Ischemia: profile of an enemy. Reperfusion injury of skeletal muscle.
Recent experimental studies of temporary skeletal muscle ischemia in dogs showed that progressive deterioration in cell membrane electrical potentials (Em) occurred after partial but not total ischemia. With intracellular adenosine triphosphate concentration within the normal range, cell membrane damage by oxygen-derived free radicals was considered. In rats subjected to 60 minutes of infrarenal aortic occlusion, intra-arterial superoxide dismutase infused during removal of the aortic clamp prevented the continued decrease in Em. These data suggest that oxygen-derived free radicals may be mediators of reperfusion injury of cell membranes.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D002463:Cell Membrane Permeability; D004285:Dogs; D005260:Female; D005609:Free Radicals; D007473:Ion Channels / Q000378:metabolism; D007511:Ischemia / Q000473:pathology*; D008564:Membrane Potentials; D009132:Muscles / Q000098:blood supply* / Q000473:pathology; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
D005609:Free Radicals; D007473:Ion Channels; D000255:Adenosine Triphosphate