A Model Of Acute Unilateral Frontal Focal Cerebral Venous Occlusion In The Rat And Low Molecular Weight Heparin Intervention

Part one A model of acute unilateral frontal focalcerebral venous occlusion in the ratObjectiveThe aim of this experimental study was to create a new focal venousinfarction model in rats.Methodsthirty-six healthy Sprague-Dawley rats were used in this experiment.They were divided randomly into two groups:(1) Sham operation(SO)group(n=16); (2) Frontal venous occlusion(VO) group(n=20). Unilateralfrontal strip craniectomy was done in front of the coronal suture. Frontalveins were observed by using the operative microscope. A linear duralincision was performed over the consecutive bridging veins using the tipof a 1ml injector pinhead. The consecutive bridging veins were sacrificedusing bipolar coagulation technique and micro-scissors. Specimens wereevaluated using histopathological techniques, MR detection and astereological method.ResultsUnilateral frontal hemispheric swelling, midline shift, brain edema,subcortical petechial hemorrhage, hemorrhagic infarction and necrosiswere the histopathological findings on microscopic examination. Brainparenchymal lesions were detected with T₂WI by MR. The brain watercontent in VO group was increased significantly(P＜0.01). The volume offrontal venous infarction in VO group was significant bigger than SOgroup. ConclusionOur results revealed that the bipolar coagulation method forocclusion of the unilateral frontal cortical veins for venous infarctionmight be a new experimental model in the evaluation of brain damageafter disturbance to the venous circulation.Part two The expression of Bcl-2 protein in thecerebral venous infarct tissue of ratsObjectiveTo study expression of anti-apoptosis protein Bcl-2 in in the cerebralvenous infarct tissue of rats.MethodsThe consecutive cerbral bridging veins were sacrificed using bipolarcoagulation technique and micro-scissors under microscope, the model ofcerebral venous infarct was made.The expression of Bcl-2 protein infrontal cerebral cortices was observed by using immunohistochemistrymethod.ResultsCompared with control group, cell expressed Bcl-2 protein increased significantly in VO group(P＜0.01).Conclusioncerebral venous occlusion could produce cerebral infarction, andalso could induce increase of bcl-2 expression, which may be one of theprotagonist in anti-apoptosis and protection of cerebral cells.Part three The effects and mechanisms of low molecularweight heparin on the acute unilateral frontalfocalcerebral venous occlusion in the ratsObjectiveTo detect the effects and mechanisms of the low molecular weightheparin on the acute unilateral frontal focal cerebral venous occlusion inthe ratsMethodsThe consecutive cerebral bridging veins were sacrificed using bipolarcoagulation technique and micro-scissors under microscope, the model ofcerebral venous infarct was made. Thirty-four healthy Sprague-Dawleyrats were divided randomly into three groups:(1) Sham operation and normal sodium was injected into abdominal cavity (SO+NS)group(n=10); (2) Frontal bridging venous occlusion and normal sodiumwas injected into abdominal cavity (VO+NS) group(n=12); (3) Frontalbridging venous occlusion and LMWH was injected into abdominalcavity (VO+LMWH) group(n=12). The water content and infarct sizewere evaluated in different group at different time.ResultsALL animal were alive after operation. The water content washigher in VO+NS group and VO+LMWH 72h group than that in SO+NSgroup(p＜0.01), there was no difference between SO+NS andVO+LMWH 7d group(P＞0.05).The infarct size was more smaller inVO+LMWH group than that in VO+NS group.ConclusionOur results revealed that treatment with LMWH can reduced brainedema and infarct size and with less hemorrhagic complications. LMWHis a safe and effective drug in treating venous infarct.