Protective Effect And Mechanism Of Normobaric Oxygen Therapy On Hemorrhagic Brain Injury In Rats

Objective:To observe different concentrations of Normobaric Oxygen on behavioralchange of rats after cerebral hemorrhag,To explore the mechanism of NormobaricOxygen to attenuates brain injury after ICH.Methods:To make all intracerebral hemorrhage(ICH)model in rats by Type IVcollagenase and heparin sodium, the rats were positioned in a stereotaxie frame. ICHwas induced in the rats:3ul Type IV collagenase and heparin sodium was sampled andthen infused stereotacticlly into the right caudate nucleus through a needle.AdultmaleSprague-Dawley(SD) rats were randomly divided into five groups: Shamoperation group, ICH group,35%oxygen therapy group,50%oxygen therapy group,90%oxygen therapy group; rats after were given35%,50%,90%of the concentrationof Normobaric Oxygen, each treatment time of6hours,1times a day, for3consecutive days, and sham-operation group. The neurological deficit (NSS) wereinvestigated at different time points of rats,HE staining was observed in brainmorphology structure;Brain water content were tested by wet dry weight, Brain tissuesamples of each index were detected in brain edema peak point (72h) with Apoptosis、Immunohistochemistry and RT-PCR.Results: In each group, The rats appeared Varying degrees of neurological deficit afterwaking up, the Neurobehavioral scores reached a peak at24h after surgery andcontinued until72h and then begin to decline. In ICH group, its scores wassignificantly higher than other groups, compared with other groups excepting for the35%oxygen therapy group(p<0.05); In oxygen therapy, the Neurobehavioral scores of90%oxygen therapy group were significantly lower than other groups(p<0.05);2. HEstaining: A large number of red blood cells were transmigrated into the area ofHematoma in ICH group; the tissues around hematoma were obviously loose and cellsdegenerated and necrosised at72h after operation, the brain tissues around hematoma were highly swollen. In each group, the pathological changes in90%oxygen therapygroup was obviously lighter than the ICH group.3. In ICH group, brain water contentbegan to increase at6h after cerebral hemorrhage, reached a peak at72h which werehighter than other point in time（p<0.05）.In each group, brain water content in90%ofthe oxygen therapy group was distinctly lower than other group（p<0.05）.4. Theprotein of HIF-1a and VEGF were expressed in the ischemic region of brain tissue,expressed mainly in the nucleus and cytoplasm of neurons, and glial cells andendothelial cells can also be found a small amount of expression. The expression ofICH group was distinctly higher than other groups(p<0.05). The expression of HIF-1aand VEGF in90%oxygen therapy group were significantly lower than the modelgroup(p<0.01).5.RT-PCR test results suggest the expression of HIF-1andVEGFmRNA transcription in a model control group is significantly enhanced, whichin90%of the oxygen therapy group decreased significantly, and the number ofneuronal apoptosis in90%oxygen therapy group was significantly less than modelcontrol group(p<0.05).Conclusion:1.Neuronal apoptosis was significantly increased after cerebralhemorrhage, and the expression of HIF-1a and VEGF were enhanced after cerebralhemorrhage.2.High concentrations of Normobaric Oxygen can improve cerebral hemorrhage inrats neurobehavioral ability of rats after ICH, reduce brain edema and reduce neuronalapoptosis.3.High concentrations of Normobaric Oxygen Therapy attenuates brain damage afterexperimental intracerbral hemorrhage by inhibition of hypoxia-inducible factor-1aexpression around the hematoma.