Effects of methylprednisolone on peritumoral brain edema

A quantitative autoradiographic study

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✓ 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.

Article Information

Address reprint requests to: Kazuo Yamada, M.D., Department of Neurosurgery, Osaka University Medical School, 1-1-50 Fukushima, Fukushima, Osaka 553, Japan.

© AANS, except where prohibited by US copyright law.

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Figures

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    Carbon-14 iodoantipyrine autoradiographs of the untreated (left) and methylprednisolone-treated (right) animals.

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    Macroscopic appearance of the untreated (left) and methylprednisolone-treated (right) animals.

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    Local blood flow and relative glucose utilization of intracerebrally implanted Walker 256 tumor. The viable part of the tumor had high blood flow and glucose utilization, whereas the necrotic center had almost no activity. No differences were noted between the untreated and methylprednisolone-treated groups except for the relative glucose utilization in the viable part of the tumor.

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    Carbon-14 deoxyglucose autoradiographs of untreated (left) and methylprednisolone-treated (right) animals.

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    Macroscopic appearance of the untreated (left) and methylprednisolone-treated (right) animals.

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    Capillary permeability of the tumor and adjacent brain tissue in the untreated and methylprednisolone-treated animals. In the untreated animals, the viable part of the tumor had a maximum increase in capillary permeability, and the periphery of the tumor and adjacent brain tissue also showed some increase in capillary permeability. In the methylprednisolone-treated animals, capillary permeability was significantly lower in the viable part and periphery of the tumor, and brain adjacent to the tumor.

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    Autoradiographs after injection of 14C-alpha-aminoisobutyric acid indicating regional capillary permeability in untreated (left) and methylprednisolone-treated (right) animals. Methylprednisolone reduced capillary permeability of the intraparenchymal tumors but had no effects on that of intraventricular tumors.

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    Macroscopic appearance of the untreated (left) and methylprednisolone-treated (right) animals.

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