A new myofilament contraction model with ATP consumption for ventricular cell model

Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic p...
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Autor*in:	Muangkram, Yuttamol [verfasserIn] Noma, Akinori Amano, Akira

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Myofilament model Mechano-energetics Actomyosin–ATPase Crossbridge kinetics Troponin system

Anmerkung:	© The Physiological Society of Japan and Springer Japan KK 2017

Übergeordnetes Werk:	Enthalten in: The journal of physiological sciences - [Tokyo] : Springer, 2006, 68(2017), 5 vom: 02. Aug., Seite 541-554
Übergeordnetes Werk:	volume:68 ; year:2017 ; number:5 ; day:02 ; month:08 ; pages:541-554

Links:	Volltext

DOI / URN:	10.1007/s12576-017-0560-x

Katalog-ID:	SPR026171627

Internformat


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520			\|a Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model.
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publishDate	2017
allfields	10.1007/s12576-017-0560-x doi (DE-627)SPR026171627 (SPR)s12576-017-0560-x-e DE-627 ger DE-627 rakwb eng Muangkram, Yuttamol verfasserin aut A new myofilament contraction model with ATP consumption for ventricular cell model 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer Japan KK 2017 Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. Myofilament model (dpeaa)DE-He213 Mechano-energetics (dpeaa)DE-He213 Actomyosin–ATPase (dpeaa)DE-He213 Crossbridge kinetics (dpeaa)DE-He213 Troponin system (dpeaa)DE-He213 Noma, Akinori aut Amano, Akira aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 68(2017), 5 vom: 02. Aug., Seite 541-554 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:68 year:2017 number:5 day:02 month:08 pages:541-554 https://dx.doi.org/10.1007/s12576-017-0560-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 68 2017 5 02 08 541-554
spelling	10.1007/s12576-017-0560-x doi (DE-627)SPR026171627 (SPR)s12576-017-0560-x-e DE-627 ger DE-627 rakwb eng Muangkram, Yuttamol verfasserin aut A new myofilament contraction model with ATP consumption for ventricular cell model 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer Japan KK 2017 Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. Myofilament model (dpeaa)DE-He213 Mechano-energetics (dpeaa)DE-He213 Actomyosin–ATPase (dpeaa)DE-He213 Crossbridge kinetics (dpeaa)DE-He213 Troponin system (dpeaa)DE-He213 Noma, Akinori aut Amano, Akira aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 68(2017), 5 vom: 02. Aug., Seite 541-554 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:68 year:2017 number:5 day:02 month:08 pages:541-554 https://dx.doi.org/10.1007/s12576-017-0560-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 68 2017 5 02 08 541-554
allfields_unstemmed	10.1007/s12576-017-0560-x doi (DE-627)SPR026171627 (SPR)s12576-017-0560-x-e DE-627 ger DE-627 rakwb eng Muangkram, Yuttamol verfasserin aut A new myofilament contraction model with ATP consumption for ventricular cell model 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer Japan KK 2017 Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. Myofilament model (dpeaa)DE-He213 Mechano-energetics (dpeaa)DE-He213 Actomyosin–ATPase (dpeaa)DE-He213 Crossbridge kinetics (dpeaa)DE-He213 Troponin system (dpeaa)DE-He213 Noma, Akinori aut Amano, Akira aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 68(2017), 5 vom: 02. Aug., Seite 541-554 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:68 year:2017 number:5 day:02 month:08 pages:541-554 https://dx.doi.org/10.1007/s12576-017-0560-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 68 2017 5 02 08 541-554
allfieldsGer	10.1007/s12576-017-0560-x doi (DE-627)SPR026171627 (SPR)s12576-017-0560-x-e DE-627 ger DE-627 rakwb eng Muangkram, Yuttamol verfasserin aut A new myofilament contraction model with ATP consumption for ventricular cell model 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer Japan KK 2017 Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. Myofilament model (dpeaa)DE-He213 Mechano-energetics (dpeaa)DE-He213 Actomyosin–ATPase (dpeaa)DE-He213 Crossbridge kinetics (dpeaa)DE-He213 Troponin system (dpeaa)DE-He213 Noma, Akinori aut Amano, Akira aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 68(2017), 5 vom: 02. Aug., Seite 541-554 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:68 year:2017 number:5 day:02 month:08 pages:541-554 https://dx.doi.org/10.1007/s12576-017-0560-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 68 2017 5 02 08 541-554
allfieldsSound	10.1007/s12576-017-0560-x doi (DE-627)SPR026171627 (SPR)s12576-017-0560-x-e DE-627 ger DE-627 rakwb eng Muangkram, Yuttamol verfasserin aut A new myofilament contraction model with ATP consumption for ventricular cell model 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Physiological Society of Japan and Springer Japan KK 2017 Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. Myofilament model (dpeaa)DE-He213 Mechano-energetics (dpeaa)DE-He213 Actomyosin–ATPase (dpeaa)DE-He213 Crossbridge kinetics (dpeaa)DE-He213 Troponin system (dpeaa)DE-He213 Noma, Akinori aut Amano, Akira aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 68(2017), 5 vom: 02. Aug., Seite 541-554 (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:68 year:2017 number:5 day:02 month:08 pages:541-554 https://dx.doi.org/10.1007/s12576-017-0560-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 68 2017 5 02 08 541-554
language	English
source	Enthalten in The journal of physiological sciences 68(2017), 5 vom: 02. Aug., Seite 541-554 volume:68 year:2017 number:5 day:02 month:08 pages:541-554
sourceStr	Enthalten in The journal of physiological sciences 68(2017), 5 vom: 02. Aug., Seite 541-554 volume:68 year:2017 number:5 day:02 month:08 pages:541-554
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Myofilament model Mechano-energetics Actomyosin–ATPase Crossbridge kinetics Troponin system
isfreeaccess_bool	false
container_title	The journal of physiological sciences
authorswithroles_txt_mv	Muangkram, Yuttamol @@aut@@ Noma, Akinori @@aut@@ Amano, Akira @@aut@@
publishDateDaySort_date	2017-08-02T00:00:00Z
hierarchy_top_id	572081235
id	SPR026171627
language_de	englisch
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author	Muangkram, Yuttamol
spellingShingle	Muangkram, Yuttamol misc Myofilament model misc Mechano-energetics misc Actomyosin–ATPase misc Crossbridge kinetics misc Troponin system A new myofilament contraction model with ATP consumption for ventricular cell model
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topic_title	A new myofilament contraction model with ATP consumption for ventricular cell model Myofilament model (dpeaa)DE-He213 Mechano-energetics (dpeaa)DE-He213 Actomyosin–ATPase (dpeaa)DE-He213 Crossbridge kinetics (dpeaa)DE-He213 Troponin system (dpeaa)DE-He213
topic	misc Myofilament model misc Mechano-energetics misc Actomyosin–ATPase misc Crossbridge kinetics misc Troponin system
topic_unstemmed	misc Myofilament model misc Mechano-energetics misc Actomyosin–ATPase misc Crossbridge kinetics misc Troponin system
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title	A new myofilament contraction model with ATP consumption for ventricular cell model
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title_full	A new myofilament contraction model with ATP consumption for ventricular cell model
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author_browse	Muangkram, Yuttamol Noma, Akinori Amano, Akira
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title_sort	new myofilament contraction model with atp consumption for ventricular cell model
title_auth	A new myofilament contraction model with ATP consumption for ventricular cell model
abstract	Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. © The Physiological Society of Japan and Springer Japan KK 2017
abstractGer	Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. © The Physiological Society of Japan and Springer Japan KK 2017
abstract_unstemmed	Abstract A new contraction model of cardiac muscle was developed by combining previously described biochemical and biophysical models. The biochemical component of the new contraction model represents events in the presence of $ Ca^{2+} $–crossbridge attachment and power stroke following inorganic phosphate release, detachment evoked by the replacement of ADP by ATP, ATP hydrolysis, and recovery stroke. The biophysical component focuses on $ Ca^{2+} $ activation and force (Fb) development assuming an equivalent crossbridge. The new model faithfully incorporates the major characteristics of the biochemical and biophysical models, such as Fb activation by transient $ Ca^{2+} $ ([$ Ca^{2+} $]–Fb), [$ Ca^{2+} $]–ATP hydrolysis relations, sarcomere length–Fb, and Fb recovery after jumps in length under the isometric mode and upon sarcomere shortening after a rapid release of mechanical load under the isotonic mode together with the load–velocity relationship. ATP consumption was obtained for all responses. When incorporated in a ventricular cell model, the contraction model was found to share approximately 60% of the total ATP usage in the cell model. © The Physiological Society of Japan and Springer Japan KK 2017
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title_short	A new myofilament contraction model with ATP consumption for ventricular cell model
url	https://dx.doi.org/10.1007/s12576-017-0560-x
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up_date	2024-07-03T19:17:45.308Z
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A new myofilament contraction model with ATP consumption for ventricular cell model

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