[abstract] HYPERBARIC OXYGEN TREATMENT DECREASED BRAIN INJURY INDUCED BY HYPOXIA-ISCHEMIA IN A NEONATAL RAT MODEL BY REDUCING APOPTOSIS

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[abstract] HYPERBARIC OXYGEN TREATMENT DECREASED BRAIN INJURY INDUCED BY HYPOXIA-ISCHEMIA IN A NEONATAL RAT MODEL BY REDUCING APOPTOSIS

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Title: [abstract] HYPERBARIC OXYGEN TREATMENT DECREASED BRAIN INJURY INDUCED BY HYPOXIA-ISCHEMIA IN A NEONATAL RAT MODEL BY REDUCING APOPTOSIS
Author: Calvert, J; Zhou, C; Nanda, A; Zhang, J
Abstract: BACKGROUND: The occurrence of hypoxia-ischemia during the perinatal period leads to neuronal damage resulting in behavioral and psychological dysfunctions, cerebral palsy, epilepsy or even death. Despite the critical clinical and socio-economic consequences of perinatal brain damage, no effective clinical therapeutic strategy has yet to be developed. Herein, we sought to determine if hyperbaric oxygen (HBO) is able to offer neuroprotectivity against a hypoxia-ischemia insult. METHODS: Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2-2.5 hrs of hypoxia (8percent O2 at 37"aC). Pups were treated with 100percent oxygen one hour after the hypoxia-ischemia insult in an HBO chamber pressurized to 3 atmospheres absolute (ATA) for a duration of 1hr. Brain injury was assessed by brain weight (ipsilateral/contralateral) , light microscopy, and sensorimotor functional tests 2wks, 5wks, and 6wks after hypoxia-ischemia. Apoptotic cell death was examined by EM, TUNEL staining, in vivo caspase-3 activity and expression, and in vivo PARP cleavage 12, 18, 24, and 48hrs after insult. RESULTS: After hypoxia-ischemia, the ipsilateral hemisphere was 52.65percent and 57.64percent (P less than 0.001) of the contralateral hemisphere at 2wks and 6wks, respectively. In HBO treated groups, the ipsilateral hemisphere was 77.77percent and 84.19percent (P less than 0.001) at 2wks and 6wks. There was much less atrophy observed in HBO treated animals under light microscopy. Sensorimotor function was also improved by HBO at 5wks after HI (Chi-square, P less than 0.001). Analysis showed a time-dependent increase in TUNEL-positive cells and HBO treatment reduced this hypoxia-ischemia-induced increase in both cortex and hippocampus at 18 and 24hrs after the insult (P less than 0.001). HBO also reduced the hypoxia-ischemia-induced increase in caspase-3 activity, expression of caspase-3 and PARP cleavage in both regions. CONCLUSIONS: The results suggest that HBO attenuates brain damage caused by a hypoxia-ischemia insult on the neonatal rat brain by reducing the progression of apoptotic neuronal injury and increasing sensorimotor function.
Description: Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org )
URI: http://archive.rubicon-foundation.org/1564
Date: 2004

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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