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Eskaf, Josephine [Author] ; Hahnenkamp, Klaus [Degree supervisor]; Deja, Maria [Degree supervisor] Universität Greifswald

Effects of Poloxamer 188 on direct mitochondrial protection in isolated mitochondria after ischemia reperfusion injury in rat isolated hearts

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  • Media type: E-Book; Thesis
  • Title: Effects of Poloxamer 188 on direct mitochondrial protection in isolated mitochondria after ischemia reperfusion injury in rat isolated hearts
  • Contributor: Eskaf, Josephine [Author]; Hahnenkamp, Klaus [Degree supervisor]; Deja, Maria [Degree supervisor]
  • Corporation: Universität Greifswald
  • Published: Greifswald, 2024
  • Extent: 1 Online-Ressource (PDF-Datei: 122 Seiten, 4256 Kilobyte); Illustrationen (farbig), Diagramme (teilweise farbig)
  • Language: English
  • Identifier:
  • RVK notation: VE 7067 : Dissertationen, Habilitationsschriften, wertvollere und umfangreichere Sonderdrucke
    YB 9504 : Dissertation, Habilitationsarbeit
  • Keywords: Poloxamer > Mitochondrium > Ischämie > Reperfusion > Postischämiesyndrom > Herzinfarkt > Ratte > Tiermodell
  • Origination:
  • University thesis: Dissertation, Universitätsmedizin der Universität Greifswald, 2024
  • Footnote: Literaturverzeichnis: Seite 87-102
    Zusammenfassung in deutscher Sprache
  • Description: Herzinfarkt, Poloxamer

    With high prevalence and mortality, myocardial infarction constitutes a social and economic burden in Germany and worldwide. Current guidelines for MI treatment require prompt reperfusion to salvage heart tissue and minimize short- and long-term complications. However, there are currently no treatments available to attenuate reperfusion injury. Ischemic as well as pharmacological post-conditioning have been identified as important clinical strategies to improve outcome. Membrane stabilizers, like Poloxamer 188 (P188), have been shown to improve myocardial ischemia reperfusion (IR) injury and mitochondrial function but have not yet been proven to directly offer mitochondrial protection. Mitochondrial function is crucial for cardiomyocyte function, and mitochondrial dysfunction plays an important role in myocardial injury. In this study, hearts from 79 Sprague Dawley rats were isolated and perfused ex-vivo with oxygenated Krebs Buffer for 20 min before 30 min of no-flow ischemia. Hearts were reperfused for 10 min with Krebs buffer or 1 mM P188. Cardiac mitochondria were isolated with 1 mM P188 vs 1 mM polyethylene glycol (PEG) vs vehicle by differential centrifugation. Mitochondrial function was assessed as adenosine triphosphate (ATP) synthesis, oxygen consumption and calcium retention for complex I and II substrates of the respiratory chain. An improvement of myocardial function with 10 min P188 post-conditioning could not be shown. Direct mitochondrial protection of P188 or PEG could not be observed in this model either. Further research is needed to ascertain whether P188 has a direct protective effect on mitochondria and, if so, on what pathways of IR injury it acts.
  • Access State: Open Access