高压氧预处理减轻大鼠脑出血后脑水肿

目的 观察高压氧预处理(Hyperbaric oxygen preconditioning,HBOP)对大鼠脑出血后脑水肿和血肿周围炎症反应及神经细胞凋亡的影响.方法 选用36只雄性Sprague-Dawley大鼠(体质量300～350 g),其中18只大鼠接受连续5次HBOP(HBOP组:3个绝对大气压,100%O2,每次1 h,1次/d,连续5 d),另18只大鼠接受连续五次假预处理(对照组:1个绝对大气压,空气,每次1 h,1次/d,连续5d).预处理结束24 h后,立体定向基底节内注射自体股动脉血100μL建立基底节脑出血模型,72 h后处死,采用干湿重法测定脑组织水含量(24只大鼠,HBOP组及对照组各12只);采用HE染色镜下观察血肿周围炎症细胞浸润,采用缺口末端标记法(TUNEL)检测神经细胞凋亡(12只大鼠,HBOP组及对照组各6只);统计学分析采用stata 7.0统计软件对脑组织水含量值进行成组设计资料的t检验.结果 HBOP组脑出血72 h后血肿周围基底节脑组织水含量显著低于对照组(81.6±0.7)%vs.(82.8±0.9)%,(P<0.01)];血肿周围炎症细胞浸润程度显著轻于对照组,血肿周围凋亡细胞显著少于对照组.结论 HBOP显著减轻脑出血后脑水肿,显著抑制脑出血后炎症反应以及减少神经细胞凋亡.

Hyperbaric oxygen preconditioning attenuates brain edema induced by infra-cerebral hemorrhage in the experimental rate

Objective To investigate the effects of hyperbaric oxygen preconditioning (HBOP) on brain edema, inflammatory reaction and neuronal cell apoptosis induced by experimental hemorrhage in rats. Method Eighteen male Spraque-Dawley rats, weighing 300 - 350 g,received five successive sessions of HBOP with 3 atmosphere absolute pressure and 100% O2 one hour daily for five successive days, and other eighteen rats received five successive sessions of pretreatment with one atmosphere absolute pressure, air, one hour daily for five successive days. Twenty-four hours after the final pre-conditioning, rats received an infusion of 100 μL autologous blood into the basal ganglion. Seventy-two hours later, rats were sacrificed for brain edema measurements in 12 rats of each group. The histopathological changes around the hematoma were observed microscopically, and the neuronal cell apoptosis was detected by using the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) in six rats of each group. Data of brain water content were analyzed by using Stata 7.0 software and statistical analysis was carried out by two-tailed Student t -test. Results Compared with the control group, HBOP significantly attenuated brain edema 72 hours after intra-cerebral hemorrhage in experimental rats (81. 6± 0. 7% vs. 82. 8± 0.9%, P < 0.01). Inflammatory cell infiltration and neuronal cell apoptosis were also significantly decreased in the HBOP group. Conclusions HBOP protects the rats against brain edema formation, and quells inflammatory reaction and neuronal cell apoptosis following intra-cerebral hemorrhage in experimental rats.