Zusammenfassung
Die genauen Vorgänge der Herzschmerzentstehung sind in vielen Bereichen noch weitgehend ungeklärt. Unterschiedliche Ansichten bestehen sowohl in der Frage nach der Art der Schmerzrezeptoren, nach der Lokalisation der Schmerzentstehung (intravaskulär, extravaskulär, myokardial, perikardial) als auch nach der Art des Stimulus (chemische Noxe als Ischämiefolge, mechanische Reizung, direkt neurogen). Dabei ist zu berücksichtigen, daß die Diskussion der Herzschmerzentstehung eng mit der Diskussion der pathophysiologischen Prozesse, die zu Herzschmerz führen, verknüpft ist. Damit sind Fragestellungen wie nach der funktionellen Bedeutung von Stenosen, der metabolischen, humoralen oder neurogenen Regulation der Koronargefäße (Yasue etal. 1974; Gunn etal. 1972; Rutishauser et al. 1973), einer durch Arteriosklerose veränderten Gefäßphysiologie (Schlant 1978), der Bedeutung von Tonusveränderungen der Koronargefäße, von Spasmen und Kollateralen eng mit der Frage der Herzschmerzentstehung verbunden.
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Droste, C. (1984). Neurophysiologie des Koronarschmerzes. In: Roskamm, H., et al. Koronarerkrankungen. Handbuch der inneren Medizin, vol 9 / 3. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69451-6_4
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