Hyperbaric oxygen improves survival in heatstroke rats by reducing multiorgan dysfunction and brain oxidative stress.
Hyperbaric oxygen has been found to be beneficial in treating heatstroke animals. We attempted to further assess the possible mechanism of therapeutic protection offered by hyperbaric oxygen in experimental heatstroke. Anesthetized rats, immediately after the onset of heatstroke, were randomized into the following groups and given: a) hyperbaric oxygen (100% O(2) at 253 kPa for 1 h); or b) normal air. They were exposed to 43 degrees C temperature to induce heatstroke. When the untreated rats underwent heat stress, their survival time values were found to be 20-24 min. Resuscitation with hyperbaric oxygen increased the survival time to new values of 152-176 min. All untreated heatstroke rats displayed cerebrovascular dysfunction (evidenced by hypotension, intracranial hypertension, and cerebral hypoperfusion, hypoxia, and ischemia), hypercoagulable state (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer, but decreased values of platelet count and protein C in plasma), and tissue ischemia/injury (evidenced by increased levels of creatinine, serum urea nitrogen, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase in plasma, and dihydrobenzoic acid, lipid peroxidation, and oxidized-form glutathione/reduced-form of glutathione ratio in hypothalamus). The cerebrovascular dysfunctions, hypercoagulable state, tissue ischemia/injury, and brain oxidative stress that occurred during heatstroke were all suppressed by hyperbaric oxygen therapy. The current results indicate that hyperbaric oxygen therapy may resuscitate rats that had a heatstroke by decreasing multiple organ dysfunction and brain oxidative stress.
Niu
Kou-Chi
KC
Institute of Undersea and Hyperbaric Oxygen Medicine, National Defense Medical Center, Taipei, 116 Taiwan.
Lin
Mao-Tsun
MT
Chang
Ching-Ping
CP
D000818:Animals; D002545:Brain Ischemia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D018883:Heat Stroke / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006358:Hot Temperature / Q000009:adverse effects; D006931:Hyperbaric Oxygenation / Q000379:methods*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002534:Hypoxia, Brain / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D019586:Intracranial Hypertension / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D007677:Kidney Function Tests; D015227:Lipid Peroxidation / Q000187:drug effects; D008111:Liver Function Tests; D008297:Male; D009102:Multiple Organ Failure / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D016019:Survival Analysis; D019851:Thrombophilia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D013997:Time Factors; D016896:Treatment Outcome
D005978:Glutathione; D019803:Glutathione Disulfide