The Observations Of Near And Distant Regional Of Brain Injuried After Fluid Percussion Brain Injury In Rats

Object:To investigate the changes of the cerebrovascular after fluid percussion brain injury in rats and to provide experimental evidence for posttraumatic cerebral ischemia.Methods:Thirty-six male Sprague; Dawley rats were randomly divided into the normal control group, sham group and posttraumatic 12h,72h, 1w,2w, groups of 6 rats each. Lateral fluid percussion brain injury model were reproduced in the present study to produce acute brain injury in rats. Take a time close to traumatic brain injury and distant regional brain tissue, detection of lactic acid, hypoxia inducible factor (HIF-1a) and Bax expression changes, using TUNEL staining of neuronal apoptosis, reflecting cerebral ischemia and neuronal apoptosis dynamics.Results:1,In near region of brain injured after TBI, the lactic acid increase at 12h after injury, lactic acid reached peak values at 72h after injury, then decreased at 1w after injury,2w later resume to the level of the controls group. The expression of Bax was observed at 12h after injury, increased at 72h, peaked at 1w, and decreased to the level of the controls at 2w. The expression of HIF-la was observed at 12h after injury, peaked at 72h, decreased at 1w after injury,2w later resume to the level of the controls group. The numbers of apoptotic cells appeared at 12h after injury then increased gradually at 72h and 1w, reached peak at 2w.2,In distant region of brain injured after TBI, the lactic acid increase at 12h after injury, lactic acid reached peak values at 72h after injury, then decreased at 1w after injury,2w later resume to the level of the controls group. The expression of HIF-la was observed at 12h after injury, peaked at 72h, decreased at 1w after injury,2w later resume to the level of the controls group.The expression of Bax was observed at 12h after injury, increased at 72h, peaked at 1w, and decreased to the level of the controls at 2w. The numbers of apoptotic cells appeared at 12h after injury then increased gradually at 72h and 1w, reached peak at 2w.Conclusions:1,Fluid percussion injury model is convenient measurement of energy in rats injured, has good stability and repeatability, can reproduce the clinical closed brain-injury, can be a good simulation of the actual traumatic brain injury, and also offers relatively unexpensive, easily to operate and can be better used in experimental research.2,There are ischemia and hypoxia in near and distant region of brain injured after TBI, its variation with the injuried region is consistent. Lactic acid, HIF-la are sensitivity of indicators of ischemia and hypoxia. According to the changes of both assess the extent of brain damage. The peak of both with cerebral edema after TBI is consistent, suggesting that lactic acid, HIF-la may promote the development of cerebral edema. expression of Bax protein can regulate apoptosis, its positive expression may have a direct causal relationship with apoptosis. But both the peak of expression is not consistent. Bax and apoptosis suggest may have a direct causal relationship but non-synchronous.4,The study apoptotic cells are detected by TUNEL at each time point,in near and distant region of brain injured after TBI,suggesting that there are apoptotic cells in region of brain injured,in near region of brain injured and distant region of brain injured.may cause brain atrophy..5,The experiment also found that the number of apoptotic cells of near region of brain injured is significantly higher than distant regions of brain injured, suggesting that the brain damage associated with cell necrosis and apoptosis.