Effects of Cyclosporin A on Neurological Outcome and Serum Biomarkers in the Same Setting of Spinal Cord Ischemia Model

Spinal cord ischemic injury is one of the feared complications during aortic cross-clamping. The aim of this study was to investigate whether cyclosporin A (CsA) has a protective effect on spinal cord during ischemia in a rabbit model. A total of 22 New Zealand white rabbits were studied in three groups. One of the groups served as a sham group (n = 7), in which only laparatomy was performed and dosed. One group served as a control group (n = 7), in which rabbits had their abdominal aortas cross-clamped for 40 min following median laparatomy. The last group was the CsA group (n = 8), in which rabbits underwent the same procedure as the control group as well as CsA infusion at 20 mg/(kg · hr) over 60 min starting with aortic cross-clamping and continuing in the first 20 min of reperfusion. Neurological outcome of rabbits was evaluated according to Johnson's scale at postoperative hours 24 and 48 in all groups, and then they were killed. Their spinal cords were harvested, and segments corresponding to L4-L6 were prepared for pathological examination. Serum neuron-specific enolase (NSE) and nitric oxide (NO) levels were measured prior to and following aortic occlusion, and comparisons were made. Physiological data were similar in all groups. Rabbits in the sham group did not have any neurological deficit. However, all rabbits in the control group showed severe neurological deficits, including total paraplegia in five. According to Johnson's scale, neurological status of the rabbits at postoperative hour 48 was better in the CsA group compared to controls (p < 0.01). Pathological examination of spinal cord specimens revealed a higher viability index in the CsA group compared to controls (p < 0.01). Serum NSE and NO levels were lower in CsA-treated animals compared to controls. Our results demonstrate that CsA, when administered during ischemia and in the early period of reperfusion, may reduce neuronal damage in the spinal cord in a rabbit model of transient spinal cord ischemia.