Trials will be continued employing the rat experimental spinal cord trauma model to determine the therapeutic effectiveness of calcium channel blockers, hyperbaric oxygen, streroids, and antioxidants. The objectives are; a) to independently and collectively test specific injury hypotheses (calcium toxicity, ischemia, free radical damage) and to provide a scientific basis for possible therapeutic approaches to human spinal cord injury. In view of the effects of lactic acidosis found this past year, studies will be designed to measure the pH in the in vivo spinal cord trauma and lactic acid myelopathy models, to determine the critical pHs that induce injury. An in vitro lactic acid injury model wil be studied as well. A selective ion analysis using a fine needle electrode will be employed to measure pH. Nerve fiber uptake of horseradish peroxidase following the acute stage of traumatic injury will be further assessed and completed. Lectin histochemistry will be employed to determine the effects of trauma on selected tracts which are identifiable by galactose binding lectins. In testing the free radical thesis of spinal cord trauma, studies will be continued on the effects of hydrogen peroxides on the untraumatized spinal cord. In addition, the xanthine oxidase system will be utilized to generate O2- to see what effect it may have on the cord. Further attempts will be made to localize calcium in the in vitro models by injury (calcium, trauma, lactic acid) by employing anion capture techniques with phosphates.
| Balentine, J D (1988) Spinal cord trauma: in search of the meaning of granular axoplasm and vesicular myelin. J Neuropathol Exp Neurol 47:77-92 |
| Sharkey, M A; Steedman, J G; Lund, R D et al. (1987) Tectal transplants into the occipital cortex of the newborn rat. Brain Res 428:119-23 |
