Der Schmerz

, Volume 2, Issue 3, pp 118–124 | Cite as

Pathophysiologie des ischämischen Herzschmerzes

  • T. Münzel
  • E. Bassenge
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Zusammenfassung

Der Herzschmerz ist eine bewußte Erfahrung, welche mit Hilfe von experimentellen Untersuchungen nur indirekt erforscht werden kann. Der exakte Mechanismus der Angina pectoris Entstehung liegt immer noch im Dunkeln. Die afferenten Fasern des sympathischen Nervensystems werden als Schmerzbahn angesehen. Vorhof und Kammer des Herzens sind in großer zahl mit sensiblen, sympathischen Nervenendigungen versorgt. Im Rückenmark konvergieren die Impulse der Sympathikusbahn mit somatischen thorakalen Bahnen auf dasselbe spinothalamische Neuron ein Umstand welcher wahrscheinlich für das Phänomen des “übertragenen Schmerzes” (=Projektion auf ein anderes Organ) verantwortlich ist. Insgesamt wurden zwei Hypothesen vorgeschlagen, welche den peripheren Mechanismus der kardialen Nozizeption erklären sollten. Die Intensitätstheorie postuliert, daß Schmerz aufgrund einer exzessiven Stimulation von rezeptiven Strukturen entsteht, welche sich normalerweise wie niederschwellige Mechanorezeptoren verhalten, während nach der Spezifitätstheorie Schmerz nur nach Erregung eines definierten nozizeptiven Apparates entsteht. Die ventrikulären sympathischen Afferenzen, ob myelinisiert oder nicht myelinisiert, antworten auf chemische und mechanische Stimuli und verhalten sich somit wie polymodale Rezeptoren. Afferent vagale Fasern tragen möglicherweise über eine Modulation der Schmerzsachwelle oder Schmerzcharakteristik zur kardialen Nozizeption bei. Aufgrund der Ergebnisse in tierexperimentellen Studien am Herzmuskel bzw. quergestreiften Skeletmuskel sind folgende Mechanismen für den Herzschmerz denkbar: a) Eine paradoxe Bewegung des ischämischen linken Ventrikels (das sogenannte Bulging) und damit die Erregung von Mechanorezeptoren durch passive Dehnung während der Kammerkontraktion. b) Die Stimulation von freien sensorischen Nervenendigungen durch chemische Algogene wie Bradykinin, PGE2, Adenosin, Histamin oder Kalium, sowie c) eine Kombination der ersten beiden Punkte: Chemische Algogene sensibilisieren Mechanorezeptoren und senken somit deren Schwelle für die Nozizeption.

Pathophysiology of ischemic cardiac pain

Abstract

Cardiac pain is a conscious experience that can be explored only indirectly with experimental approaches. The exact machanisms eliciting cardiac pain still remain obscure. The afferent fibres running in the cardiac sympathetic nerves are regarded as the essential pathway for the transmission of cardiac pain. Atria and ventricle are abundantly supplied with sympathetic sensory innervation. In the spinal cord, impulses transmitted by the sympathetic pathway converge with impulses from somatic thoracic structures onto the same ascending spinothalamic neuron which probably explains the mechanism of referred pain (=projection of pain to another organ). Two hypotheses have been put forward to explain the peripheral mechanism for nociception. The intensity mechanism assumes that pain results from an excessive stimulation of receptive structures normally stimulated at lower levels whereas a specific sensation is considered to result from an excitation of a well defined nociceptive apparatus. Ventricular sympathetic afferent fibres whether myelinated or unmyelinated, always possess some mechanosensitivity and respond to normal chemical and mechanical stimuli, thus displaying properties of polymodal receptors. Afferent vagal fibres may contribute to the mechanisms of cardiac nociception by modulating the threshold and characteristics of pain. Experimental studies identified three main mechanisms, which may be responsible for eliciting cardiac pain during ischemic periods in humans: a) nonphysiological motion of the ischemic left ventricular wall (bulging) and an excitation of mechanical receptors by passive stretching. b) The excitation of free sensory nerve endings by chemicals such as bradykinin, PGE2, adenosin, histamin or potassium. c) A combination of a and b: algogenic chemicals may sensitize mechanical receptors and therefore lower their threshold for nociception.

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Copyright information

© Springer-Verlag 1988

Authors and Affiliations

  • T. Münzel
    • 1
  • E. Bassenge
    • 1
  1. 1.Institut für Angewandte Physiologie der UniversitätFreiburg i. Br.

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