title: Attenuation of Heat-Induced Hypothalamic Ischemia, Inflammation, and Damage by Hyperbaric Oxygen in Rats.
abstract: The present study was attempted to assess the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO2; 100% O2at 253 kpa) in treating experimental heatstroke. Anesthetized rats were divided into five major groups: normothermic control (NC) rats treated with normobaric air (NBA; 21% O2at 101 kpa; NC + NBA); NC rats treated with HBO2(NC + HBO2); heatstroke (HS) rats treated with NBA (HS + NBA); HS rats treated with hyperbaric air (HBA; 21% at 253 kpa; HS + HBA); and HS rats treated with HBO2(HS + HBO2). HS groups were exposed to heat (43°C) for exactly 68 min and then allowed to recover at 26°C. HBA or HBO2was adopted 68 or 78 min after the start of heat exposure. Survival time values for (HS + NBA) rats, (HS + HBA) rats at 68 min, (HS + HBA) rats at 78 min, (HS + HBO2) rats at 68 min, and (HS + HBO2) rats at 78 min were found to be 90 ± 3, 133 ± 12, 109 ± 9, 240 ± 18, and 170 ± 15 min, respectively. Resuscitation with HBA or HBO2at 68 min was superior to those treated at 78 min in prolonging the survival time values. All (HS + NBA) animals displayed hyperthermia, hypotension, and increased cellular levels of ischemia, oxidative stress and damage markers, pro-inflammatory cytokines, and an indicator of polymorphonuclear cell accumulation in their hypothalamus as compared to those of NCs. Heat-induced hyperthermia was not affected by HBA or HBO2treatment. However, heat-induced hypotension and hypothalamic ischemia, oxidative stress, neuronal damage, and inflammation were all significantly reduced by HBA or HBO2therapy. Compared to those of HBA therapy, HBO2therapy had a significantly higher beneficial effect in treating heatstroke. Our results suggested that HBO2improved heatstroke outcomes, in part, by restoring normal hypothalamic function. Delaying the onset of HBO2therapy reduced the therapeutic efficiency.
authors.affiliation: Graduate Institute of Clinical Medicine, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.|Department of Surgery, Buddhist Tzu Chi General Hospital, Taipei, Taiwan.
authors.forename: Po-An
authors.initials: PA
authors.lastname: Tai
authors.affiliation: Graduate Institute of Disease Prevention and Control, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.|Department of Neurosurgery, Mackay Memorial Hospital, Taipei, Taiwan.
authors.forename: Chen-Kuei
authors.initials: CK
authors.lastname: Chang
authors.affiliation: Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan.
authors.forename: Ko-Chi
authors.initials: KC
authors.lastname: Niu
authors.affiliation: Graduate Institute of Disease Prevention and Control, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.|Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan.
authors.forename: Mao-Tsun
authors.initials: MT
authors.lastname: Lin
authors.affiliation: Graduate Institute of Disease Prevention and Control, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
authors.forename: Wen-Ta
authors.initials: WT
authors.lastname: Chiu
authors.affiliation: Graduate Institute of Clinical Medicine, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.|Department of Neurosurgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
authors.forename: Jia-Wei
authors.initials: JW
authors.lastname: Lin
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism* / Q000628:therapy; D018883:Heat Stroke / Q000150:complications / Q000378:metabolism*; D006358:Hot Temperature / Q000009:adverse effects*; D006931:Hyperbaric Oxygenation / Q000379:methods*; D007031:Hypothalamus / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D018836:Inflammation Mediators