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Tytuł oryginału: Oxidative stress and neutrophil activation - the two keystones of ischemia/reperfusion injury.
Autorzy: Kamiński Karol A., Bonda Tomasz A., Korecki Janusz, Musiał Włodzimierz
Źródło: Int. J. Cardiol. 2002: 86 (1) s.41-59, il., bibliogr. 212 poz.
Sygnatura GBL: 305,693

Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Streszczenie angielskie: The widespread introduction of fibrinolytics and recently also PTCA in the treatment of myocardial infarction has changed the picture of modern cardiology. But this therapy also raises new problems and challenges. One of them is the occurrence of ectensive tissue injury caused by reperfusion. Reinstitution of oxegen to the ischemia tissues initiates various processes leading to generation of reactive oxygen species (ROSs). Acting on the plasma membrane ROS damage its organization and release various proinflammatory agents. Different proteins, including receptors, ionic channels, transporters or components of transduction pathways are substrates of oxidation by ROSs. Theis changed structure results in altered functioning and disruption of vital cellular processes. Another key factor of reperfusion injury is activation and infiltration of infarcted are by polymorphonuclear leukocytes (PMNs). Multiple studies identified stages of PMN activation and substances being involved in it. Main interest lies in cellular adhesion molecules, particularly selectins and á2 integrins, as their atagonists were repeatedly found to diminish neutrophil activation and infarct size. Nevertheless new publications strike at the foundations of the established order and confront the realtion between neutrophil infiltration and infarct size. PMNs are linked by close ties to other cells involved in inflammatory response. Seemingly also in cardiac ischemia-reperfusion injury, the activity of neutrophils is modulated by lymphocytes and macrophages. The article describes mutual interactions between different factors involved in the reperfusion injury that may enable preparing new treatments, hopefully as effective and successful as reperfusion therapy.

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