title: Preconditioned hyperbaric oxygenation protects skin flap grafts in rats against ischemia/reperfusion injury.
abstract: Hyperbaric oxygen (HBO) therapy is an effective therapy for ischemia/reperfusion (I/R) injury of the brain, small intestine, testes and liver. However, the detailed molecular mechanisms underlying the effect of HBO therapy remain undetermined. In the current study, the hypothesis that preconditioning rats with HBO protects grafted skin flaps against subsequent I/R injury was investigated. In addition, the molecular mechanisms underlying HBO therapy were characterized by analyzing the roles of the following important inflammatory factors: High mobility group protein 1 (HMGB1) and nuclear factor-κ B (NF-κB). A total of 40 rats were randomly divided into the following five groups: (i) Sham surgery (SH); (ii) ischemia followed by reperfusion 3 days following surgery (I/R3d); (iii) ischemia followed by reperfusion 5 days following surgery (I/R5d); (iv) HBO preconditioning (HBO-PC) and ischemia followed by reperfusion 3 days following surgery (HBO-PC+3d); and (v) HBO-PC and ischemia followed by reperfusion 5 days following surgery (HBO-PC+5d). For the surgical procedure, all pedicled skin flaps were first measured and elevated (9x6 cm). The feeding vessels of the skin flaps were subsequently clamped for 3 h and released to restore blood flow. The rats in the HBO-PC+3d and HBO-PC+5d groups received 1 h HBO for 3 and 5 consecutive days, respectively, prior to surgery. Following surgery, the rats were euthanized, and grafted tissues were collected for western blotting and immunohistochemistry. HBO-PC increased blood perfusion in epigastric skin flaps and attenuated I/R injury following skin flap graft. Additionally, the elevated expression of HMGB1 and NF-κB proteins during I/R injury was attenuated by HBO-PC treatment. HBO-PC may therefore be applied to reduce I/R injury and improve the survival rate of grafted skin flaps. The molecular mechanisms underlying the effect of HBO therapy are associated with the attenuation of inflammatory responses.
authors.affiliation: Department of Orthopaedics, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Nan
authors.initials: N
authors.lastname: Kang
authors.affiliation: Department of Orthopaedics, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Hai
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Fang
authors.initials: F
authors.lastname: Liang
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Chun-Jin
authors.initials: CJ
authors.lastname: Gao
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Xue-Hua
authors.initials: XH
authors.lastname: Liu
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006085:Graft Survival; D024243:HMGB1 Protein / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D007150:Immunohistochemistry; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D010101:Oxygen Consumption; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control*; D012867:Skin / Q000098:blood supply / Q000378:metabolism; D016038:Skin Transplantation; D013524:Surgical Flaps; D019172:Transplantation Conditioning
chemical_list: D024243:HMGB1 Protein; D016328:NF-kappa B