Hyperbaric oxygen preconditioning attenuates brain edema induced by infra-cerebral hemorrhage in the experimental rate
10.3760/cma.j.issn.1671-0282.2010.06.016
- VernacularTitle:高压氧预处理减轻大鼠脑出血后脑水肿
- Author:
Zhenhua SHI
;
Hongzhi XU
;
Jianbo DING
;
Qing XIE
;
Zhiyong QIN
- Publication Type:Journal Article
- Keywords:
Hyperbaric oxygen;
Preconditioning;
Rat;
Intracerebral hemorrhage;
Brain edema;
Inflammatory reaction;
Apoptosis;
Animal model
- From:
Chinese Journal of Emergency Medicine
2010;19(6):610-614
- CountryChina
- Language:Chinese
-
Abstract:
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.
