmural uniformity of stress and sarcomere length at end-diastole, 30 and changes in residual stress resulting from nonuniform hypertrophy have been described as an adaptive response to hemodynamic overload in arteries. Yet the most striking alterations in myocardial residual stresses have been developmental responses to ECM gene mutations in the tightskin mouse, Tsk, and the osteogenesis imperfecta murine, oim.…”

Section: Mechanical Interactions Between Myocytes and The Ecmmentioning

confidence: 99%

Dance Band on the Titanic

Sussman

McCulloch

Borg

2002

Circulation Research

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Abstract-Biomechanical signaling is a complex interaction of both intracellular and extracellular components. Both passive and active components are involved in the extracellular environment to signal through specific receptors to multiple signaling pathways. This review provides an overview of extracellular matrix, specific receptors, and signaling pathways for biomechanical stimulation in cardiac hypertrophy. Key Words: mechanical signaling Ⅲ cardiac hypertrophy Ⅲ extracellular matrix W hile all cells, tissues, and organisms depend on external mechanical inputs to maintain their phenotypes, cardiac cells are also constantly generating active forces of contraction. Mechanical forces are intimately linked to chemical signals that lead to many interrelated modifications both inside and outside the various cell types of the heart. Outside the cells, these modifications include dynamic restructuring of the extracellular matrix (ECM) and its signaling components and alterations in the quantity and type of cell surface receptors. Within the cell, changes occur in signaling proteins, contractile apparatus, and cytoskeleton. Because these structural alterations prompt alterations in mechanical properties of the cells and ECM, they result in a redistribution of mechanical stimuli until a new (mechanical and biological) equilibrium is achieved. This dynamic system works well in the physiological adaptation to a variety of signals that result in normal cardiac growth or development; however, when this equilibrium goes out of balance, the result can be pathological growth and abnormal physiology. In this review, we focus on the components that regulate biomechanosignaling in the cardiac myocyte and their integration.Mechanical stress provides critical information for maintenance of myocardial structure and function. Because dynamic changes in stress occur with every contraction/relaxation cycle as well as with short-and long-term hemodynamic alterations, this information must be integrated using multiple sensors. Chronic elevation of force exerted on cardiomyocytes prompts signaling reactivity and remodeling that transforms the structural characteristics and physical properties of the myocardium altering the balance of forces between different regions and components of the tissue. Increased physical stress on the heart can be normal and beneficial, but pathological conditions such as hypertension, ischemia, or contractile abnormalities that increase stress excessively lead to maladaptive remodeling that may precede the onset of heart failure. Because of the close interplay between the myocytes and the ECM, it is not surprising that cellular and extracellular remodeling tends to occur in tandem, such as fibrosis that accompanies pressure-overload hypertrophy.Mechanotransduction-the transformation of a mechanical stimulus into cellular responses-is a hallmark of myocardial cells. Mechanical stress and strain activate a panoply of signaling pathways too numerous to be adequately addressed in this review. Accordingly, the over...

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Effect of residual stress on transmural sarcomere length distributions in rat left ventricle

Cited by 79 publications

References 0 publications

Homogeneity of Cardiac Contraction Despite Physiological Asynchrony of Depolarization: A Model Study

Homogeneity of Cardiac Contraction Despite Physiological Asynchrony of Depolarization: A Model Study

Optimization of Cardiac Fiber Orientation for Homogeneous Fiber Strain During Ejection

Dance Band on the Titanic

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