Inhibition of lipid peroxidation in CNS trauma.
It is believed that the key mechanism of protection of the injured spinal cord by methylprednisolone (MP) is the inhibition of posttraumatic lipid peroxidation. Large, i.v. bolus doses are required to achieve this effect, but the biphasic dose-response curve limits the dose size to approximately 30 mg/kg. The mechanism for the reversed effect at higher concentrations is believed currently to be membrane disruption. Early treatment is required because injury mediated by lipid peroxidation is largely irreversible. Furthermore, the time course of the protective effects parallels the tissue pharmacokinetics, defining the need for repeated maintenance dosing by bolus or infusion. The optimum duration of treatment has not been ascertained, but it would appear to extend throughout the period during which biochemical conditions that promote peroxidation exist within the injured cord.
Hall
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CNS Disease Research, Upjohn Company, Kalamazoo, Michigan.
D000818:Animals; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects* / Q000502:physiology; D008775:Methylprednisolone / Q000008:administration & dosage / Q000627:therapeutic use*; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
D008775:Methylprednisolone