Modification Of The Suture-occuluded Method For Middle Cerebral Artery Occlusion In Rats

Background and Objective:With the development of an aging population, cerebrovascular disease has become one of the three important diseases that lead significant harm to human health. Among which cerebral ischemia has been gained increasing attention because of its high morbidity, deformity and mortality. The disease not only impaires the elderly's health,but also brings burden to the society.Recent years, with the development of thrombolytic and endovascular treatment for acute cerebral infarction, restoring the blood supply is the main treatment, but sometimes it not only fails to restore its function, but induces more severe brain dysfunction, known as cerebral ischemia-reperfusion injury.Many previous studies have shown that MK-801 could exhibit its protective effects against brain ischemia injury, resulting in reducing the infarct size, decreasing the content of inflammatory effects in ischemia area in vivo.In our present study, we modify the the suture-occuluded method for middle cerebral artery occlusion,and use the protective effects against ischemia-reperfusion of MK-801 to verify the practice of the method.Methods:Middle cerebral artery occlusion (MCAO) was used to establish the focal cerebral ischemia model. The rats were divided into 3 groups in random: sham group, ischemia-reperfusion group, permanent MCAO group. 0.9%NaCl of the same capacity was given to the sham group and the model group. MCAO models were made after an aesthesia and fixation after the drug was given 15 minutes. The blood was deprived 90 minutes and was reperfused 24 hours. Scores of neurological deficit were observed and the cerebral infarction size was measured by 2,3,5-triphenytetrazolium chloride(TTC) staining technique. The morphological changes of cerebral cortical neurons through Cresyl fast violet staining were observed. The content of Tumor necrosis factor-α(TNF-α)in brain was measured by ELISA.Results:After 90 minutes of cerebral ischemia and 24 hours of reperfusion, scores of neurological deficit were lower significantly in the IR group treated with MK-801. The levels of TNF-αin brain were obviously decreased(p<0.01).Conclusions:The animal model of MCAO was successfully constructed and the model was stable and reliable.MK-801 had a neuro-protective effect against neuronal damage following focal Ischemia-reperfusion in the SD rats. One of the neuro-protective mechanisms of MK-801 is that it can inhibit the formation of mediator of inflammation.