Attenuation of motor nerve terminal repetitive discharge by the 21-aminosteroid tirilazad: evidence of a neural calcium antagonist action.

Pretreatment with the 21-aminosteroid antioxidant compound tirilazad mesylate has been previously shown to retard the axotomy-induced anterograde degeneration of soleus motor nerve terminals in the cat. In the present study, we examined tirilazad's effects (7.7, 13.

Lack of effect of postinjury treatment with methylprednisolone or tirilazad mesylate on the increase in eicosanoid levels in the acutely injured cat spinal cord.

Methylprednisolone (MP) improves motor recovery in spinal cord-injured patients when administered in a 24 h intensive high dose regimen beginning within 8 h after spinal cord injury (SCI). The rationale for this regimen has been based upon the need for high doses (i.e.

Brain hydroxyl radical generation in acute experimental head injury.

The time course and intensity of brain hydroxyl radical (.OH) generation were examined in male CF-1 mice during the first hour after moderate or severe concussive head injury. Hydroxyl radical production was measured using the salicylate trapping method in which the production of 2,3- and/or 2,5-dihydroxybenzoic acid (DHBA) in brain 15 min after salicylate administration was used as an index of .

Biochemistry and pharmacology of lipid antioxidants in acute brain and spinal cord injury.

Oxygen radical-mediated lipid peroxidation (LP) has been suggested increasingly to be an important factor in posttraumatic neuronal degeneration. Thus, numerous studies have evaluated the neuroprotective efficacy of pharmacological agents with lipid antioxidant activity in models of spinal cord and brain injury. Intensive pretreatment of animals with the endogenous lipid peroxyl radical scavenger vitamin E (i.