Abstract. The aim of the present study was to investigate the effect of hyperbaric oxygen (HBO) on lipid peroxidation and visual development in a neonatal rat model of hypoxic-ischemic brain damage (HIBD). The rat models of HIBD were established by delayed uterus dissection and were divided randomly into two groups (10 rats each): HIBD and HBO-treated HIBD (HIBD+HBO) group. Another 20 rats that underwent sham-surgery were also divided randomly into the HBO-treated and control groups. The rats that underwent HBO treatment received HBO (0.02 MPa, 1 h/day) 24 h after the surgery and this continued for 14 days. When rats were 4 weeks old, their flash visual evoked potentials (F-VEPs) were monitored and the ultrastructures of the hippocampus were observed under transmission electron microscope. The levels of superoxide dismutase (SOD) and malonyldialdehyde (MDA) in the brain tissue homogenate were detected by xanthine oxidase and the thiobarbituric acid colorimetric method. Compared with the control group, the ultrastructures of the pyramidal neurons in the hippocampal CA3 area were distorted, the latencies of F-VEPs were prolonged (P<0.01) and the SOD activities were lower while the MDA levels were higher (P<0.01) in the HIBD group. No significant differences in ultrastructure, the latency of F-VEPs or SOD/MDA levels were identified between the HBO-treated HIBD group and the normal control group (P>0.05). HBO enhances antioxidant capacity and reduces the ultrastructural damage induced by hypoxic-ischemia, which may improve synaptic reconstruction and alleviate immature brain damage to promote the habilitation of brain function.
IntroductionHypoxic-ischemic brain damage (HIBD) occurs at a rate of 3-5/1,000 full-term live births in developed countries and ≤10-fold higher in developing countries (1). Following hypoxia-ischemia (HI), ~45% of newborns succumb or have permanent cognitive impairments, potentially including cerebral palsy, and there are currently no effective therapies (2).Hyperbaric oxygen (HBO) therapy has been identified as a clinical therapy for HIBD for a number of years. Animal experiments and clinical trials have shown that HBO performed within 6 h after HIBD may achieve favorable outcomes and promote the long-term neurological recovery (3-6). In addition, numerous studies in China have demonstrated that HBO can reduce the disability and mortality of HIBD (7). However, there are concerns regarding the safety and validity of HBO treatment due to oxygen toxicity, which may increase the infarct area (3). A previous study demonstrated an increase in lipid and protein oxidation products in the lung tissues of rats accompanied by increased antioxidant enzyme activities when HBO was continued for >20 sessions (8). In addition to the lung being the entering site of hyperoxic injuries, CNS is mainly accepted as another important target for oxygen exposure in toxic amounts (9). However, whether HBO will exacerbate lipid peroxidation causing secondary injury to the brain or lead to neonatal pulmonary and retina...