Free radical mediated damage in skeletal muscle.
Skeletal muscle subjected to prolonged ischemia will develop significant injury, however it can withstand periods of ischemia that would be irreversible in other tissues such as brain and heart. Reperfusion injury has been measured and suggested to occur secondary to oxygen free radicals. The increases in vascular permeability and resistance following ischemia/reperfusion can be blunted using free radical scavengers. Also skeletal muscle necrosis can be reduced if these scavengers are provided in high concentration during reperfusion. Recently increases in hydroxy-conjugated dienes, a marker of lipid peroxidation, have been found in reperfused skeletal muscle, providing chemical evidence for free radical injury during reperfusion. These studies have provided some insight into ischemia/reperfusion injury in skeletal muscle, but more investigations are required to detail the mechanisms involved in this injury.
Lindsay
T
T
Division of Vascular Surgery, University of Toronto, R. Fraser Elliott Vascular Research Laboratory, Ontario, Canada.
Romaschin
A
A
Walker
P M
PM
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004285:Dogs; D005609:Free Radicals; D007511:Ischemia / Q000378:metabolism; D015227:Lipid Peroxidation; D009132:Muscles / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D009336:Necrosis; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D014969:Xanthine Oxidase / Q000378:metabolism
D005609:Free Radicals; D014969:Xanthine Oxidase; D010100:Oxygen; D002118:Calcium