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Pathophysiologie der Gefäßwand — Bedeutung für internistische Erkrankungen

  • Conference paper
Verhandlungen der Deutschen Gesellschaft für Innere Medizin

Part of the book series: Verhandlungen der Deutschen Gesellschaft für Innere Medizin ((VDGINNERE,volume 97))

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Zusammenfassung

Das gesamte Gefäßsystem wird vom Endothel in einer einzelligen Schicht ausgekleidet. Dabei stellt das Endothel nicht nur eine Diffusionsbarriere dar, sondern leistet einen wesentlichen Beitrag bei der Regulation des Gefäßtonus. Diese den Gefäßtonus modulierende Funktion des Endothels wurde 1981 von Furchgott et al. aufgedeckt, als sie zeigen konnten, daß Azetylcholin (ACh) in Gefäßen mit intaktem Endothel eine Dilatation hervorruft, in In-vitro-Gefäßpräparaten, deren Endothel infolge der Präparation meistens weitgehend geschädigt ist, aber eine Konstriktion auslöst. So hängt die Wirkung einer Vielzahl von im Blut zirkulierenden, vasoaktiven Substanzen (sog. Agonisten) auf die Vasomotorik vom funktionellen Zustand des Endothels ab:

  1. a)

    Ist die Endothelfunktion intakt, so kommen diese Agonisten nicht unmittelbar mit der glatten GefäßmuskuIatur in Kontakt, sondern stimulieren zunächst einmal, meist über einen rezeptorgekoppelten Mechanismus, das Endothel, wodurch es zur nachfolgenden Freisetzung von verschiedenen Lokalhormonen (sog. Autakoiden) kommt Diese Autakoide, wie der „endothelium-derived relaxant factor“ (EDRF; wahrscheinlich mit dem Stickoxid-(NO-)Radikal identisch) und verschiedene Prostaglandine (z. B. Prostazyklin, PGI2) bewirken bei abluminal gerichteter Freisetzung Vasodilatation und bei luminal gerichteter Freisetzung in erster Linie eine Hemmung der Thrombozytenadhäsion und -aggregation.

  2. b)

    Ist die Endothelfunktion dagegen mangelhaft (z. B. bei Atheromatose, bei der Hypertonie und bei immunologischen Reaktionen an der Endotheloberfläche) oder bei mechanischer Zerstörung des Endothels (z. B. durch Ballonkathetermanipulationen oder scherkraftbedingt bei stark turbulentem Fluß im Gebiet der Stenosen), dann fällt zum einen die Autakoidfreisetzung durch das Endothel weitgehend aus, zum anderen treffen die im Blut zirkulierenden Agonisten teilweise direkt auf die Gefäßmuskulatur, da die Schutzfunktion des Endothels nicht mehr gegeben ist. Über die Stimulation spezifischer Rezeptoren an der Gefäßmuskulatur (H1-, HT2-, P2x-, M1,2-, α1,2-, AVP-, VP-, u. a.) lösen die meisten dieser Agonisten dann eine Konstriktion aus. In den letzten Jahren sind eine Reihe von Erkrankungen, die möglicherweise auf eine gestörte Endothelfunktion zurückzuführen sind, daraufhin genauer untersucht worden. Bei verschiedenen Krankheitsbildern mit gestörter Vasomotorik, wie z. B. beim Morbus Raynaud und bei verschiedenen Formen der Angina pectoris (Übersicht bei Bassenge u. Heusch 1990), konnte die ursächliche Beteiligung einer mangelhaften endothelialen Autakoidfreisetzung mit weitgehender Sicherheit festgestellt werden. Da es sich bei diesen Erkrankungen jedoch meistens um ein multifaktorielles Geschehen handelt, dessen Teilkomponenten sehr variabel sind, und in dem nervöse, präsynaptische, humorale, hormonale, metabolische und endothelvermittelte Faktoren und Mechanismen interagieren, läßt sich die Stärke der einzelnen Teilkomponenten noch nicht genau abschätzen.

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Authors and Affiliations

  1. Mainz, Deutschland

    J. Meyer

  2. Institut für Angewandte Physiologie der Universität, Freiburg, Deutschland

    E. Bassenge & Ch. Huckstorf

  3. Physiologisches Institut I, Universität Tübingen, Deutschland

    P. C. Dartsch

  4. Klinische Forschergruppe der Medizinischen Klinik, Universität Würzburg, Würzburg, Deutschland

    U. Walter, M. Halbrügge, C. Nolte, M. Eigenthaler & S. M. Lohman

  5. Departement Innere Medizin, Abteilungen Klinische Pharmakologie und Kardiologie, und Departement Forschung, Labor für Gefäßforschung, Universitatskliniken, Kantonsspital, Basel, Schweiz

    T. F. Löscher

  6. Abteilung für experimentelle Kardiologie, Max-Planck-Institut, Bad Nauheim, Deutschland

    W. Schaper

  7. Medizinische Klinik, Universität Würzburg, Deutschland

    P. Schanzenbächer

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  1. J. Meyer
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  2. E. Bassenge
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  3. Ch. Huckstorf
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  5. U. Walter
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  6. M. Halbrügge
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  7. C. Nolte
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  8. M. Eigenthaler
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  9. S. M. Lohman
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  10. T. F. Löscher
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  11. W. Schaper
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  12. P. Schanzenbächer
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  1. Humboldtstr. 14, W-6200, Wiesbaden, Germany

    Klaus Miehlke

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© 1991 Springer-Verlag Berlin Heidelberg

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Meyer, J. et al. (1991). Pathophysiologie der Gefäßwand — Bedeutung für internistische Erkrankungen. In: Miehlke, K. (eds) Verhandlungen der Deutschen Gesellschaft für Innere Medizin. Verhandlungen der Deutschen Gesellschaft für Innere Medizin, vol 97. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84710-3_26

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  • DOI: https://doi.org/10.1007/978-3-642-84710-3_26

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-55080-8

  • Online ISBN: 978-3-642-84710-3

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