Abstract
The glucocorticoid steroids (e.g. methylprednisolone) are highly effective in the treatment of tumor-associated brain edema. However, they have been disappointing in the management of post-traumatic edema. Recently, it has been shown that methylprednisolone can beneficially affect the injured nervous system by inhibition of injury-induced free radical-mediated lipid peroxidation. However, higher doses are required to protect the injured nervous system than those needed to reduce tumor-associated edema. A novel non-glucocorticoid 21-aminosteroid tirilazad mesylate (U74006F), which more effectively inhibits lipid peroxidation and protects the injured nervous system, has been shown to be ineffective in limiting experimental tumor-associated edema. These results suggest that the mechanisms of tumor-associated edema are distinct from those involved in post-traumatic pathophysiology.
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© 1991 Springer Science+Business Media Dordrecht
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Hall, E.D., Del Maestro, R.M. (1991). Role of Oxygen Radicals in Cerebral Edema Mechanisms: Rationale for the Use of Steroids. In: Paoletti, P., Takakura, K., Walker, M.D., Butti, G., Pezzotta, S. (eds) Neuro-Oncology. Developments in Oncology, vol 66. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3152-0_44
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DOI: https://doi.org/10.1007/978-94-011-3152-0_44
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