Baumeister Steffen, Ofer Nina, Kleist Christian, Terne Peter, Opelz Gerhard, Gebhard Martha Maria, Germann Günter, Heitmann Christoph
Department of Hand, Plastic, and Reconstructive Surgery, Burn Center, BG Trauma Center Ludwigshafen, Germany.
Plast Reconstr Surg. 2004 Dec;114(7):1832-41. doi: 10.1097/01.prs.0000143577.36583.1b.
Ischemia-reperfusion injury is a dominant factor limiting tissue survival in any microsurgical tissue transplantation, a fact that also applies to allogeneic hand transplantation. The clinical experience of the 12 human hand transplantations indicates that shorter ischemia times result in reduced tissue damage and, ultimately, in better hand function. Heat stress preconditioning and the accompanying up-regulation of the heat shock protein 72 have been shown to reduce the ischemia-reperfusion injury following ischemia of various organs, including organ transplantation. The aim of this study was to reduce the ischemia-reperfusion injury in a model of composite tissue allotransplantation. Allogeneic hind limb transplantations were performed from Lewis (donor) to Brown-Norway rats. Donor rats in group A (n = 10) received a prior heat shock whereas rats in group B (n = 10) did not receive any prior heat shock. Group C served as a control group without transplantation. The transplantations were performed 24 hours after the heat shock, at which time the heat shock protein 72 was shown to be up-regulated. The outcome was evaluated 24 hours after transplantation by nitroblue tetrazolium staining and wet-to-dry weight ratio of muscle slices (anterior tibial muscle). The nitroblue tetrazolium staining showed a significant reduction of necrotic muscle in group A (prior heat shock) (p = 0.005). The wet-to-dry ratio was significantly reduced in group A (prior heat shock), indicating less muscle edema and less tissue damage (p = 0.05). Heat shock preconditioning 24 hours before an ischemic event leads to an up-regulation of heat shock protein 72 in muscle and to a tissue protection reducing ischemia-reperfusion injury in composite tissue transplantation.
缺血再灌注损伤是限制任何显微外科组织移植中组织存活的主要因素，这一事实也适用于同种异体手移植。12例人体手移植的临床经验表明，较短的缺血时间可减少组织损伤，并最终改善手部功能。热应激预处理及伴随的热休克蛋白72上调已被证明可减轻包括器官移植在内的各种器官缺血后的缺血再灌注损伤。本研究的目的是在复合组织同种异体移植模型中减轻缺血再灌注损伤。从Lewis大鼠（供体）到Brown-Norway大鼠进行同种异体后肢移植。A组（n = 10）的供体大鼠接受预先热休克，而B组（n = 10）的大鼠未接受任何预先热休克。C组作为未进行移植的对照组。热休克24小时后进行移植，此时热休克蛋白72显示上调。移植后24小时通过硝基蓝四氮唑染色和肌肉切片（胫前肌）的湿重与干重比评估结果。硝基蓝四氮唑染色显示A组（预先热休克）坏死肌肉明显减少（p = 0.005）。A组（预先热休克）的湿重与干重比显著降低，表明肌肉水肿减轻且组织损伤减少（p = 0.05）。缺血事件前24小时进行热应激预处理可导致肌肉中热休克蛋白72上调，并在复合组织移植中减轻缺血再灌注损伤，起到组织保护作用。
