Normobaric Hypoxia-induced Brain Damage and Mechanism in Wistar Rat

摘要

To evaluate normobaric hypoxia-induced brain damage and discuss the mechanism in wistar rat brain injury, the water content of brain, brain infarction area ratio, the level of lactic acid and Na+-K+-ATPase activity were detected. The expression of HIF-1α was confirmed using immunohistochemistry. Histopathological changes of brain in rat model due to hypoxia were investigated using hematoxylin and eosin stain (HE). Results showed that the levels of lactic acid were positively correlated with the degree of hypoxia which caused a concentration-dependent decrease in total Na+-K+-ATPase activity. Compared with the control group, brain water content of rat model had significant difference under serious hypoxia condition. Brain infarction ratio increased sharply when lactic acid level increased and Na+-K+-ATPase activity decreased obviously. Histopathological examination confirmed that there was a necrotic feature in one single hippocampal gyrus neuron cell. HIF-1α (hypoxia induced factor-1α) was induced by hypoxia at 6% O2. Expression of HIF-1α enhanced the hypoxia adaptation capability of the rat model through regulating the expression of multiple genes. Lactic acid, Na+-K+-ATPase and HIF-1α played an important role in brain injury as a possible mechanism.