The cariomyopathic hamster as model of early myocardial aging
Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocard...
Ausführliche Beschreibung
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| Autor*in: |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1999 |
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| Umfang: |
6 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Molecular and cellular biochemistry - 1973, 198(1999) vom: Jan./Feb., Seite 1-6 |
| Übergeordnetes Werk: |
volume:198 ; year:1999 ; month:01/02 ; pages:1-6 ; extent:6 |
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| 520 | |a Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. | ||
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| 700 | 1 | |a Peruzzi, Giuseppe |4 oth | |
| 700 | 1 | |a Di Nardo, Paolo |4 oth | |
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(DE-627)NLEJ198051611 DE-627 ger DE-627 rakwb eng The cariomyopathic hamster as model of early myocardial aging 1999 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. Springer Online Journal Archives 1860-2002 Minieri, Marilena oth Fiaccavento, Roberta oth Carosella, Luciana oth Peruzzi, Giuseppe oth Di Nardo, Paolo oth in Molecular and cellular biochemistry 1973 198(1999) vom: Jan./Feb., Seite 1-6 (DE-627)NLEJ188989099 (DE-600)2003615-2 1573-4919 nnns volume:198 year:1999 month:01/02 pages:1-6 extent:6 http://dx.doi.org/10.1023/A:1006926411659 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 198 1999 1/2 1-6 6 |
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(DE-627)NLEJ198051611 DE-627 ger DE-627 rakwb eng The cariomyopathic hamster as model of early myocardial aging 1999 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. Springer Online Journal Archives 1860-2002 Minieri, Marilena oth Fiaccavento, Roberta oth Carosella, Luciana oth Peruzzi, Giuseppe oth Di Nardo, Paolo oth in Molecular and cellular biochemistry 1973 198(1999) vom: Jan./Feb., Seite 1-6 (DE-627)NLEJ188989099 (DE-600)2003615-2 1573-4919 nnns volume:198 year:1999 month:01/02 pages:1-6 extent:6 http://dx.doi.org/10.1023/A:1006926411659 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 198 1999 1/2 1-6 6 |
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(DE-627)NLEJ198051611 DE-627 ger DE-627 rakwb eng The cariomyopathic hamster as model of early myocardial aging 1999 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. Springer Online Journal Archives 1860-2002 Minieri, Marilena oth Fiaccavento, Roberta oth Carosella, Luciana oth Peruzzi, Giuseppe oth Di Nardo, Paolo oth in Molecular and cellular biochemistry 1973 198(1999) vom: Jan./Feb., Seite 1-6 (DE-627)NLEJ188989099 (DE-600)2003615-2 1573-4919 nnns volume:198 year:1999 month:01/02 pages:1-6 extent:6 http://dx.doi.org/10.1023/A:1006926411659 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 198 1999 1/2 1-6 6 |
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(DE-627)NLEJ198051611 DE-627 ger DE-627 rakwb eng The cariomyopathic hamster as model of early myocardial aging 1999 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. Springer Online Journal Archives 1860-2002 Minieri, Marilena oth Fiaccavento, Roberta oth Carosella, Luciana oth Peruzzi, Giuseppe oth Di Nardo, Paolo oth in Molecular and cellular biochemistry 1973 198(1999) vom: Jan./Feb., Seite 1-6 (DE-627)NLEJ188989099 (DE-600)2003615-2 1573-4919 nnns volume:198 year:1999 month:01/02 pages:1-6 extent:6 http://dx.doi.org/10.1023/A:1006926411659 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 198 1999 1/2 1-6 6 |
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(DE-627)NLEJ198051611 DE-627 ger DE-627 rakwb eng The cariomyopathic hamster as model of early myocardial aging 1999 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. Springer Online Journal Archives 1860-2002 Minieri, Marilena oth Fiaccavento, Roberta oth Carosella, Luciana oth Peruzzi, Giuseppe oth Di Nardo, Paolo oth in Molecular and cellular biochemistry 1973 198(1999) vom: Jan./Feb., Seite 1-6 (DE-627)NLEJ188989099 (DE-600)2003615-2 1573-4919 nnns volume:198 year:1999 month:01/02 pages:1-6 extent:6 http://dx.doi.org/10.1023/A:1006926411659 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 198 1999 1/2 1-6 6 |
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The cariomyopathic hamster as model of early myocardial aging |
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Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. |
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Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. |
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Abstract Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early α to β myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging. |
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