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Pathophysiologie — Kontraktile Proteine

  • Chapter
Herzinsuffizienz

Part of the book series: Aktuelle Therapieprinzipien in Kardiologie und Angiologie ((THERAPIEPRINZ.))

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Zusammenfassung

Eine vermehrte hämodynamisehe Belastung kompensiert das Herz auf zellulärer Ebene durch eine Größenzunahme der Myozyten und entsprechende Massenzunahme intrazellulärer Moleküle (Vliegen et al. 1987; Campbell et al. 1989). Diese myokardiale Hypertrophie ist jedoch kein uniform ablaufender Prozeß. Statt dessen wird die quantitative und qualitative Änderung intrakardialer Moleküle bei der Herzhypertrophie von einer Fülle von exogenen und endogenen Faktoren beeinflußt. So hängt das Ausmaß der Hypertrophie von der untersuchten Spezies (Rouleau et al. 1989), der intrakardialen Lokalisation der hypertrophierenden Myozyten (Vescovo et al. 1989) und der Art der Belastung ab (Moalic et al. 1981). Aber nicht nur das Ausmaß, sondern auch die Qualität der Hypertrophie ist je nach Spezies und Ursache der Hypertrophie verschieden (Moalic et al. 1981; Hamrell u. Low 1978). Daraus resultiert ein für die jeweilige Spezies sowie für die Art und das Ausmaß der Hypertrophie spezifische Isoformzusammensetzung kardialer Moleküle.

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Authors
  1. H. Katus
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Editors and Affiliations

  1. Abt. Innere Medizin III, Med. Klinik, Bergheimer Straße 58, D-6900, Heidelberg, Deutschland

    Rainer Dietz

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© 1992 Springer-Verlag Berlin Heidelberg

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Katus, H. (1992). Pathophysiologie — Kontraktile Proteine. In: Dietz, R. (eds) Herzinsuffizienz. Aktuelle Therapieprinzipien in Kardiologie und Angiologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77021-0_14

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  • DOI: https://doi.org/10.1007/978-3-642-77021-0_14

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-54670-2

  • Online ISBN: 978-3-642-77021-0

  • eBook Packages: Springer Book Archive

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