Induction of heat-shock protein 72 in rat skeletal muscle does not increase tolerance to ischemia-reperfusion injury

Ischemia-reperfusion injury is implicated in the failure of free flap and r eplant surgeries and is associated with the pathogenesis of a wide variety of clinical diseases including stroke, myocardial infarction, spinal injury , and compartment syndromes. We used a skeletal muscle flap model to test i f the induction of heat-shock protein 72 (HSP72) by mild hyperthermia provi des tolerance against ischemia-reperfusion injury. Immunocytochemistry and Western blot analysis verified increased production of HSP72 in the gracili s muscle of globally heated rats. Neutrophil accumulation in the microvascu lature and postischemic muscle survival after ischemia-reperfusion were una ltered by preischemic hyperthermia, indicating HSP72 induction is not suffi cient to provide resistance against severe injury in skeletal muscle. (C) 1 999 John Wiley & Sons, Inc.