Log in

Relevant bibliographies by topics / Cardiac myocytes

Contents

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers

Academic literature on the topic 'Cardiac myocytes'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Cardiac myocytes.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Cardiac myocytes"

1

Orita, Hiroyuki, Manabu Fukasawa, Hideaki Uchino, Kana Fukui, Minoru Kohi, and Masahiko Washio. "Modulation of the viability of immature cardiac myocytes by cardiac fibroblasts after hypothermic preservation—its values as a technique for evaluation of storage solutions." Cardiology in the Young 5, no. 2 (April 1995): 110–17. http://dx.doi.org/10.1017/s1047951100011665.

Full text

Abstract:

AbstractWe evaluated the modulation of the viability of immature cardiac myocytes by cardiac fibroblasts after hypothermic preservation using three types of storage solutions—saline, University of Wisconsin solution, and MCDB 107 medium. Cardiac myocytes and fibroblasts were isolated from neonatal rat ventricles, and cultures of myocytes only or co-cultures with fibroblasts (myocyte: fibroblast 2:1) were established. On the fourth day of culture, the cultures were incubated at 4 °C for 6, 12, 18 and 24 hours in the different storage solutions. Enzymes were measured in the storage solutions immediately before and after hypothermic incubation. The cultures were then incubated for an additional 24 hours at 37 °C to evaluate the recovery of the myocyte beating rate. The myocyte beating rate in the co-culture groups showed significantly higher recovery ratios than the corresponding groups in which only myocytes were cultured. Complete recovery was observed in the group co-cultured in MCDB medium 24 hours after hypothermic incubation (83.4% of control—beating rate prior to hypothermic incubation) compared to the other co-cultured groups (15.4, 0%, respectively). Release of enzymes in the co-cultures was significantly suppressed compared to the cultured myocytes, and the greatest suppression was found after 24 hours of incubation in MCDB medium (CPK: 36.6 mIU/flask, LDH: 281.2 mIU/flask) compared to the other two co-cultured groups (CPK: 181.1, 281.1; LDH: 501.7, 773.2). Cardiac fibroblasts diminished myocytic injury after hypothermic preservation using various storage solutions, in which MCDB 107 medium showed the best overall protective effect. Thus, cardiac fibroblasts may play an important role in controlling myocytic viability under various hypothermic conditions.

APA, Harvard, Vancouver, ISO, and other styles

2

Krishnan, Anirudh, Emily Chilton, Jaishankar Raman, Pankaj Saxena, Craig McFarlane, Alexandra F. Trollope, Robert Kinobe, and Lisa Chilton. "Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?" Cells 10, no. 9 (September 21, 2021): 2501. http://dx.doi.org/10.3390/cells10092501.

Full text

Abstract:

Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

APA, Harvard, Vancouver, ISO, and other styles

3

Jonker, Sonnet S., Lubo Zhang, Samantha Louey, George D. Giraud, Kent L. Thornburg, and J. Job Faber. "Myocyte enlargement, differentiation, and proliferation kinetics in the fetal sheep heart." Journal of Applied Physiology 102, no. 3 (March 2007): 1130–42. http://dx.doi.org/10.1152/japplphysiol.00937.2006.

Full text

Abstract:

The generation of new myocytes is an essential process of in utero heart growth. Most, or all, cardiac myocytes lose their capacity for proliferation during the perinatal period through the process of terminal differentiation. An increasing number of studies focus on how experimental interventions affect cardiac myocyte growth in the fetal sheep. Nevertheless, fundamental questions about normal growth of the fetal heart remain unanswered. In this study, we determined that during the last third of gestation the hearts of fetal sheep grew primarily by four processes. 1) Myocyte proliferation contributed substantially to daily cardiac mass gain, and the number of cardiac myocytes continued to increase to term. 2) The (hitherto unrecognized) contribution to cardiac growth by the increase in myocyte size associated with the transition from mononucleation to binucleation (terminal differentiation) became considerable from ∼115 days of gestational age (dGA) until term (145dGA). Because binucleation became the more frequent outcome of myocyte cell cycle activity after ∼115dGA, the number of binucleated myocytes increased at the expense of the number of mononucleated myocytes. Both the interval between nuclear divisions and the duration of cell cycle activity in myocytes decreased substantially during this same period. Finally, cardiac growth was in part due to enlargement of 3) mononucleated and 4) binucleated myocytes, which grew in cross-sectional diameter but not length during the last third of gestation. These data on normal cardiac growth may enable a more detailed understanding of the consequences of experimental and pathological interventions in prenatal life.

APA, Harvard, Vancouver, ISO, and other styles

4

Kabaeva, Zhyldyz, Mei Zhao, and Daniel E. Michele. "Blebbistatin extends culture life of adult mouse cardiac myocytes and allows efficient and stable transgene expression." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 4 (April 2008): H1667—H1674. http://dx.doi.org/10.1152/ajpheart.01144.2007.

Full text

Abstract:

The characterization of cellular phenotypes of heart disorders can be achieved by isolating cardiac myocytes from mouse models or genetically modifying wild-type cells in culture. However, adult mouse cardiac myocytes show extremely low tolerance to isolation and primary culture conditions. Previous studies indicate that 2,3-butanedione monoximine (BDM), a nonspecific excitation-contraction coupling inhibitor, can improve the viability of isolated adult mouse cardiac myocytes. The mechanisms of the beneficial and unwanted nonspecific actions of BDM on cardiac myocytes are not understood. To understand what contributes to murine adult cardiac myocyte stability in primary culture and improve this model system for experimental use, the specific myosin II inhibitor blebbistatin was explored as a media supplement to inhibit mouse myocyte contraction. Enzymatically isolated adult mouse cardiac myocytes were cultured with blebbistatin or BDM as a media supplement. Micromolar concentrations of blebbistatin significantly increased the viability, membrane integrity, and morphology of adult cardiac myocytes compared with cells treated with previously described 10 mM BDM. Cells treated with blebbistatin also showed efficient adenovirus gene transfer and stable transgene expression, and unlike BDM, blebbistatin does not appear to interfere with cell adhesion. Higher concentrations of BDM actually worsened myocyte membrane integrity and transgene expression. Therefore, the specific inhibition of myosin II activity by blebbistatin has significant beneficial effects on the long-term viability of adult mouse cardiac myocytes. Furthermore, the unwanted effects of BDM on adult mouse cardiac myocytes, perhaps due to its nonspecific activities or action as a chemical phosphatase, can be avoided by using blebbistatin.

APA, Harvard, Vancouver, ISO, and other styles

5

Evans, Heather J., Janea K. Sweet, Robert L. Price, Michael Yost, and Richard L. Goodwin. "Novel 3D culture system for study of cardiac myocyte development." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (August 2003): H570—H578. http://dx.doi.org/10.1152/ajpheart.01027.2002.

Full text

Abstract:

Insufficient myocardial repair after pathological processes contributes to cardiovascular disease, which is a major health concern. Understanding the molecular mechanisms that regulate the proliferation and differentiation of cardiac myocytes will aid in designing therapies for myocardial repair. Models are needed to delineate these molecular mechanisms. Here we report the development of a model system that recapitulates many aspects of cardiac myocyte differentiation that occur during early cardiac development. A key component of this model is a novel three-dimensional tubular scaf-fold engineered from aligned type I collagen strands. In this model embryonic ventricular myocytes undergo a transition from a hyperplastic to a quiescent phenotype, display significant myofibrillogenesis, and form critical cell-cell connections. In addition, embryonic cardiac myocytes grown on the tubular substrate have an aligned phenotype that closely resembles in vivo neonatal ventricular myocytes. We propose that embryonic cardiac myocytes grown on the tube substrate develop into neonatal cardiac myocytes via normal in vivo mechanisms. This model will aid in the elucidation of the molecular mechanisms that regulate cardiac myocyte proliferation and differentiation, which will provide important insights into myocardial development.

APA, Harvard, Vancouver, ISO, and other styles

6

Li, F., M. R. McNelis, K. Lustig, and A. M. Gerdes. "Hyperplasia and hypertrophy of chicken cardiac myocytes during posthatching development." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 2 (August 1, 1997): R518—R526. http://dx.doi.org/10.1152/ajpregu.1997.273.2.r518.

Full text

Abstract:

For characterization of the growth pattern of cardiac myocytes during posthatching development, cardiac myocytes were enzymatically isolated from the ventricles of 1-, 15-, 29-, and 42-day-old chickens for measurement of myocyte nucleation, length, width, volume, and number, and for immunolabeling of cytoskeletal proteins. Ventricular myocyte number increased 156% from day 1 to day 42. Average cell volume increased more than 400%, and myocytes lengthened 125%, but cell width only increased 53% during this period. All myocytes were mononucleated at day 1. At day 15, 18% of myocytes became binucleated with < 1% of myocytes containing more than two nuclei. Interestingly, binucleated myocytes were able to divide with two nuclei going through mitosis at the same time. As demonstrated by staining with tubulin and alpha-actinin antibodies, two mitotic spindles and two cleavage furrows were formed in dividing binucleated myocytes. At day 42, binucleated myocytes increased to 44% with 11% of myocytes containing more than two nuclei. Sarcomeric alpha-actinin was partially disassembled in prometaphase and was reorganized into regular Z lines of sarcomeres in telophase. Desmin was disassembled in prophase and was reassembled during late telophase. These results suggest that chicken myocytes undergo hypertrophy and continue to proliferate during posthatching maturation, although it is currently believed that myocytes of all vertebrates withdraw from the cell cycle shortly after birth. We provide direct evidence for the first time of in vivo myocyte division in 6-wk-old chicken hearts.

APA, Harvard, Vancouver, ISO, and other styles

7

Pinsky, David J., Walif Aji, Matthias Szabolcs, Eleni S. Athan, Youping Liu, Yi Ming Yang, Richard P. Kline, Kim E. Olson, and Paul J. Cannon. "Nitric oxide triggers programmed cell death (apoptosis) of adult rat ventricular myocytes in culture." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 3 (September 1, 1999): H1189—H1199. http://dx.doi.org/10.1152/ajpheart.1999.277.3.h1189.

Full text

Abstract:

Excessive nitric oxide (NO) production within the heart is implicated in the pathogenesis of myocyte death, but the mechanism whereby NO kills cardiac myocytes is not known. To determine whether NO may trigger programmed cell death (apoptosis) of adult rat ventricular myocytes in culture, the NO donor S-nitroso- N-acetylpenicillamine (SNAP) was shown to kill purified cardiac myocytes in a dose-dependent fashion. In situ analysis of ventricular myocytes plated on chamber slides using nick-end labeling of DNA demonstrated that SNAP induces cardiac myocyte apoptosis, which was confirmed by the identification of oligonucleosomal DNA fragmentation on agarose gel electrophoresis. Similarly, treatment of cardiac myocytes with cytokines that induce inducible NO synthase was shown to cause an NO-dependent induction of apoptosis. Addition of reduced hemoglobin to scavenge NO liberated by SNAP extinguished both the increase in percentage of apoptotic cells and the appearance of DNA ladders. Treatment with SNAP (but not with N-acetylpenicillamine or SNAP + hemoglobin) not only induced apoptosis but resulted in a marked increase in p53 expression in cardiac myocytes detected by Western blotting and immunohistochemistry. These data indicate that NO has the capacity to kill cardiac myocytes by triggering apoptosis and suggest the involvement of p53 in this process.

APA, Harvard, Vancouver, ISO, and other styles

8

Chen, Hua, Xueyin N. Huang, Alexandre F. R. Stewart, and Jorge L. Sepulveda. "Gene expression changes associated with fibronectin-induced cardiac myocyte hypertrophy." Physiological Genomics 18, no. 3 (August 11, 2004): 273–83. http://dx.doi.org/10.1152/physiolgenomics.00104.2004.

Full text

Abstract:

Fibronectin (FN) is an extracellular matrix protein that binds to integrin receptors and couples cardiac myocytes to the basal lamina. Cardiac FN expression is elevated in models of pressure overload, and FN causes cultured cardiac myocytes to hypertrophy by a mechanism that has not been characterized in detail. In this study, we analyzed the gene expression changes induced by FN in purified rat neonatal ventricular myocytes using the Affymetrix RAE230A microarray, to understand how FN affects gene expression in cardiac myocytes and to separate the effects contributed by cardiac nonmyocytes in vivo. Pathway analysis using z-score statistics and comparison with a mouse model of cardiac hypertrophy revealed several pathways stimulated by FN in cardiac myocytes. In addition to the known cardiac myocyte hypertrophy markers, FN significantly induced metabolic pathways including virtually all of the enzymes of cholesterol biosynthesis, fatty acid biosynthesis, and the mitochondrial electron transport chain. FN also increased the expression of genes coding for ribosomal proteins, translation factors, and the ubiquitin-proteasome pathway. Interestingly, cardiac myocytes plated on FN showed elevated expression of the fibrosis-promoting peptides connective tissue growth factor (CTGF), WNT1 inducible signaling pathway protein 2 (WISP2), and secreted acidic cysteine-rich glycoprotein (SPARC). Our data complement in vivo studies and reveal several novel genes and pathways stimulated by FN, pointing to cardiac myocyte-specific mechanisms that lead to development of the hypertrophic phenotype.

APA, Harvard, Vancouver, ISO, and other styles

9

Brady, A. J., J. B. Warren, P. A. Poole-Wilson, T. J. Williams, and S. E. Harding. "Nitric oxide attenuates cardiac myocyte contraction." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H176—H182. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h176.

Full text

Abstract:

Cardiac muscle fibers have microvessels in close proximity, the distance from the nearest capillary being no greater than 8 microns. We performed experiments on isolated, electrically stimulated, contracting guinea pig cardiac myocytes to test whether NO from endothelium or nitrovasodilators or directly superfused in solution might affect myocyte contractility. In endothelium-myocyte coculture experiments, 10(-7) M bradykinin reduced myocyte shortening by 11 +/- 3.5%. This effect was abolished in the presence of NG-nitro-L-arginine methyl ester and was unaffected by indomethacin. Sodium nitroprusside, but not organic nitrovasodilators, reduced myocyte contraction amplitude by 23% at 3 x 10(-5) M. This effect was reversed by methylene blue. Superfusion with NO solution had an effect similar to sodium nitroprusside, as did exposure to 8-bromoguanosine 3',5'-cyclic monophosphate. Thus the present study shows that cardiac myocyte contraction is attenuated by NO, which appears to act via production of guanosine 3',5'-cyclic monophosphate within the myocytes. Because cardiac myocytes in vivo are in such close proximity to endothelium, the effects of endothelial products on cardiac myocyte contractility may be important in myocardial function.

APA, Harvard, Vancouver, ISO, and other styles

10

Jiang, Jianming, Patrick G. Burgon, Hiroko Wakimoto, Kenji Onoue, Joshua M. Gorham, Caitlin C. O’Meara, Gregory Fomovsky, et al. "Cardiac myosin binding protein C regulates postnatal myocyte cytokinesis." Proceedings of the National Academy of Sciences 112, no. 29 (July 7, 2015): 9046–51. http://dx.doi.org/10.1073/pnas.1511004112.

Full text

Abstract:

Homozygous cardiac myosin binding protein C-deficient (Mybpct/t) mice develop dramatic cardiac dilation shortly after birth; heart size increases almost twofold. We have investigated the mechanism of cardiac enlargement in these hearts. Throughout embryogenesis myocytes undergo cell division while maintaining the capacity to pump blood by rapidly disassembling and reforming myofibrillar components of the sarcomere throughout cell cycle progression. Shortly after birth, myocyte cell division ceases. Cardiac MYBPC is a thick filament protein that regulates sarcomere organization and rigidity. We demonstrate that many Mybpct/t myocytes undergo an additional round of cell division within 10 d postbirth compared with their wild-type counterparts, leading to increased numbers of mononuclear myocytes. Short-hairpin RNA knockdown of Mybpc3 mRNA in wild-type mice similarly extended the postnatal window of myocyte proliferation. However, adult Mybpct/t myocytes are unable to fully regenerate the myocardium after injury. MYBPC has unexpected inhibitory functions during postnatal myocyte cytokinesis and cell cycle progression. We suggest that human patients with homozygous MYBPC3-null mutations develop dilated cardiomyopathy, coupled with myocyte hyperplasia (increased cell number), as observed in Mybpct/t mice. Human patients, with heterozygous truncating MYBPC3 mutations, like mice with similar mutations, have hypertrophic cardiomyopathy. However, the mechanism leading to hypertrophic cardiomyopathy in heterozygous MYBPC3+/− individuals is myocyte hypertrophy (increased cell size), whereas the mechanism leading to cardiac dilation in homozygous Mybpc3−/− mice is primarily myocyte hyperplasia.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Cardiac myocytes"

1

Kuwahara, Koichiro. "Involvment of cardiotrophin-1 cardiac myocyte-nonmyocyte interactions during hypertrophy of rat cardiac myocytes in vitro." Kyoto University, 2000. http://hdl.handle.net/2433/180849.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Egdell, Robin Michael. "Arrhythmogenic phenomena in isolated cardiac myocytes." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322380.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Iancu, Radu Vlad. "cAMP COMPARTMENTATION IN ADULT CARDIAC MYOCYTES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1220587638.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Sirna, Josephine Barbara. "Iron regulation in neonatal rat cardiac myocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0001/MQ33937.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Patel, Trupti. "Mechanisms of Pathogen Sensing in Cardiac Myocytes." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486584.

Full text

Abstract:

Bacterial sepsis and septic shock are major causes ofdeath in the critically ill. The majority ofthese deaths are due to the development ofmyocardial contractile dysfunction. The pathophysiology ofthis phenomenon is incompletely understood,. with previous work focussing on the influence ofcirculating inflammatory mediators ofnon-cardiac origin. Despite the recognised importance ofthese factors in contrit>uting to myocardial dysfunction, how the heart itselfresponds to bacterial pathogens directly has not been fully elucidated. The aims ofthis study were, first, to characterise the functional changes induced in isolated cardiac myocytes by whole bacteria. With the recent identification ofToll-like receptors (TLR)s (pattern recognition receptors (PRR)s) within the cardiac compartment, the second aim was to examine their roles in any changes seen. Finally, the role ofkey inflammatory mediators was examined. A novel method ofevaluating how Gram positive Staphylococcus aureus (S. aureus) or Gram negative Escherichia coli (E. call) directly modified 'populations' ofcardiac rat and mouse myocytes is described. Bacteria not' only decreased the propot:tion ofviable rod-shaped cells, they also decreased the proportion ofcells able to contract to electrical stimulation. S. aureus was found to have more pronounced effects than E. coli. In separate experiments, extracellular oxidants mimicked the effects ofbacteria on cardiac myocytes. The effects ofS. aureus and E. coli were mediated by TLR2ffLR6 and TLR4 respectively. Although no role for nitric oxide was found in bacteria-induced changes in myocyte function, the adverse effects ofS. aureus were partly prevented by specific cyclo-oygenase-2 inhibitors. However, the central hormone mediating the effects of bacteria (and oxidants) was found to be endothelin-l (ET-l), acting on ETA receptors. Caspase activation, without leading to apoptosis, was also implicated in mediating the phenotype changes induced by bacteria. Finally, cardiac myocytes ofthe noncontracting phenotype showed a reduced myofilament sensitivity to calcium, explaining the functional changes seen. Although the data are limited, a similar phenomenon was seen in failing human myocytes.

APA, Harvard, Vancouver, ISO, and other styles

6

Gavino, Belinda Joy E. "Nickel induced rhabdomyosarcoma in cultured cardiac myocytes." Tallahassee, Fla. : Florida State University, 2008. http://purl.fcla.edu/fsu/lib/digcoll/undergraduate/honors-theses/341766.

Full text

Abstract:

Thesis (Honors paper)--Florida State University, 2008.
Advisor: Dr. P. Bryant Chase, Florida State University, College of Arts and Sciences, Dept. of Biological Science. Includes bibliographical references.

APA, Harvard, Vancouver, ISO, and other styles

7

Vierheller, Janine. "Modelling excitation coupling in ventricular cardiac myocytes." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19158.

Full text

Abstract:

Um die Kontraktion einer Herzmuskelzelle durch den Kalziumeinstrom zu ermöglichen, ist die Kopplung von Erregung und Kontraktion (ECC) von zentraler Bedeutung. Durch das elektrische Signal einer Nachbarzelle wird die Depolarisation des Sarkolemmas verursacht, wodurch sich die L-Typ-Kalziumkanäale (LKK) öffnen und der Amplifizierungsprozess eingeleitet wird. Letzterer ist bekannt als Kalzium induzierte Kalzium Freisetzung (CICR). Durch die LKK wird ein Kalziumeinstrom in die Zelle ermöglicht, welcher zur Öffnung der Ryanodinrezeptoren (RyR) des Sarkoplasmatischen Retikulums (SR) führt. Durch die Kalziumfreisetzung des SR wird dieses im Cytoplasma akkumuliert. Modelle für diese Prozesse werden seit mehreren Jahrzenten entwickelt. Bisher fehlte jedoch die Kombination aus räumlich aufgelösten Kalziumkonzentrationen der dyadischen Spalte mit stochastischen Simulationen der einzelnen Kalziumkanäle und die Kalziumdynamiken in der ganzen Zelle mit einem Elektrophysiologiemodell einer ganzen Herzmuskelzelle. In dieser Arbeit entwickleten wir ein neues Modell, in welchem die Konzentrationsgradienten von einzelnen Kanälen bis zum Ganzzelllevel räumlich aufgelöst werden. Es wurde der quasistatische Ansatz und die Finite-Elemente-Methode zur Integration partieller Differentialgleichungen verwendet. Es wurden Simulationen mit unterschiedlichen RyR Markow-Kette-Modellen, verschiedenen Parametern für die Bestandteile des SR, verschiedenen Konditionen des Natrium-Kalzium-Austauschers und unter Einbindung der Mitochondrien durchgeführt. Ziel war es, das physiologische Verhalten einer Kaninchen-Herzmuskelzelle zu simulieren. In dem neu entwickelten Multiskalenmodell wurden Hochleistungsrechner verwendet, um detaillierte Informationen über die Verteilung, die Regulation und die Relevanz von den im ECC involvierten Komponenten aufzuzeigen. Zukünftig soll das entwickelte Modell Anwendung bei der Untersuchung von Herzkontraktionen und Herzmuskelversagen finden.
Excitation contraction coupling (ECC) is of central importance to enable the contraction of the cardiac myocyte via calcium in ux. The electrical signal of a neighbouring cell causes the membrane depolarization of the sarcolemma and L-type Ca2+ channels (LCCs) open. The amplifcation process is initiated. This process is known as calcium-induced calcium release (CICR). The calcium in ux through the LCCs activates the ryanodine receptors (RyRs) of the sarcoplasmic reticulum (SR). The Ca2+ release of the SR accumulates calcium in the cytoplasm. For many decades models for these processes were developed. However, previous models have not combined the spatially resolved concentration dynamics of the dyadic cleft including the stochastic simulation of individual calcium channels and the whole cell calcium dynamics with a whole cardiac myocyte electrophysiology model. In this study, we developed a novel approach to resolve concentration gradients from single channel to whole cell level by using quasistatic approximation and finite element method for integrating partial differential equations. We ran a series of simulations with different RyR Markov chain models, different parameters for the SR components, sodium-calcium exchanger conditions, and included mitochondria to approximate physiological behaviour of a rabbit ventricular cardiac myocyte. The new multi-scale simulation tool which we developed makes use of high performance computing to reveal detailed information about the distribution, regulation, and importance of components involved in ECC. This tool will find application in investigation of heart contraction and heart failure.

APA, Harvard, Vancouver, ISO, and other styles

8

Grandi, Eleonora <1978&gt. "Computational analysis of excitability in cardiac myocytes." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/497/1/TesiEleonoraGrandi.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Grandi, Eleonora <1978&gt. "Computational analysis of excitability in cardiac myocytes." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/497/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Mathavan, Neashan Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "Parameter optimization in simplified models of cardiac myocytes." Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2009. http://handle.unsw.edu.au/1959.4/44709.

Full text

Abstract:

Atrial fibrillation (AF) is a complex, multifaceted arrhythmia. Pathogenesis of AF is associated with multiple aetiologies and the mechanisms by which it is sustained and perpetuated are similarly diverse. In particular, regional heterogeneity in the electrophysiological properties of normal and pathological tissue plays a critical role in the occurrence of AF. Understanding AF in the context of electrophysiological heterogeneity requires cell-specific ionic models of electrical activity which can then be incorporated into models on larger temporal and spatial scales. Biophysically-based models have typically dominated the study of cellular excitability providing detailed and precise descriptions in the form of complex mathematical formulations. However, such models have limited applicability in multidimensional simulations as the computational expense is too prohibitive. Simplified mathematical models of cardiac cell electrical activity are an alternative approach to these traditional biophysically-detailed models. Utilizing this approach enables the embodiment of cellular excitation characteristics at minimal computational cost such that simulations of arrhythmogensis in atrial tissue are conceivable. In this thesis, a simplified, generic mathematical model is proposed that characterizes and reproduces the action potential waveforms of individual cardiac myocytes. It incorporates three time-dependent ionic currents and an additional time-independent leakage current. The formulation of the three time-dependent ionic currents is based on 4-state Markov schemes with state transition rates expressed as nonlinear sigmoidal functions of the membrane potential. Parameters of the generic model were optimized to fit the action potential waveforms of the Beeler-Reuter model, and, experimental recordings from atrial and sinoatrial cells of rabbits. A nonlinear least-squares optimization routine was employed for the parameter fits. The model was successfully fitted to the Beeler-Reuter waveform (RMS error: 1.4999 mV) and action potentials recorded from atrial tissue (RMS error: 1.3398 mV) and cells of the peripheral (RMS error: 2.4821 mV) and central (RMS error: 2.3126 mV) sinoatrial node. Thus, the model presented here is a mathematical framework by which a wide variety of cell-specific AP morphologies can be reproduced. Such a model offers the potential for insights into possible mechanisms that contribute to heterogeneity and/or arrhythmia.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Cardiac myocytes"

1

sirna, Josephine Barbara. Iron regulation in neonatal rat cardiac myocytes. Ottawa: National Library of Canada, 1998.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

2

Wu, Bingruo. Expression of inhibin subunits in rat heart and cardiac myocytes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

3

Rizek, Randy. Ionic selectivity and regulation of maitotoxin-activated nonselective cation channels in rat cardiac myocytes. Ottawa: National Library of Canada, 2003.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

A, Clark William, Decker Robert S, Borg Thomas K. 1943-, and National Heart, Lung, and Blood Institute., eds. Biology of isolated adult cardiac myocytes: Proceedings of the National Heart, Lung, and Blood Institute-sponsored workshop "Biology of isolated adult cardiac myocytes," held September 22-25, 1987, at Asilomar Conference Center, Pacific Grove, California, USA. New York: Elsevier, 1988.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

5

Hariharan, Venkatesh. The Effects of Arrhythmogenic Right Ventricular Cardiomyopathy-Causing Proteins on the Mechanical and Signaling Properties of Cardiac Myocytes. [New York, N.Y.?]: [publisher not identified], 2014.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

6

Larry and Horti Fairberg Cardiac Workshop (6th 2009 Haifa, Israel). Analysis of cardiac development: From embryo to old age. Edited by Beyar Rafael, Landesberg Amir, and New York Academy of Sciences. Boston: Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

7

S, Sideman, Beyar Rafael, Landesberg Amir, and New York Academy of Sciences, eds. Interactive and integrative cardiology. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

8

1944-1988, Robinson T. F., and Kinne Rolf K. H, eds. Cardiac myocyte-connective tissue interactions in health and disease. Basel: Karger, 1990.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

9

pepper, C. B. Modulation of cardiac myocytr contraction by the vascular endothelium. Birmingham: University of Birmingham, 1996.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

10

Jenkins, Kim. The role of phosphoinositide hydrolysis and protein kinase C activation in cardiac myocyte hypertrophy. Birmingham: University of Birmingham, 1994.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "Cardiac myocytes"

1

Barnett, Vincent A. "Cellular Myocytes." In Handbook of Cardiac Anatomy, Physiology, and Devices, 147–58. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-372-5_10.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Barnett, Vincent A. "Cellular Myocytes." In Handbook of Cardiac Anatomy, Physiology, and Devices, 201–14. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19464-6_12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Deten, Alexander, Hans Christian Volz, Wilfried Briest, and Heinz-Gerd Zimmer. "Differential cytokine expression in myocytes and non-myocytes after myocardial infarction in rats." In Cardiac Cell Biology, 47–55. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-4712-6_7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Price, Robert L., Stephen T. Haley, Tara Bullard, Jeffrey Davis, Thomas K. Borg, and Louis Terracio. "Confocal Microscopy of Cardiac Myocytes." In Confocal Microscopy, 185–99. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-60761-847-8_8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Kaestner, Lars. "Calcium signalling in cardiac myocytes." In Calcium signalling, 24–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-34617-0_9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Chudasama, N. L., S. O. Marx, and S. F. Steinberg. "Scaffolding Proteins in Cardiac Myocytes." In Handbook of Experimental Pharmacology, 301–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72843-6_13.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Lang, Sarah E., and Margaret V. Westfall. "Gene Transfer into Cardiac Myocytes." In Methods in Molecular Biology, 177–90. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2572-8_15.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Takahashi, Eiji, and Katsuhiko Doi. "Oxygen Transport to Ischemic Cardiac Myocytes." In Advances in Experimental Medicine and Biology, 145–48. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5865-1_18.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Guatimosim, Silvia, Cristina Guatimosim, and Long-Sheng Song. "Imaging Calcium Sparks in Cardiac Myocytes." In Methods in Molecular Biology, 205–14. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-950-5_12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Shannon, T. R. "Integrated Calcium Management in Cardiac Myocytes." In Lecture Notes in Mathematics, 63–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11406501_3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Cardiac myocytes"

1

Lieber, Samuel C., Nadine Aubry, Jayashree Pain, Gissela Diaz, Song-Jung Kim, and Stephen S. Vatner. "Measurement of the Transverse Apparent Elastic Modulus in Mammalian Cardiac Myocytes." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-41469.

Full text

Abstract:

Transverse mechanical properties of mammalian cardiac myocytes, was determined by using atomic force microscopy (AFM). The AFM can be used as a nano-indentation device allowing transverse stiffness measurements to be conducted on biological cells in a physiological environment. This enables real-time biomechanical and physiological processes to be monitored with nano-scale resolution. Cellular mechanical properties were determined by indenting the cell’s body, and analyzing the indentation data with classical infinitesimal strain theory (CIST). This calculation was accomplished by modeling the AFM probe as a blunted cone. The blunted cone geometry fits the AFM force indentation data well and was used to calculate the apparent elastic modulus of the cardiac myocyte body. The mechanical properties of male 344 x Brown Norway F1 hybrid (F344×BN) rat cells was measured and an apparent elastic modulus of 35.1 ± 0.7 kPa (n = 53) was calculated. Further studies are being conducted on myocytes isolated from aged hearts to determine whether age effects cardiac mechanical properties at the level of the single myocyte.

APA, Harvard, Vancouver, ISO, and other styles

2

Zhang, Xu, and Yi Zhao. "Selective Electrical Stimulation of Adult Cardiomyocyte for Studying Intercellular Mechanical Transmission." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14753.

Full text

Abstract:

Heart diseases rank the top among the leading causes of death in the United States, and account for nearly 40% of all deaths 1. As the most important component of heart muscle, cardiac myocytes are the basic units to generate contractile forces and regulate heart function. There are extensive molecular and electrophysiological studies suggesting that the defective intercellular communication in cardiac myocytes is an underlying cause of left ventricular dysfunction in several heart diseases 2,3. However, there are limited evidences in terms of mechanical contractility and electromechanical transmission, which are the direct measures of intercellular communication in myocardium. This is largely due to the lack of appropriate tools that can quantitatively assess the mechanical performance of adult cardiac myocytes. In this study, a microengineered device is developed for quantitative assessment of cardiac mechanical performance in isolated adult myocytes. This device is capable of applying electrical stimulation to selected cardiac myocytes, measuring mechanical force generation in single cells, and examining intercellular mechanical transmission in longitudinally connected doublets of adult cardiac myocytes.

APA, Harvard, Vancouver, ISO, and other styles

3

Isomura, Akihiro, Takahiro Harada, and Kenichi Yoshikawa. "Spontaneous Formiation Cell Clusters in Cultured Cardiac Myocytes." In 2006 IEEE International Symposium on MicroNanoMechanical and Human Science. IEEE, 2006. http://dx.doi.org/10.1109/mhs.2006.320322.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Francis Ijebu, Funebi, Qince Li, Kuanquan Wang, Haibo Sui, Lufang Zhou, Yong Feng, and Henggui Zhang. "Computational Modeling of Cardiac Metabolism in Atrial Myocytes." In 2018 Computing in Cardiology Conference. Computing in Cardiology, 2018. http://dx.doi.org/10.22489/cinc.2018.184.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Roos, Kenneth P., A. Christyne Bliton, Bradford A. Lubell, John M. Parker, Mark J. Patton, and Stuart R. Taylor. "High Speed Striation Pattern Recognition In Contracting Cardiac Myocytes." In OE/LASE '89, edited by Gary C. Salzman. SPIE, 1989. http://dx.doi.org/10.1117/12.951892.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Xu, Menghao, and Yongshen Liang. "The numerical model of Ca2+ nanospark in cardiac myocytes." In 2023 3rd International Conference on Applied Mathematics, Modelling and Intelligent Computing (CAMMIC 2023), edited by Xuebin Chen and Hari Mohan Srivastava. SPIE, 2023. http://dx.doi.org/10.1117/12.2685983.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Wong, Jonathan, Oscar Abilez, and Ellen Kuhl. "Computational Modelling of Optogenetics in Cardiac Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80810.

Full text

Abstract:

Channelrhodopsin-2 (ChR2) is a light-activated ion channel that can allow scientists to electrically activate cells via optical stimulation. Using a combination of existing computational electrophysiological and mechanical cardiac cell models with a novel ChR2 ion channel model, we created a model for ChR2-transduced cardiac myocytes. We implemented this model into a commonly available finite element platform and simulated both the single cell and the tissue electromechanical response. Our simulations show that it is possible to stimulate cardiac tissue optically with ChR2-transduced cells.

APA, Harvard, Vancouver, ISO, and other styles

8

Bowlin, G. L., Barbara Wise, L. Terracio, and D. G. Simpson. "Bioengineered Muscle Implants." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2546.

Full text

Abstract:

Abstract Fundamental research has defined many of the mechanistic events that mediate congenital malformations and the pathological disease processes that alter cardiac structure and function. Despite these efforts, there are a limited number of clinical treatment options available for many of these conditions. In many cases, even for disease processes that cause focal defects in the ventricular wall, the only viable treatment is the complete replacement of the damaged organ by transplant. Unfortunately, the supply of cardiac tissue that is available for transplant therapy remains chronically, and critically, short of demand. The reconstruction of a specific domain of dysfunctional ventricular tissue with a cell-based therapy is a potential avenue of treatment. One of the most direct strategies in this type of treatment regime is the injection of a suspension of fetal or neonatal cardiac myocytes into the injured domain. In small animal models, two limitations have become apparent with this strategy. First, differentiated myocytes do not undergo migration when they are injected into scar tissue and as a result they tend to remain concentrated in the vicinity of the injection site. Second, the myocytes that survive in the injection site are not well integrated into the healthy tissue and contract at rates that are independent of the surrounding myocardium. The long-term objective of this project is to circumvent the limitations of injection therapy by fabricating a cardiac muscle prosthesis that mimics the three dimensional architecture of the intact heart.

APA, Harvard, Vancouver, ISO, and other styles

9

Shimayoshi, Takao, Yuta Yamamoto, and Tetsuya Matsuda. "A Preliminary Computational Model for Hypoxic Acidosis in Cardiac Myocytes." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513112.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Liu, Honghai, Julie X. Yun, Russel K. Pirlo, Delpine Dean, Hai Yao, Martine Laberge, and Bruce Z. Gao. "The Dependence of Mechanical Properties of Adult Rat Myocytes on Cell Alignment." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193024.

Full text

Abstract:

In response to damage, stress and cell death cardiac muscle undergoes remodeling in which cardiomyocytes de-differentiate and re-differentiate. An understanding of the mechanisms involved in this process may lead to therapies to promote and enhance the repair of damaged cardiac tissue. However, due to the complexity of native environments, it is hard to investigate this remodeling process directly on tissues isolated from the body. Therefore, it is important to construct a cell-culture model that will replicate the most relevant characteristics of that tissue in controlled environments with greater capability to be assessed. Native cardiac myocytes have an aligned arrangement in which neighboring cardiomyocytes are electrically and mechanical coupled through contact junctions. When adult cardiomyocytes are placed into a culture dish, the cells will be randomly oriented and lose their native phenotypes gradually due to the lack of proper aligned cell-cell connections. To address this issue, we have implemented our laser cell micropatterning system to create an adult cardiomyocyte culturing model with aligned rows of cells connected end to end. In this abstract, we describe the experimental procedure to achieve the laser alignment of adult cardiomyocytes and the results of mechanical property testing of the myocytes investigated using Multimode Picoforce Nanoscope Atomic Force Microscope (AFM) (Veeco).

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!