| Background and PurposeCerebral edema was a common syndrome in dangerous patients of Neurology and Neurosurgy and was an important reason that caused death and mutilation. Pathologically, its type include and cytotoxicitic cerebral edema. Vasogenic cerebral edema(VBE) is a severe complication based on some diseases, such as cerebral vascular diseases, inflammation, brain trauma and brain tumors. And it is the most familiar type of brain edema and the most common cause of death of these diseases.The pathogenesis of VBE was an increase in BBB permeability which resulted in the leakage of plasma protein in blood capillary, water and electrolure and resulted in amplification of extraluminal of cell, increased content of extracellular fluid. The principal characteristic of VBE is the major edema area is in white matter. In a series of experiment study, we have studied the activities of 12 kinds of enzymes in the brain capillary and the plexus chorioideus. Ten of them change in VBE. We suggested that the enzyme barrier might be related with the formation of VBE. Enzyme system plays an adjustment role in the active transport of substance in the course of striding over blood capillary membran such as amino acid and protein besides the barrier function.The super release and collecting of calecholamine such as noradrenaline (NE)and adnephrin(E)is important in mechanism of neuronal damage after brain injury. Monoamine oxidase (MAO) is a metabolism enzyme to calecholamine, which is an extensive existing oxidase in brain. Monoamine oxidase, alkaline phosphatase, glutamyl transpeptidase and lactate dehydrogenase in cerebrospinal fluid and brain tissue increased in the earlierperiod of VBE. These enzymes are closely related to the exchange and transport of substance. In present study, we observed the neuroprotective effect of monoclonal antibody of monoamine oxidase on vasogenic cerebral edema in rats from the standpoint of enzyme barrier so that to prove that enzyme barrier plays an important role in VBE and to find a new treatment of VBE.Materials and Methods75 male Wistar rats were randomly divided into 5 groups: normal group, VBE group, mannitol group, negative control group and MCA-MAO group. The VBE animal model was made by injecting into abdominal cavity of Wistar rats. The head of normal group was broke directly. After injection of Phenylephrine, the head of VBE group was broke. After being injected Phenylephrine 30 minutes, the mannitol group was injected the 20% mannitol from venae femoral vein and negative control group and MCA-MAO group were separately injected the Saline and MCA-MAO(500ul/kg). Water content of gray matter and white matter were measured by Infrared Moisture Analyzer respectively. The permeability of the blood- brain barrier (BBB) was determined by Evan's blue (EB) extravasation. The MAO activities of every group were presented by histochemical method. The image analyzer system was presented to measure the activity of MAO of every group respectively.ResultsThe brain water content of gray mater and white matter in normal group was 66.64 + 6.306%, 61.71 ?.74% respectively, 78.28 + 7.53%, 76.35?8.14% in VBE group, 65.38 + 9.01 %, 67.15?.85% in mannitol group, 75.35 + 6.31% 74.76+7.12% in negative control group, 68.15 + 6.21% 62.37?.23% in MCA-MAO group. Compared to normal group, the brain water content of gray and white matter in mannitol group and MCA-MAO group was reduced markedly (P.01). It was clear that both of mannitol and MCA-MAO had an important role in resisting cerebral edema. Themannitol group can reduce the water content of brain gray and white matter, but there isn't significant difference between brain gray matter and white matter. But MCA-MAO had remarkable dehydration on brain edema and the dehydration on white matter was more obvious than the mannitol group as compared with mannitol group (P<0.01).Evan's blue permeability results of brain capillary: The permeability of EB of normal group, VBE group, mannitol group, negative control group and MCA-MAO group was 0.02... |
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