Attenuation Of Heat-Induced Hypothalamic Ischemia, Inflammation, And Damage By Hyperbaric Oxygen In Rats

The present study was attempted to assess the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO2; 100% O-2 at 253 kpa) in treating experimental heatstroke. Anesthetized rats were divided into five major groups: normothermic control (NC) rats treated with normobaric air (NBA; 21% O-2 at 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 degrees C) for exactly 68 min and then allowed to recover at 26 degrees C. HBA or HBO2 was 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 HBO2 at 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 HBO2 treatment. However, heat-induced hypotension and hypothalamic ischemia, oxidative stress, neuronal damage, and inflammation were all significantly reduced by HBA or HBO2 therapy. Compared to those of HBA therapy, HBO2 therapy had a significantly higher beneficial effect in treating heatstroke. Our results suggested that HBO2 improved heatstroke outcomes, in part, by restoring normal hypothalamic function. Delaying the onset of HBO2 therapy reduced the therapeutic efficiency.