| pubmed-article:6886781 | pubmed:abstractText | Peritumoral brain edema was produced by intracerebral transplantation of Walker 256 tumor in rats. Local cerebral blood flow (LCBF), local cerebral glucose utilization (LCGU), and capillary permeability were studied in untreated and methylprednisolone-treated rats by quantitative autoradiography. In the untreated group, LCBF and LCGU were widely depressed in the cortex and deep structures of the hemisphere ipsilateral to the tumor. In the methylprednisolone-treated animals, LCBF and LCGU were significantly better than in the untreated animals. Capillary permeability was highly increased in the viable part of the tumor in the untreated animals. In the methylprednisolone-treated group, capillary permeability of the tumor was significantly lower than that in the untreated group. These results may suggest that increase in capillary permeability of the tumor is the major source for edema fluid production, and that methylprednisolone improves brain edema by decreasing capillary permeability of the tumor. Decrease in edema fluid formation may result in restoration of blood flow and glucose metabolism in the adjacent brain tissue, and may improve clinical symptoms and signs. | lld:pubmed |
