The Research Of Edaravone Pretreatment’s Protective Mechanism To Rats’ Brainstem Ischemical Reperfusion Injury

Objective: Presently，therapists gradually find that, in theprocess of rescueing or treating the severe ischemicdisease, the mainfactors caused injure to tissues were not the ischemia itself, but rather thesuperfluous free radical attacking cell in the tissues which regained thesupply of blood. Such injury could be called tissues ischemia-reperfusioninjury. Cerebrovascular disease (VCD) is a kind of disease which causedby various cerebrovascular pathologicalchanges. Its common character isthe brain-function deletion locally and diffusely. It is also a familiar andcomose illness which severely threaten the human’s health and lives. Andits fatality rate、 disability rate and recrudescence rate are all high.Cerebral infarction（CI）accounting for the classification of Clinic VCD is2/3. About1/5ischemic apoplexy are caused by the obturation of basilarartery. Their fatality rate、disability rate are all obviously higher than theinternal carotid artery. The harm of brainstem infarction is most serious.Edaravone as a particular scavenger has been used to protect CerebralIschemia reperfusion(CIR) injury. A large numbers of clinical researchshave confirmed that Edaravone can inhibit hydrocephalus and late-onsetneurocyte’s death through eliminating free radicals and lipidoveroxidation.Then it can effectively improve neurologic defective symptom. Coordinate expression, Edaravone plays a protective role inischemical reperfusion injury of multifarious viscera and tissues. But thereports of Edaravone has action to brainstem ischemical reperfusioninjury have not been found in Domestic. So we adopted the model thatbetween basilar artery first no branch area and second no branch of ratswhere we practise ischemia reperfusion experiment, then used Edaravonepretreatment to rats, observing the effect of MDA SOD and so on,discussing and researching Edaravone’s protective action to brainstemischemical reperfusion injury. They could offer experimental evidence toclinic. Methods:55healthy male SD rats used in experimental animalswere divided into3group at random: sham operation(normal) group(N),having5, brainstem ischemia reperfusion group(IR) and Edaravonepretreatment group(E). According to different ischemia time, we dividedIR group and E group into ischemia1h reperfusion7h(1hr7h)、ischemia2h reperfusion6h(2hr6h)、ischemia3h reperfusion5h(3hr5h)、ischemia4h reperfusion4h (4hr4h)、 ischemia6h reperfusion2h (6hr2h) fivesubgroups. Every subgroup had5rats. In N groups, we exposed basilarartery first no branch area and second no branch and observed8h. In IRgroups, we used Micro-bulldogclamp to clamp corresponding time point.In E groups, we injected Edaravone(6mg/kg) into tail’s vein of rats before10min of experiments, and the others are the same to IR groups. TTC issensitive to light and deliquescent to fattiness. The brainstem tissues of every groups was coloured with TTC. After HE coloration, the brainstemtissues at various stages was observed by light microscope. The bloodsamples was collected after put the rats to death. The activities of SODand the contents of MDA、 NO at various subgroups were mensuratingwith spectrophotometry. The levels of cytokines TNF-a were alsoanalyzed by use of radioimmuno-assay. Results: By TTC coloration, Ngroup，s tissues was red, It would be red when it reacted with normaltissues and it will be white when it reacted with ischemical tissues in IRgroups and E groups. Pathology of light microscope after HE colorationof brainstem tissues was that there was no change on N groups and on IRgroups and E groups that neurocytes were denaturated、 dead andhemorrhagic, cells were obvious dropsy and gliocytes were diffusehyperplasia. But the changes of E groups were more alleviative than theIR groups. Compared with the N groups, the contents of MDA、No andTNF-a at various time stage were higher in IR groups and E groups,especially the IR groups. And compared with the IR groups, the levels inE groups were depressed. In general, along with the ischemia timeextension, the contents were also increasing. About the activities of SODin brainstem tissues of rats, the IR groups and E groups are lower than theE groups, which are higher than the IR groups. Conclusion: Edaravoneplayed a tremendous role in brainstem ischemical reperfusion injury ofrats. Its mechanism have to do with the eliminating oxyradical、 confronting the overoxidation of lipid、inhibiting the releasion of TNF-aand so on. Of or relating to the mechanism,the activities of SOD and thelevels of MDA、NO indirectly reacted that Edaravone have protectivefunction. And Edaravone can appropriately lengthen the reperfusiontime window.