Mild Hypothermia On HICH Rat Mitochondrial Na~+-K~+-ATP Enzyme And Mitochondrial Structure

Objective:Hypertensive cerebral hemorrhage on the human body injuries include damage to primary and secondary damage, secondary damage to brain tissue damage than the primary injury is more serious. Primary damage is that the formation of blood hematoma is direct pressure on the brain tissue. Secondary injury refers to the secondary brain ischemia oxygen around the hematoma, hematoma of the disintegration products on the toxicity of neurons to brain tissue surrounding hematoma neurons from near to far edema, degeneration, hemorrhage, apoptosis and necrosis. Mitochondria are important organelles within cells. the citric acid cycle, electron transport and oxidative phosphorylation were carried out in mitochondria. In physiological circumstances, it is the cell's energy conversion devices and support cell survival. More than ten years, mild hypothermia (33℃-35℃) for cerebral protection is extensive experimental study abroad.Cerebral protective effect of mild hypothermia in neurosur-gery has been hot and difficult, but the specific protection mechanisms are not completely unclear. Through the normal temperature control group and the mild hypothermia group, we observed mitochondrial Na+-K+-ATP enzyme and microstructure changes and will study of mild hypothermia on HICH protection mechanisms.Methods:Healthy adult male SD rats were 72 and body mass (250±25) g, by the Dalian Medical University Medical Experimental Animal Center. SD Rats were randomly divided into two cerebral hemorrhage group (A group), mild hypothermia-treated group (B group) and control group (C group). According to the stereotactic brain atlas, We used micro-syringe and extracted autologous blood 50μL in rats and made hypertensive intra- cerebral hemorrhage (HICH) model.A group:After the success of cerebral hemorrhage model produced, give room temperature treatment; B group: After the success of cerebral hemorrhage model produced, give hypothermia; C group:Surgical procedure with the A group and B group,injected 0.9% normal saline 50μL. Respectively, after 2h,24 h,3d,7d four time each group SD rats were decapitated brain tissue around the hematoma wall, extracted mitochondria, Used the modified Lowry's method to detect mitochondrial Na+-K+-ATP enzyme and observed the microstructure of mitochondria in the electron microscope. the three groups were compared each time.Result:In 2h,24 h,3d,7d four time, Na+-K+-ATP activity in hypothermia-treated group (B group) was significantly higher than the hemorrhage group (A group); The control group (C group) was significantly higher than cerebral hemorrhage group (A group); control group (C group) was higher than mild hypothermia treatment group (B group). Cerebral hemorrhage group (A group) with time, increased blood-brain barrier endothelial cell responsiveness, astrocytes swelled,Narrow capillaries severely, mitochondria swelled, spinal was unclear, spinal was fracture.In the hypothermia group (B group), astrocytes swelled mildly, neurons shrank slightly, a small number of mitochondria cristae blurred, and to 7 d, neuronal morphology was not very different from normal brain tissue and significantly better than the cerebral hemorrhage group (A group).Conclusion:The results suggest that Mild hypothermia protects the relative integrity of mitochondria, preserved the greatest degree of mitochondrial energy metabolism,and reduced neuronal apoptosis and necrosis. The results also showed that In the hemorrhage group (A group) Na+-K+-ATP activity were significantly decreased and In the hypothermia group (B group), mild hypothermia can increase Na+-K+-ATP activity. Initially, we proved that Mild hypothermia can reduced brain damage after brain hemorrhage and improved prognosis.