| Cerebral ischemia reperfusion injury is one of the most popular complications, and temporary brain hypoxia usually can result in injury of brain’s functions. Besides recovering blood, many other medicines play important roles in the pathophysiology of cerebral ischemia reperfusion injury.Dexmedetomidine is an adjuvant in anesthesia and it plays the role of sedation and analgesia. Recently, there are many studies showing that Dex can protect nerves, but the mechanism is unclear. So we assume that Dex has the role of nerve protection and the protection can be mediated by ATP sensitive potassium channel. This experiment includes two parts:1. The effect of dexmedetomidine on cognitive function and apoptosis controlling gene in rats under brain middle cerebral artery obstruction. Objective:Investigate the effect of Dex on cognitive dysfunction and apoptosis controlling gene of rats undergone cognitive dysfunction obstruction. Methods:120male Wistar rats were randomly divided into5groups:sham operation group (group C),I/R group, Dex group. Dex+Yohimbine group, Dex+5-HD.Middle cerebral artery occlusion model was made by reforming Longa method. The learning and memory functions were measured with Morris water maze, and bcl-2and bax were measured by Western-blot. Results:The shorter escaping latency period is,the sooner the speed of learn and memory functions are.It was found in the experiment that escaping latency period of rats in group D and group I/R was significantly delayed, and between the two groups, the escaping latency period in group D was shorter. Significant difference exists. The escaping latency period of rats in group Y was significantly delayed compared with group C and D. No significant difference exists between group Y and group I/R. There was a significant difference between group H and group C or group D, but no significant difference exists between group H and group I/R.Space explore test:In this experiment, the swimming time and the times through platform were used to judge the memory ability. Big value means better memory ability. In the experiment, it was found that the swimming time of rats in group D and group I/R was shorter and the times of crossing plat significantly decreased.The swimming time of rats in group D was much longer,and the times of crossing plat was much more. The swimming time and the times of crossing plat of rats in group Y were significantly decreased, compared with group C and group D.There was no significantly different between group Y and group I/R.There was no significant difference between group H and group D. But compared with group I/R, a significant difference exists. The results of Bcl-2and bax with western blot:Comparison in Bcl-2:the expression of bcl-2significantly increased in group D, compared with group C and group I/R. The expression of bcl-2in group I/R were significantly decreased compared with group C. The expression of bcl-2in group Y were significantly decreased, compared with group C and group D, but no significant difference compared with group I/R. The expression of bcl-2in group H significantly increased, compared with group C and group I/R, but no significant difference between group H and group D. Comparison of bax:There was no significant increasing in the bax expression in group D, compared with group C. But compared with group I/R, the bax expression of rats in group D decreased significantly. The bax expression in group I/R enhanced significantly compared with group C. The bax expression in group Y increased compared with group C and no significant difference compared with group I/R. The bax expression in group H decreased compared with group I/R, but enhanced less than group D. Conclusion:1. Dex can decrease the cerebral ischemia reperfusion injury to rat’s learning and memory ability.2. Dex can improve the bcl-2expression, promote the bax expression, and protect brain.3. Dex can protect brain by a2-adrenoceptor.4. Specific blocking agent to KATP channel can’t block the effect of Dex on cognitive function and apoptosis gene, which suggests that Dex’s protection function to cerebral ischemia reperfusion injury of rats possibly was not mediated by KATP channel.2. The effect of Dex on amino acid after cerebral ischemia reperfusion injury in ratsObjective:To investigate Dex’s effect on amino acid after cerebral ischemia reperfusion injury in rats.Methods:36male Wistar rats were randomly divided into3groups:sham operation group (group C),I/R group, Dex group.The content of glu and GABA of brain were measured, and ultrastructure changes in cerebral cortex were examined under electron microscopy. Results:Compared with group C, Glu of rats in group D and I/R significantly increasing. Compared with group I/R, Glu of rats in group D significantly decreased. Compared with group C, GABA of rats in D and I/R significantly increased. There was a significantly increased. Between group D and I/R, there was no significant difference on GABA. The changes of cerebral ultrasructure: cerebral structure was normal in group C. Kytoplasmwater thesaurismosis of nerve cell, oligodendrocyte and gitter cell could be obviously seen in group I/R, as well the integrity of cell membrane was broken. Vacuolar degeneration in plast iosome, nervous process was more critical than in group D. Vascular endothelial cell(VEC) was damaged and congestion in micrangium could also be observed significantly. On the opposition, these changes in group D relieved obviously. Conclusion:Dex can decrease the content of Glu and increase the content of GABA, and decrease the injury of cerebral ultrasructure.In conclusion, Dex has the role of brain protection, and it can improve the cognitive function of cerebral ischemia reperfusion injury in rats. The protection is possibly made through mediating a2-adrenoceptor and depressing apoptosis by the reduction of Glu release. |
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