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 replant 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 if the induction of heat-shock protein 72 (HSP72) by mild hyperthermia provides tolerance against ischemia-reperfusion injury. Immunocytochemistry and Western blot analysis verified increased production of HSP72 in the gracilis muscle of globally heated rats. Neutrophil accumulation in the microvasculature and postischemic muscle survival after ischemia-reperfusion were unaltered by preischemic hyperthermia, indicating HSP72 induction is not sufficient to provide resistance against severe injury in skeletal muscle.