title: Reduction of skeletal muscle injury in composite tissue allotransplantation by heat stress preconditioning.
abstract: 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.
authors.affiliation: Department of Hand, Plastic, and Reconstructive Surgery, Burn Center, BG Trauma Center Ludwigshafen, Germany. stbaumeister@yahoo.com
authors.forename: Steffen
authors.initials: S
authors.lastname: Baumeister
authors.forename: Nina
authors.initials: N
authors.lastname: Ofer
authors.forename: Christian
authors.initials: C
authors.lastname: Kleist
authors.forename: Peter
authors.initials: P
authors.lastname: Terne
authors.forename: Gerhard
authors.initials: G
authors.lastname: Opelz
authors.forename: Martha Maria
authors.initials: MM
authors.lastname: Gebhard
authors.forename: Günter
authors.initials: G
authors.lastname: Germann
authors.forename: Christoph
authors.initials: C
authors.lastname: Heitmann
mesh_terms: D000818:Animals; D050884:HSP72 Heat-Shock Proteins; D018882:Heat Stress Disorders; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006614:Hindlimb / Q000637:transplantation*; D006979:Hyperthermia, Induced; D007202:Indicators and Reagents / Q000032:analysis; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D009580:Nitroblue Tetrazolium / Q000032:analysis; D009929:Organ Size; D051381:Rats; D011917:Rats, Inbred Lew; D015427:Reperfusion Injury / Q000517:prevention & control*; D014184:Transplantation, Homologous / Q000379:methods*; D015854:Up-Regulation
chemical_list: D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D007202:Indicators and Reagents; D009580:Nitroblue Tetrazolium