Lille S, Su C Y, Schoeller T, Suchy H, Lyons S, Russell R C, Neumeister M, Lai C C
Institute of Plastic and Reconstructive Surgery, Department of Surgery, Southern Illinois University School of Medicine, Springfield 62702, USA.
Muscle Nerve. 1999 Mar;22(3):390-3. doi: 10.1002/(sici)1097-4598(199903)22:3<390::aid-mus12>3.0.co;2-1.
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.
缺血再灌注损伤与游离皮瓣和再植手术失败有关，并且与包括中风、心肌梗死、脊髓损伤和骨筋膜室综合征在内的多种临床疾病的发病机制相关。我们使用骨骼肌瓣模型来测试轻度热疗诱导热休克蛋白72（HSP72）是否能提供对缺血再灌注损伤的耐受性。免疫细胞化学和蛋白质印迹分析证实，全身加热大鼠的股薄肌中HSP72的产生增加。缺血前热疗并未改变缺血再灌注后微血管中的中性粒细胞聚集和缺血后肌肉存活情况，这表明诱导HSP72不足以提供对骨骼肌严重损伤的抵抗力。
