延迟高压氧治疗对缺氧缺血性脑损伤新生大鼠的远期影响

目的　探讨延迟高压氧 (hyperbaricoxygen,HBO)治疗对缺氧缺血性脑损伤 (hypoxic-ischemicbraininjury,HIBD)新生大鼠的远期影响。方法　7日龄大鼠随机分为对照组(n=18,假手术处理)、HIBD组(n=17)和HBO组(n=17,制备HIBD模型后 48~72h开始 2个绝对大气压HBO治疗,稳压 30min/次,间隔 24h,连续 5次),以大鼠 37~41日龄的学习记忆功能 (Morris水迷宫实验 )和 42日龄的脑形态组织学(脑损伤程度、脑重量、海马CA1区存活神经元数、AchE纤维面积百分比和NOS神经元数)来判断干预效果。结果　HBO组、HIBD组的空间学习记忆功能严重不良,脑形态组织学也明显缺损。水迷宫平均逃逸潜伏期HBO组 (56±23)s]、HIBD组 (56±22)s]较对照组 (23±16)s]延长(P<0 05);平台象限搜索时间HBO组 (30±5)s]、HIBD组 (29±6)s]较对照组 (51±5)s]缩短 (P<0.05);平台象限搜索距离HBO组 (572±92)cm]、HIBD组 (548±92 )cm]较对照组 (989±101)cm]缩短(P<0.05);左脑重量HBO组 (598±46)mg]、HIBD组 (601±59)mg]较对照组 (984±18)mg]减轻 (P<0 05 );海马CA1区存活神经元数HBO组 ( 97±27 )个 /mm]、HIBD组 (100±27)个 /mm]较对照组 ( 183±8 )个 /mm]减少 (P<0 05 );AchE纤维面积百分比HBO组 (18.4±2.2)% ]、

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

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.