An Experimental Study Of Treating Vasogenic Brain Edema With Inhibiting Monoamine Oxidase Activity

Object and significance: Vasogenic Brain 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 principal characteristic of VBE is the major edema area is in white matter. Because its edema fluid is full of protein, the absorption will be very slowly, which causes the long-lasting brain edema and the high death rate. Up to date, we do not find a kind of medicine whose selective dehydration area is white matter. The problem of how to find the mechanism and the treatment of VBE puzzled the fields of neurology and neurosurgery for nearly a century. 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. Monoamine oxidase (MAO) is a member of the enzyme barrier, which is an extensive existing oxidase in brain. In present study, we observed the effect of MAO on blood-brain barrier (BBB) and VBE by inhibiting the MAO activity in the VBE model to determine its role in VBE formation and find a new treatment of VBE. Materials and Methods: The male Wistar rats were employed and divided into 4 groups randomly: normal group, VBE group, mannitol treat group and enzyme inhibitor treat group. The VBE model was caused by hypertension encephalopathy after injecting Phenylephrine into peritoneal cavity. Water content of gray matter and white matter was measured by Infrared Moisture Analyzer respectively. The BBB permeability reflected by Even's blue extravasations. The MAO activities of every group were presented by histocjiemical method. The image analyzer system was presented to measire the activities respectively. Results After injection of Phenylephrine, the blood pressure increased 40-5OmmHg in ten minutes. The mice presented symptoms of hypertension encephalopathy. No blutene chloaide was found in general and slice observation. The water content of gray and white matter of VI3E group was all increased (rising 11.64% and 14.64% respectively). Dehydration of gray matter of mannitol group is obvious (12.9%) while the dehydration of white matter is not obvious (9.2%). Dehydration of gray and white matter of MAO inhibitor group is obvious (13.18% and 18.11% respectively), which present the selective therapy effect on white matter edema. Evan's blue extravasations results of brain capillary show that VBE group extravasates more than normal group (0.225 OD/g verse 0.079 OD/g). After administration of mannitol, the exfravasations did not change (0.228 OD/g). But the extravasations decreased obviously in the MAO inhibitor group which reflected the reduction of the permeability of brain capillary. MAO histoohemical staining results show that MAO shows certain expression in normal BBB capillary and higher expression in VBE group. The MAO activity did not reduce obviously after administration of mannitol. But it reduced obviously after administration of MAO inhibitor. Unit area optical density measured by image analyzer system: normal group 0.482 cJ.034, VBE group 0.97 0.104, tnannitol treatment group 0.880?.096, MAO inhibitor treatment group 0.601 .174. Mannitol group and VBE group did not show obvious changes as the MAO inhibitor grou...