Abstract | BACKGROUND: METHODS: RESULTS: Mild hypothermia that was started within 0 to 60 minutes delayed the consumption of SOD, GSH-Px, GSH, and ATP (P < 0.05 or P < 0.01) in ischemic tissue, as compared to a normothermic ischemia group. In contrast, mild hypothermia beginning at 90 minutes had little effect on the levels of SOD, GSH-Px, GSH, and ATP (P > 0.05). CONCLUSIONS: Postischemic mild brain hypothermia can significantly delay the consumption of endogenous antioxidant enzymes and energy metabolites, which are critical to the process of cerebral protection by mild hypothermia. These results show that mild hypothermia limits ischemic injury if started within 60 minutes, but loses its protective effects when delayed until 90 minutes following cerebral ischemia.
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Authors | Hong Zhang, Jun-jian Zhang, Yuan-wu Mei, Sheng-gang Sun, E-tang Tong |
Journal | Chinese medical journal
(Chin Med J (Engl))
Vol. 124
Issue 17
Pg. 2764-6
(Sep 2011)
ISSN: 2542-5641 [Electronic] China |
PMID | 22040438
(Publication Type: Journal Article)
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Chemical References |
- Antioxidants
- Adenosine Triphosphate
- Glutathione Peroxidase
- Superoxide Dismutase
- Glutathione
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Topics |
- Adenosine Triphosphate
(metabolism)
- Animals
- Antioxidants
(metabolism)
- Brain Ischemia
(enzymology, metabolism)
- Glutathione
(metabolism)
- Glutathione Peroxidase
(metabolism)
- Hypothermia, Induced
- Male
- Rats
- Rats, Sprague-Dawley
- Superoxide Dismutase
(metabolism)
- Temperature
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