title: Antioxidant status following acute ischemic limb injury: a rabbit model.
abstract: Although ischemic injury to skeletal muscle is a matter of great clinical importance, relatively little is known about the mechanisms which determine systemic responses. One purpose of this study is to elucidate the systemic antioxidant status following an episode of acute ischemic limb injury and subsequent reperfusion. Twelve New Zealand white rabbits were used in this study. After the animals were anesthetized, an ischemic insult was created in the right hind limb for twelve hours, followed by four hours of reperfusion. Several series of blood samples were obtained. At the end of the experiment, the animals were killed and necropsies undertaken in order to evaluate the antioxidant status of various visceral organs. The results link ischemia and reperfusion injury to a significant decline in antioxidative activity in various tissues. The weakening in antioxidant status after ischemic limb injury was most pronounced in the heart tissue, followed in descending order by the spleen, skeletal muscle, lung, liver, and kidney tissue. The levels of specific antioxidants and reactive oxygen species in various organs changed significantly, and the changes were tissue specific. Endogenous radical scavenging systems were not entirely overwhelmed in most of the tissues studied. But higher levels of malondialdehyde (MDA) found in cardiac tissue suggest that the production of oxygen free radicals is accelerated by an ischemic injury. Based on the study, we believe that the cardiac tissue is particularly susceptible to the effects of ischemia and reperfusion injury. Damage to cardiac tissue is probably the major cause of mortality following acute ischemic injury in a limb.
authors.affiliation: Department of Orthopedic Surgery, National Taiwan University Hospital, College of Medicine, Taipei, ROC. drjssun@ha.mc.ntu.edu.tw
authors.forename: J S
authors.initials: JS
authors.lastname: Sun
authors.forename: F J
authors.initials: FJ
authors.lastname: Lu
authors.forename: W C
authors.initials: WC
authors.lastname: Huang
authors.forename: S M
authors.initials: SM
authors.lastname: Hou
authors.forename: Y H
authors.initials: YH
authors.lastname: Tsuang
authors.forename: Y S
authors.initials: YS
authors.lastname: Hang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D006614:Hindlimb / Q000098:blood supply*; D006861:Hydrogen Peroxide / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008163:Luminescent Measurements; D008168:Lung / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D011817:Rabbits; D015427:Reperfusion Injury / Q000378:metabolism*; D013154:Spleen / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D020122:tert-Butylhydroperoxide / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D008315:Malondialdehyde; D020122:tert-Butylhydroperoxide; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione