Role in post-traumatic hypoperfusion secondary ischemia

Role in post-traumatic hypoperfusion (secondary ischemia) 

Strong support for a pathophysiological role of these radical and/or peroxidative reactions has been provided by investigations showing that the pharmacological inhibition of lipid peroxidation can attenuate the development of post-traumatic spinal cord hypoperfusion. As noted above, post-traumatic 

Based upon the atypical pharmacological characteristics of methyl-prednisolone s effects on the injured spinal cord and brain, it was postulated that the neuroprotective action (i.e. inhibition of lipid peroxidation and related pathophysiological events) was not glucocorticoid-receptor-mediated. Therefore, it was further reasoned it should be possible to design an analog that would lack the glucocorticoid-receptor-based actions and still retain the ability 

METHYLPREONISOLONE SODIUM SUCCINATE U72099E - NON-GLUCOCORTICOID STEROID 

Subsequently, it was found that the substitution of a complex amine on the non-glucocorticoid steroid nucleus in place of the 21-hydroxyl functionality results in a dramatic enhancement of the lipid antioxidant activity. Many of these 21-aminosteroid compounds effectively inhibit iron-catalyzed lipid peroxidation in rat-brain tissue homogenates under assay conditions where the glucocorticoid steroid methylprednisolone and the non-glucocorticoid analog U-72099E are completely ineffective [20,21]. Of these, U-74006F (tirilazad mesylate Fig. 2) has shown excellent activity in experimental models of spinal-cord and brain injury. 

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