Constitutive properties of hypertrophied myocardium:  cellular contribution to changes in myocardial stiffness

Harris, Todd S.; Baicu, Catalin F.; Conrad, Chester H.; Koide, Masaaki; Buckley, J. Michael; Barnes, Michael C.; Cooper, George; Zile, Michael R.

doi:10.1152/ajpheart.00480.2001

Cited by 33 publications

(32 citation statements)

References 48 publications

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“…In many disease states, a decrease in compliance is mediated by changes in the content or physical properties of collagen; however, other factors may contribute such as amyloidosis, cellular disarray, coronary vascular engorgement, myocardial ischemia, and the cardiomyocytes (10,16). In addition, it is unclear why the 9-mo-old mast cell-deficient hearts displayed somewhat enhanced slopes when the effects of balloon volume on developed pressure, ϩdP/dt max , and ϪdP/dt max were examined.…”

Section: Discussionmentioning

confidence: 99%

Cardiac function in hearts isolated from a rat model deficient in mast cells

Kennedy

Hauer‐Jensen²,

Joseph³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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2004.-Several studies have examined the role of mast cells in the myocardial response to injury such as that caused by hypertension and ischemia-reperfusion. However, little is known about the influence of mast cells on normal myocardial structure and function. The present experiments examined cardiac function in Langendorff-perfused hearts isolated from 6-and 9-mo-old male mast cell-deficient (Ws/Ws) and mast cell-competent rats. A fluid-filled balloon catheter was used to measure left ventricular diastolic and systolic function at increasing preload volumes. At 6 mo of age, mast cell-deficient rats showed a slight cardiac hypertrophy (as monitored by heart weight and heart weight-to-body weight ratio) but no significant change in maximum observed systolic or diastolic function. In contrast, at 9 mo of age, the mast cell-deficient group showed no signs of hypertrophy but displayed a diastolic dysfunction characterized by decreased compliance without a significant decline in maximum observed basal ϪdP/dt max. There were no significant differences in maximum observed values for measures of systolic function (developed pressure and ϩdP/dtmax). In summary, the results of this study in adult rats suggest that mast cells influence cardiac function in the absence of injury and that observed differences between mast cell-competent and -deficient animals vary with age. Thus it is important to consider these "physiological" actions and resulting changes in function when studying effects of insult in mast cell-deficient models.compliance; diastolic dysfunction; Langendorff-perfused hearts MAST CELLS are part of the innate immune system that provides the first line of defense against tissue damage. In addition to their critical role in immunoglobulin E-dependent, histaminemediated hypersensitivity, mast cells release and modulate cytokines, growth factors, chemokines, proteases, and other mediators, which in turn regulate a vast array of important biological processes. Many mast cell mediators (e.g., histamine, heparin, tryptase, chymase, TNF-␣, and interleukin-4) are preformed and stored in large amounts in secretory granules, available for immediate release (21). Studies have demonstrated that mast cells reside in the myocardium even under physiological conditions, with their distribution along the coronary capillaries being more dense in the arteriolar section (30).Several studies have examined the potential role of mast cells in the myocardial response to injury. However, in many cases, the results of these studies have been contradictory. For example, numerous investigators have monitored the contribution of mast cells to preconditioning as well as ischemic injury. Parikh and Singh (27, 28) suggested that ischemia-and norepinephrine-induced preconditioning are mediated in part by degranulation of resident mast cells in the rat heart, whereas Wang et al. (37) reported that mast cell degranulation is not involved in ischemic cardiac preconditioning in rabbits. Similarly, the role of mast cells in the acute tissue damage...

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Section: Discussionmentioning

confidence: 99%

Cardiac function in hearts isolated from a rat model deficient in mast cells

Kennedy

Hauer‐Jensen²,

Joseph³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…What then is the precise physical nature of the impediment to contraction produced by microtubule network densification? I addressed this question in a collaboration with N. Wang and M. R. Zile by directly probing the viscoelastic properties of the tensegrity network of physically interrelated cytoskeletal filaments in living cardiocytes (26) and then confirming these findings at the level of whole cell and tissue mechanics (14,31). Figure 15 (top) shows the appearance of beads that are attached via integrin receptors to the cardiocyte cytoskeleton.…”

Section: Materials Properties Of the Microtubule Networkmentioning

confidence: 91%

“…In normal cardiocytes, although very recent data suggest that microtubules may contribute to longitudinal shear stiffness (22), the normal microtubule network actually has very little effect on cytoskeletal material properties in terms of influencing sarcomere (29), cardiocyte (31), myocardial (14), or cardiac (19) mechanics. What then is the precise physical nature of the impediment to contraction produced by microtubule network densification?…”

Section: Materials Properties Of the Microtubule Networkmentioning

confidence: 99%

Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction

Cooper

2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…21 Likewise, an increase in microtubule density and distribution has been shown in some forms of pressure overload to act as a viscous load and increase myocardial and cardiomyocyte viscoelastic stiffness. 7,[22][23][24][25] This change in diastolic function is reversible when microtubules are acutely depolymerized by chemical or physical agents. 7,[22][23][24][25] …”

Section: Cardiomyocytementioning

confidence: 99%

New Concepts in Diastolic Dysfunction and Diastolic Heart Failure: Part II

2002

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A s described in Part I of this 2-part article, 1 diastolic heart failure is common and causes significant alterations in prognosis. In Part II, experimental studies that have provided insight into the mechanisms that cause diastolic heart failure will be described. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] In addition, current treatment strategies and the design of future clinical trials of diastolic heart failure will be discussed. The development of truly effective therapy for diastolic heart failure depends on gaining a clear understanding of the basic mechanisms that alter diastolic function and the ability to efficiently target these mechanisms to correct these abnormalities in diastolic function. Mechanisms That Cause Diastolic DysfunctionConceptually, the mechanisms that cause abnormalities in diastolic function that lead to the development of diastolic heart failure can be divided into factors intrinsic to the myocardium itself (myocardial) and factors that are extrinsic to the myocardium (extramyocardial; Table 1). Myocardial factors can be divided into structures and processes within the cardiac muscle cell (cardiomyocyte), within the extracellular matrix (ECM) that surrounds the cardiac muscle cell, and that activate the autocrine or paracrine production of neurohormones. Each of these mechanisms are active in the major pathological processes that result in diastolic dysfunction and heart failure. Myocardial and extramyocardial mechanisms, cellular and extracellular mechanisms, and neurohumoral activation each play a role in the development of diastolic heart failure caused by ischemia, pressure-overload hypertrophy, and restrictive and hypertrophic cardiomyopathy. CardiomyocyteDiastolic dysfunction can be caused by mechanisms that are intrinsic to the cardiac muscle cells themselves. These include changes in calcium homeostasis caused by (1) abnormalities in the sarcolemmal channels responsible for short-and long-term extrusion of calcium from the cytosol, such as the sodium calcium exchanger and the calcium pump; (2) ATPase function, such as phospholamban, calmodulin, and calsequestrin. Changes in any of these processes can result in increased cytosolic diastolic calcium concentration, prolongation in the calcium transient, and delayed and slowed diastolic decline in cytosolic calcium concentration. These changes have been shown to occur in cardiac disease and cause abnormalities in both active relaxation and passive stiffness. 2 The myofilament contractile proteins consist of thickfilament myosin and thin-filament actin proteins. Bound to actin are a complex of regulatory proteins that include tropomyosin and troponin (Tn) T, C, and I. During relaxation, ATP hydrolysis is required for myosin detachment from actin, calcium dissociation from Tn-C, and active sequestration of calcium by the SR. Modification of any of these steps, the myofilament proteins involved in these steps, or the ATPase that catalyzes them can alter diastolic function. [2][3][4][5][6] Thus, relaxation is...

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Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffness

Cited by 33 publications

References 48 publications

Cardiac function in hearts isolated from a rat model deficient in mast cells

Cardiac function in hearts isolated from a rat model deficient in mast cells

Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction

New Concepts in Diastolic Dysfunction and Diastolic Heart Failure: Part II

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