The Effect of Nimodipine on Single High Dose Irradiation-Induced Apoptosis in the Rat Spinal Cord

OBJECTIVE: Radiation injury includes radiation necrosis and apoptosis. Though some of its mechanism in brain are reported, those in spinal cord are not determined yet. The purpose of this study is to see whether nimodipine, one of calcium channel blockers, is effective for the prevention of high dose irradiation-induced apoptosis in the rat spinal cord. METHODS: Forty eight Sprague-Dawley rats were divided into four experimental groups, such as non-treated group(control group) after 5Gy and 10Gy irradiation(n=24), and nimodipine-treated group after 5Gy and 10Gy irradiation(n=24). Each group was divided by irradiation doses. After the drug was administered, the spinal cord was exposed to 5Gy and 10Gy dose of gamma rays using Ir-192. All spinal cord underwent histological examination at 4 hours, 8 hours, 12 hours after irradiation to evaluate the number of apoptotic cells. Apoptotic cells were detected by TUNEL assay, and determined by direct visual counting at x200, magnification RESULTS: In nimodipine-treated group, apoptotic cell counts were reduced significantly, compared to that of control group after irradiation(p < 0.05). CONCLUSION: These results suggest that nimodipine treatment may have effects on the prevention of radiationinduced apoptosis. If it could be established that calcium channel blockers inhibit radiation injury, they might be useful in radiation therapy.

The Effect of Nimodipine on Experimental Spinal Cord Injury

Nimodipine the potent, centrally active, clacium channel blocker, is known to increase cerebral and spinal blood flow. In the present study, the authors investigated the effect on Nimodipine on injured spinal cord. The experiment was a randomized blind study in which four groups of five cats received Nimodipine(0.05mg/kg) intravenously, and control groups of five cats received only Diluent. As a step in the investigation of the possible effect of spinal cord trauma on biochemical and ultrastructural changes in the injured cord, activities of lipid peroxidation were measured in the frozened-dried sample of the spinal cord and fine structure of the mylinated nerve fiber in the white matter were observed. An increase of lipid peroxidation level was found as early as 1 hour after the injury and the highest concentration was reached at 5 hours after the injury(P<0.01). Fine structures of the myelinated nerve fibers were changed progressively with the lapse of time after the injury. The effect of Nimodipine on lipid peroxidation and fine ultrastructural changes of myelinated nerve fibers were studied, and the result of this study revealed that Nimodipine groups showed a lower level of lipid peroxidation with statistical significance(P<0.05) and preservation of ultrastructural myelinated nerve fiber was prominent.