Anästhesiol Intensivmed Notfallmed Schmerzther 2002; 37(6): 314-325
DOI: 10.1055/s-2002-32233
Übersicht
© Georg Thieme Verlag Stuttgart · New York

Die neurogene Entzündung

I. Grundlegende Mechanismen, Physiologie und PharmakologieNeurogenic InflammationI. Basic Mechanisms, Physiology and PharmacologyM.  K.  Herbert1 , P.  Holzer2
  • 1Klinik für Anaesthesiologie der Universität Würzburg
  • 2Institut für Exp. und Klin. Pharmakologie der Universität Graz, Österreich
Further Information

Publication History

Publication Date:
13 June 2002 (online)

Zusammenfassung

Die Aktivierung dünner sensorischer Nervenfasern durch noxische Reize bewirkt eine Freisetzung der Neuropeptide Substanz P und Calcitonin Gene-related Peptide, CGRP, aus den peripheren Nervenendigungen. Diese Neuropeptide und nachfolgend freigesetzte Mediatoren rufen am Ort der noxischen Reizung ein Ödem, eine Hyperämie und ferner ein Erythem hervor, dessen Ausdehnung über die Reizstelle hinausgeht (sog. flare response). Da diese Entzündungszeichen von der Funktion und Integrität peripherer sensorischer Neurone abhängen, wurde diese Reaktion neurogene Entzündung genannt. Da fast alle Gewebe von Säugern, inklusive dem Menschen, von afferenten nozizeptiven Neuronen innerviert sind, kann diese neurogene Entzündung überall im Körper auftreten. Obgleich seit mehr als einem Jahrhundert bekannt war, dass an dieser Reaktion, die mit antidromer Vasodilatation, Axonreflex, triple response, neurogener Entzündung beschrieben wurde, sensorische Afferenzen beteiligt sind, rückte die neurogene Entzündung erst in den vergangenen zwanzig Jahren als ein physiologisch und pathophysiologisch relevanter Prozess ins Bewusstsein. Eine Vielzahl endogener und exogener Substanzen können sensorische Nervenendigungen aktivieren und sensibilisieren und somit Schmerz oder eine nozizeptive Reaktion und eine neurogene Entzündung auslösen. Es wurde eine große Zahl pharmakologisch unterschiedlicher Substanzen und Mediatorantagonisten gefunden, die die neurogene Entzündung modulieren oder vermindern. Von besonderem Interesse sind hierbei Capsaicin und andere Agonisten und Antagonisten am Vanilloidrezeptor, da sie nozizeptive Neurone desensibilisieren und somit eine neurogene Entzündung vermindern oder gar verhindern können.

Abstract

Activation of sensory unmyelinated neurons by noxious stimuli evokes the release of neuropeptides, such as substance P and calcitonin gene-related peptide (CGRP) from peripheral nerve endings. These neuropeptides and subsequently released mediators cause a local oedema, hyperaemia and an erythema which extends beyond the site of stimulation (so-called flare response). Since these inflammatory signs depend on the function and integrity of peripheral sensory nervous systems, the response has been termed neurogenic inflammation. Due to the fact that nearly all tissues in mammals including humans are innervated by afferent sensory neurons, this neurogenic inflammation can occur ubiquitously throughout the body. Albeit first evidence showing that sensory neurons contribute to the inflammatory signs, described as antidromic vasodilatation, axon reflex, triple response, neurogenic inflammation, elicited at the level of tissue that they innervate was first obtained more than one hundred years ago, it was in the last two decades that inflammation caused by the release of neuropeptides from afferent nerve endings was recognised as a physiologically and pathologically relevant process. A large number of exogenous and endogenous substances and autacoids may stimulate or sensitise sensory nerve endings, thus simultaneously producing pain and nociceptive responses, as well as neurogenic inflammation. On the basis of recent research a variety of pharmacological substances and antagonists of putative mediators have been identified to modulate or suppress neurogenic inflammation, thus providing a rationale for therapeutical strategies for various diseases in which neurogenic inflammation is suggested to be involved. Among them, capsaicin and other newly developed agonists and antagonists at the vanilloid receptor have attracted particular attention, since they were found to be capable of desensitizing nociceptive nerve structures and thus of preventing development of neurogenic inflammation or even of abolishing an ongoing inflammatory process.

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Priv.-Doz. Dr. med. Michael K. Herbert

Klinik für Anaesthesiologie der Universität Würzburg


Josef-Schneider-Straße 2

97080 Würzburg

Email: mherbert@anaesthesie.uni-wuerzburg.de

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