| Background and Objective Cerebral edema is a kind of pathological change that liquid increased of brain tissue results in brain's volume and weight enlargement under various factors. Pathologically, its type includes cytotoxicitic cerebral edema and vasogenic cereral edema(VCE). VCE is most frequently met in clinic, and caused by cereralvasocular diseases, brain tumor and brain trauma. VCE is the necessary pathological course of these diseases, Its development degree directly relates to the prognosis of illness. Usually, if the paitent could pass through the period of cerebral edema, the mortality is almost 0. Hence, the key of mortality solution is anesis of VCIE. At present, the treatment of VCE is searching after. We have produced the doctrine of enzymatic barrier before, and demonstrated that the change of some enzyme of enzymatic barrier is the important cause of VCE production. It can palliate VCE distinctly by inhibiting the activity of enzyme of enzymatic barrier in correlation to VCE . On the basis of the doctrine, we study furtherly the method of inhibiting enzymatic activity, and prove furtherly the effect of enzymatic barrier during VCE, also provide a new method to treat VCE. Materials and Methods To immune a BALB/C small mice by alkaline phosphatase(AKP) for three weeks. After the mice was strengthed immune for three days, spleen of the mice was taken out and mixed together with the SP2/0 myeloma cell in logarithmic growth phase. Examing the positive hole of hybridoma cells of excreting anti-alkaline phosphatase monoclonal antibody(AAP) by indirect ELISA method. The positive hole of hybridoma cells were cultured in vitro. The cultured liquid was extracted. The male Wistar rats were employed and divided into 5 groups randomly: normal group, VCE group, mannitol group, negative control group and anti- alkaline phosphatase inonoclonal antibody group. VCE animal model was made by injecting Phenylephrine into peritoneal cavity. After 30 minutes, the mannitol group were injected the 20% mannitol from venae femoralis and the negative control group and monoclonal antibody group were separately injected the cultured liquid with myeloma cell and the cultured liquid with hybridoma cells. Brain water content of gray and white matter were measured by Moistrue Analyzer respectively. The BBB permeability was reflected by Evan's blue(EB) extravasation. AKP enzymic activity was presented by enzyme histOchemical method and detected the mean optical density by image analysis system. Result The brain water content of gray and white matter in normal group was 66.64% .36%, 61.71% .74% respectively, and 78.28% 53 76.35% 8.14% in VCE, 75.35% .31%, 74.76% .12% in negative control group, 68.43% .17%, 63.56% 6.45 in monoclonal antibody group. The statistic analysis indicated that there was significant difference between the VCE group and the normal group (P<0.0 1); there wasn't significant difference between the VCE group and the negative control group(P > 0.05); and significant difference between the monoclonal antibody group and the negative control group and between the mannitol group and the VCE group (P < 0.0 1). EB extravasation: EB extravasation of normal group, CE group, mannitol group, the negative control group and AAP group were 0.079 0 01 0.225 0.023 0 228 0.028, 0.225 0.03 5, 0.087 0.01 6ODIg respectively. The satistic analysis indicated that there was...
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