Concepts related to the study of reactive oxygen and cardiac reperfusion injury.
The phenomenon of reperfusion injury remains poorly defined. Questions remain about whether injury occurs in addition to that produced by hypoxia or ischemia, or whether the observed changes simply reflect the unmasking of an underlying injury. Various pathological processes which occur upon the return of oxygen to hypoxic and ischemic heart tissue have been quantitated to assess the extent of reperfusion injury, yet it is not known if they reflect identical or different processes. In addition, the mechanism(s) responsible for these diverse changes may not be the same in the various model systems used to study reperfusion injury. Although reactive oxygen species clearly are formed at reperfusion, conclusive evidence that they are producing injury, particularly during the first seconds, is not available. Several sources of these reactive oxygen species have been proposed but none have been clearly linked with injury in several species or model systems. As research in the field of reperfusion injury continues, it is imperative for scientists to clearly define the system they are using so that studies examining mechanisms of cell lysis at reperfusion are not confused with those assessing the occurrence and mechanisms of damage in addition to that produced by oxygen deprivation.
Kehrer
J P
JP
Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas, Austin 78712-1074.
D000818:Animals; D005609:Free Radicals; D006321:Heart / Q000503:physiopathology; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009206:Myocardium / Q000166:cytology; D010100:Oxygen / Q000633:toxicity*
D005609:Free Radicals; D010100:Oxygen