Abstract |
The aims of the present paper were to ascertain whether the heat-induced ischemia and oxidative damage to the hypothalamus and lethality in mice could be ameliorated by hyperbaric oxygen therapy. When normobaric air-treated mice underwent heat treatment, the fractional survival and core temperature at 4 hours after heat stress were found to be 0 of 12 and 34 degrees C +/- 0.3 degrees C, respectively. In hyperbaric oxygen-treated mice, when exposed to the same treatment, both fractional survival and core temperature values were significantly increased to new values of 12/12 and 37.3 degrees C +/- 0.3 degrees C, respectively. Compared to normobaric air-treated heatstroke mice, hyperbaric oxygen-treated mice displayed lower hypothalamic values of cellular ischemia and damage markers, prooxidant enzymes, proinflammatory cytokines, inducible nitric oxide synthase-dependent nitric oxide, and neuronal damage score. The data indicate that hyperbaric oxygen may improve outcomes of heatstroke by normalization of hypothalamic and thermoregulatory function in mice.
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Authors | Po-An Tai, Chen-Kuei Chang, Ko-Chi Niu, Mao-Tsun Lin, Wen-Ta Chiu, Jia-Wei Lin |
Journal | Journal of biomedicine & biotechnology
(J Biomed Biotechnol)
Vol. 2010
Pg. 609526
( 2010)
ISSN: 1110-7251 [Electronic] United States |
PMID | 20625500
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cytokines
- Inflammation Mediators
- Nitric Oxide Synthase Type II
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Topics |
- Animals
- Brain Ischemia
(enzymology, etiology, pathology, therapy)
- Cytokines
(metabolism)
- Extracellular Space
(metabolism)
- Heat Stroke
(complications, pathology, therapy)
- Hyperbaric Oxygenation
- Hypothalamus
(enzymology, pathology)
- Inflammation Mediators
(metabolism)
- Male
- Mice
- Mice, Inbred ICR
- Neurons
(metabolism, pathology)
- Nitric Oxide Synthase Type II
(metabolism)
- Oxidative Stress
- Survival Analysis
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