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[Long-term effects of delayed hyperbaric oxygen therapy on hypoxic-ischemic brain injury in neonatal rats].

Meina Liu, Si-qi Zhuang, Xiaoyü Li, Huaqiao Wang, Qunfang Yuan

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Abstract

OBJECTIVE: To evaluate the long-term effects of delayed hyperbaric oxygen (HBO) therapy on neonatal rats with hypoxic-ischemic brain injury (HIBD). METHOD: Postnatal 7 days newborn rats (n = 52) were randomly set to three groups: control (n = 18, sham operation), HIBD (n = 17), or HBO (n = 17). Pups in the HBO group were subjected to hyperbaric oxygen treatment with 2 atmosphaera absolutus, 5 x 30 min at a 24 h intervals since 48-72 h after the HIBD model. All the animals were tested for the spatial learning and memory ability in the Morris water maze from postnatal days 37 to 41. At day-42, rats were decapitated and the brains were analyzed for morphological and histological changes, including brain shapes and weights, survival neurons, percentage of AchE positive area and NOS positive neurons in hippocampal CA1 region. RESULTS: Rats in HBO and HIBD groups displayed significant morphological and histological damages, as well as severe spatial learning and memory disability. The average escape latency of Morris water maze in HBO group [(56 +/- 23) s] and HIBD group [(56 +/- 22) s] were longer than the control [(23 +/- 16) s] (P < 0.05). The swimming time in HBO group [(30 +/- 5) s] and HIBD group [(29 +/- 6) s] were shorter than the control [(51 +/- 5) s] (P < 0.05). The swimming length in HBO group [(572 +/- 92) cm] and HIBD group [(548 +/- 92) cm] were shorter than the control [(989 +/- 101) cm] (P < 0.05). The weight of left brains in HBO group [(598 +/- 46) mg] and HIBD group [(601 +/- 59) mg] were lighter than the control [(984 +/- 18) mg] (P < 0.05). The survival neurons of hippocamal CA1 region in HBO group [(97 +/- 27)/mm] and HIBD group [(100 +/- 27)/mm] were less than the control [(183 +/- 8)/mm] (P < 0.05). The percentage of AchE-positive fibers in HBO group [(18.4 +/- 2.2)%] and HIBD group [(18.5 +/- 2.2)%] were less than the control [(27.5 +/- 2.2)%,] (P < 0.05). NOS-positive neurons in HBO group [(21 +/- 5)/mm(2)] and HIBD group [(19 +/- 4)/mm(2)] were also less than the control [(34 +/- 6)/mm(2)] (P < 0.05). CONCLUSION: Delayed HBO therapy resulted in no protection against either HIBD-induced brain morphological and histological deficits or spatial learning and memory disability.

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OBJECTIVE: To evaluate the long-term effects of delayed hyperbaric oxygen (HBO) therapy on neonatal rats with hypoxic-ischemic brain injury (HIBD). METHOD: Postnatal 7 days newborn rats (n = 52) were randomly set to three groups: control (n = 18, sham operation), HIBD (n = 17), or HBO (n = 17). Pups in the HBO group were subjected to hyperbaric oxygen treatment with 2 atmosphaera absolutus, 5 x 30 min at a 24 h intervals since 48-72 h after the HIBD model. All the animals were tested for the spatial learning and memory ability in the Morris water maze from postnatal days 37 to 41. At day-42, rats were decapitated and the brains were analyzed for morphological and histological changes, including brain shapes and weights, survival neurons, percentage of AchE positive area and NOS positive neurons in hippocampal CA1 region. RESULTS: Rats in HBO and HIBD groups displayed significant morphological and histological damages, as well as severe spatial learning and memory disability. The average escape latency of Morris water maze in HBO group [(56 +/- 23) s] and HIBD group [(56 +/- 22) s] were longer than the control [(23 +/- 16) s] (P < 0.05). The swimming time in HBO group [(30 +/- 5) s] and HIBD group [(29 +/- 6) s] were shorter than the control [(51 +/- 5) s] (P < 0.05). The swimming length in HBO group [(572 +/- 92) cm] and HIBD group [(548 +/- 92) cm] were shorter than the control [(989 +/- 101) cm] (P < 0.05). The weight of left brains in HBO group [(598 +/- 46) mg] and HIBD group [(601 +/- 59) mg] were lighter than the control [(984 +/- 18) mg] (P < 0.05). The survival neurons of hippocamal CA1 region in HBO group [(97 +/- 27)/mm] and HIBD group [(100 +/- 27)/mm] were less than the control [(183 +/- 8)/mm] (P < 0.05). The percentage of AchE-positive fibers in HBO group [(18.4 +/- 2.2)%] and HIBD group [(18.5 +/- 2.2)%] were less than the control [(27.5 +/- 2.2)%,] (P < 0.05). NOS-positive neurons in HBO group [(21 +/- 5)/mm(2)] and HIBD group [(19 +/- 4)/mm(2)] were also less than the control [(34 +/- 6)/mm(2)] (P < 0.05). CONCLUSION: Delayed HBO therapy resulted in no protection against either HIBD-induced brain morphological and histological deficits or spatial learning and memory disability.

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Available abstract

OBJECTIVE: To evaluate the long-term effects of delayed hyperbaric oxygen (HBO) therapy on neonatal rats with hypoxic-ischemic brain injury (HIBD). METHOD: Postnatal 7 days newborn rats (n = 52) were randomly set to three groups: control (n = 18, sham operation), HIBD (n = 17), or HBO (n = 17). Pups in the HBO group were subjected to hyperbaric oxygen treatment with 2 atmosphaera absolutus, 5 x 30 min at a 24 h intervals since 48-72 h after the HIBD model. All the animals were tested for the spatial learning and memory ability in the Morris water maze from postnatal days 37 to 41. At day-42, rats were decapitated and the brains were analyzed for morphological and histological changes, including brain shapes and weights, survival neurons, percentage of AchE positive area and NOS positive neurons in hippocampal CA1 region. RESULTS: Rats in HBO and HIBD groups displayed significant morphological and histological damages, as well as severe spatial learning and memory disability. The average escape latency of Morris water maze in HBO group [(56 +/- 23) s] and HIBD group [(56 +/- 22) s] were longer than the control [(23 +/- 16) s] (P < 0.05). The swimming time in HBO group [(30 +/- 5) s] and HIBD group [(29 +/- 6) s] were shorter than the control [(51 +/- 5) s] (P < 0.05). The swimming length in HBO group [(572 +/- 92) cm] and HIBD group [(548 +/- 92) cm] were shorter than the control [(989 +/- 101) cm] (P < 0.05). The weight of left brains in HBO group [(598 +/- 46) mg] and HIBD group [(601 +/- 59) mg] were lighter than the control [(984 +/- 18) mg] (P < 0.05). The survival neurons of hippocamal CA1 region in HBO group [(97 +/- 27)/mm] and HIBD group [(100 +/- 27)/mm] were less than the control [(183 +/- 8)/mm] (P < 0.05). The percentage of AchE-positive fibers in HBO group [(18.4 +/- 2.2)%] and HIBD group [(18.5 +/- 2.2)%] were less than the control [(27.5 +/- 2.2)%,] (P < 0.05). NOS-positive neurons in HBO group [(21 +/- 5)/mm(2)] and HIBD group [(19 +/- 4)/mm(2)] were also less than the control [(34 +/- 6)/mm(2)] (P < 0.05). CONCLUSION: Delayed HBO therapy resulted in no protection against either HIBD-induced brain morphological and histological deficits or spatial learning and memory disability.

Key concepts: Morris water navigation task, Medicine, Brain damage, Hippocampal formation, Hyperbaric oxygen, Spatial learning, Anesthesia, Hippocampus

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[Long-term effects of delayed hyperbaric oxygen therapy on hypoxic-ischemic brain injury in neonatal rats]. — Research Paper | ScholarLens