Zusammenfassung
Gegen Ende der 60er Jahre, als die Bedrohung durch die koronare Herzerkrankung zu politischem Handeln zwang, schrieb das National Heart and Lung Institute der USA ein besonderes Programm zur Förderung von Forschungsprojekten aus, die sich direkt mit der experimentellen Therapie experimenteller Infarkte befaßten [6]. Es wurden aber auch Programme gefördert, die sich mit Methodenentwicklungen und geeigneten Tiermodellen beschäftigten. Viele neue wie schon bekannte Pharmaka, Naturstoffe und physikalische Methoden wurden einem empirischen Screening mit relativ einfachen Methoden unterzogen, mit dem Ziel der Hemmung der Infarktausbreitung nach akutem Koronarverschluß. Von den oft nicht besonders gut reproduzierbaren Resultaten blieb eigentlich als Goldstandard nur die rechtzeitige Reperfusion übrig. Der optimale Erfolg der Reperfusion, wie unsere Experimente zeigten [42, 46, 47], war abhängig von drei Faktoren:
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von der Zeit, die seit dem Koronarverschluß vergangen war
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vom O2-Verbrauch des Myokards vor und während des Koronarverschlusses (hoher MVO2 erfordert frühere Reperfusion) und
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von der Kollateraldurchblutung (niedrige Kollateraldurchblutung erfordert frühere Reperfusion).
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© 1990 Dr. Dietrich Steinkopff Verlag, GmbH & Co. KG, Darmstadt
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Schaper, W., Schott, R.J., Kobayashi, M. (1990). Reperfusion des ischämischen Myokards — Schutz oder Schaden?. In: Heusch, G. (eds) Pathophysiologie und rationale Pharmakotherapie der Myokardischämie. Steinkopff. https://doi.org/10.1007/978-3-642-72437-4_8
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