Effects Of Etomidate Postconditioning On The Brain Tissue MDA And SOD In Rats Induced By Cerebral Ischemia-reperfusion

The restoration of blood flow after ischemia can also cause further tissue demage anddysfunction in some cases which we called it reperfusion injury.ObjectiveTo establish the cerebral ischemia reperfusion injury model of rats. To observe the effects ofEtomidate postconditioning on the brain tissue malondialdehyde(MDA)concentration andsuperoxide dismutase(SOD)activity in rats induced by cerebral ischemia-reperfusion(CIR) so asto investigate cerebral protection mechanism of Etomidate.and the dose of Etomidate whosecerebral protection is better.MethodsThe establishment of the cerebral ischemia reperfusion model: Animalweighing�'Anesthesia�'Fixation of animal�'Exposed rats’ femoral vein to standby coveredwith warm saline gauze�'Neck incision to exposed the bilateral common carotid artery andligate them�'After20mins’ ischemia, give them the drug treatment for1min�'Restoration ofblood flow.Experimental animal:A total of40adult Wistar rats were randomly divided into5groups(n=8each):Sham operation group (Sham),cerebral ischemia reperfusion group (I/R),Etomidatepostconditioning group1,2,3(Eto1,2,3group respectively be given0.3mg/kg，0.9mg/kg,2.7mg/kgdoses of Etomidate).Then,make the cerebral ischemia model by ligating two-sides commoncarotid arteries except the Sham group.After20min, we will give Eto1,2,3group respectively0.3mg/kg，0.9mg/kg,2.7mg/kg doses of Etomidate, in the same time sham group and I/R groupwill be injected an equal volume of saline solution from femoral vein. Restoration of blood flowafter1min’ ischemic postconditioning.Sacrificed all rats after24hours’ reperfusion. Seperated the Rat’s head to get its brain. To fixthe brain tissue48hours with10%paraformaldehycle after coronary cutting from the opticchiasm plane for about4mm wide. Paraffin embedding conventionally. Then observe the coronalslices (thickness5μm) whichare alreadybe stained by HE under light microscope, and find theirhistological changed.Put another0.5g brain tissue into PH7.4PBC buffer to make up the10%tissue homogenate.After20minutes’ centrifugal5000/min, take supernatant to test the biochemical indexesaccording to kit. Using thiobarbituric acid (TBA) method to test the content of MDA. Using hydroxylamine oxidation method to test the SOD activity.ResultsCompared with the Sham group, the MDA content in the rat brain tissue significantlyincreased in I/R group(P <0.05), SOD activity significantly decreased (P <0.05);Compared with the I/R group, the MDA content in the rat brain tissue in Eto1,2,3groupsdecreased (all P <0.05), while the SOD activity increased (all P <0.05).Meanwhile, the Eto3groups have the higher MDA content and lower SOD activity than Eto1、2group (P<0.05).And Eto1group compared with Eto2group, the MDA content and SOD activity had nosignificant difference.Conclusion1Though the testing of MDA content, SOD activity and the observation under the lightmicroscope from the HE staining, we found that the rat brain tissue under the ischemiareperfusion was really damaged than a sham operation group does.2Etomidate postconditioning shows an effect against ischemia reperfusion brain injury, themechanism of the protection may be related to inhibiting of the oxygen free radicals.3Eto1,2group have better cerebral protection than Eto3group.