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- W204908957 abstract "Prolonged myocardial ischemia results in a variety of severe cellular, metabolic and ultra-structural damages. It is therefore generally accepted that reperfusion is an absolute prerequisite for the survival of ischemic tissue. However, reperfusion may precipitate arrhythmias, cause myocardial stunning and accelerate necrotic process. Oxygen free radicals have been suggested as possible mediators of reperfusioninduced injury and there is circumstantial evidence that supports this hypothesis. Indirect evidence in support of this concept derives from studies in which antioxidant enzymes, enzyme inhibitors, free radical scavengers and iron chelators are able to protect against reperfusion injury in a number of experimental studies.In vivopolymorphonuclear leukocytes (PMNs) have been hypothesized to induce and to amplify the process of reperfusion injury in post-ischemic myocardium. Within vivo models, there are many different cellular and humoral factors making it difficult to determine the importance of specific components in the pathogenesis of myocardial injury. Both ischemia and reperfusion promote the expression of pro-inflammatory gene products and bioactive agents. Furthermore, ischemia induces a pro-inflammatory state that increases tissue vulnerability towards further injury during reperfusion.KeywordsNitric OxideReperfusion InjuryCardiac IschemiaSpin TrapSpin AdductThese 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." @default.
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- W204908957 date "2003-01-01" @default.
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- W204908957 title "Identification and role of inflammatory oxygen free radicals in cardiac ischemia and reperfusion injury" @default.
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- W204908957 doi "https://doi.org/10.1007/978-3-0348-8047-3_11" @default.
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