Abstract
Free radical reactions are considered to be an important pathophysiologic determinant of a broad range of inflammatory and ischemic diseases. The latter disease state, in particular, is still a very active area of free radical research since the discovery of the so-called oxygen paradox [1, 2]. Indeed, the sudden reoxygenation of the myocardium after a transient period of global ischemia results in cellular necrosis and intracellular calcium overload. Current hypotheses on the involvement of oxygen-derived free radicals in the course of the reperfusion event are essentially based on animal studies, in which the inclusion of free radical scavengers in the perfusion medium significantly improved hemodynamic and biochemical parameters [3-6]. In addition, electron spin resonance, low level chemiluminescence and reflectance studies on perfused rat heart suggest that free radical production is already present in the ischemic phase and that shortly after the onset of the oxygen readmission, a burst of free radical generation occurs [7–9].KeywordsMembrane PhospholipidFatty Acid IncorporationRadioactive Fatty AcidAntioxidant NetworkFatty Acid TurnoverThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Published Version
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