The effects of barnidipine on an experimental ischemia reperfusion model of spinal cord injury and comparison with methyl prednisolone

OBJECTIVE: Increased intracellular calcium concentration plays an important role in the secondary mechanism of spinal cord injury. In the presenting experimental study, we aimed to evaluate the healing effect of barnidipine, which has a high affinity for L-type calcium channels, on acute spinal cord injury and to compare its effects with those of methylprednisolone. METHODS: A total of 32 Spraque Dawley albino adult female rats were divided into 4 groups; group 1: sham-operated (n=8), group 2: only ischemia (n=6), group 3: barnidipine-treated (n=8), and group 4: methylprednisolone-treated (n=6). An ischemia-reperfusion model was created by clipping the abdominal aorta in the rats. Motor examination was performed 1 hour after the surgical procedure and before sacrification. Immediately following the second motor examination, rats were sacrificed and tissue samples were taken for histopathological examination and for testing of tissue malondialdehyde (MDA) levels. RESULTS: A significant correlation of motor examination was found between the sham-operated and barnidipine-treated groups and the sham-operated and only ischemia groups at the 1(st) and 24(th) hour (p<0.008). There was no significant difference between the only ischemia and barnidipine-treated groups and only ischemia and methylprednisolone-treated groups (p>0.008). Light microscopic examination of the sham-operated group revealed findings consistent with normal spinal cord structure. In group 2, 3, and 4, light microscopic examination revealed polymorphonuclear leukocyte infiltration and a small amount of axonal swelling. There was no significant correlation between the ischemia and barnidipine-treated groups and the barnidipine and methylprednisolone groups in terms of MDA levels (p>0.008). CONCLUSION: A single dose of barnidipine (10 mg/kg) and methylprednisolone are not effective and not sufficient to prevent spinal ischemia-reperfusion injury in rats.