BACKGROUND: Severe neurological injury still represents one of the most devastating complications occurring after surgical repair of thoracoabdominal aneurysms. We aimed to investigate the role of rosuvastatin (RSV) against ischemia/reperfusion injury in an experimental model of spinal cord ischemia in rats. METHODS: Experimental groups included control group (n = 8), ischemia/reperfusion group (n = 8) undergoing aortic occlusion without pharmacologic treatment, and RSV-treated group (n = 8) receiving 10 mg/kg/day of RSV orally for 3 days before spinal cord ischemia. Spinal cord ischemia was induced by occlusion of the abdominal aorta between the left renal artery and aortic bifurcation for 45 minutes, followed by reperfusion. Neurological status was assessed before spinal ischemia and at 48 hours postoperatively. Spinal cords were harvested for histopathologic examination with hematoxylin-eosin staining and biochemical analysis for tissue malondialdehyde, superoxide dismutase, and glutathione peroxidase levels. RESULTS: Decreased spinal cord tissue malondialdehyde levels (p = .01) and increased tissue superoxide dismutase (p = .01) and glutathione peroxidase (p = .09) levels were observed in the RSV-treated group, as compared with the ischemia group. Histopathologic analyses demonstrated typical changes of ischemic necrosis in the ischemia group; however, RSV attenuated tissue necrosis. Total injury score in the RSV-treated group was significantly decreased, as compared with the ischemia group (p < .05). The Tarlov scores at 48 hours postoperatively were higher in the RSV group as compared with the ischemia group. CONCLUSION: RSV administration before spinal cord ischemia reduces spinal cord tissue injury by increasing antioxidant enzyme levels and may reduce the incidence of associated neurological dysfunction.
BACKGROUND: Severe neurological injury still represents one of the most devastating complications occurring after surgical repair of thoracoabdominal aneurysms. We aimed to investigate the role of rosuvastatin (RSV) against ischemia/reperfusion injury in an experimental model of spinal cord ischemia in rats. METHODS: Experimental groups included control group (n = 8), ischemia/reperfusion group (n = 8) undergoing aortic occlusion without pharmacologic treatment, and RSV-treated group (n = 8) receiving 10 mg/kg/day of RSV orally for 3 days before spinal cord ischemia. Spinal cord ischemia was induced by occlusion of the abdominal aorta between the left renal artery and aortic bifurcation for 45 minutes, followed by reperfusion. Neurological status was assessed before spinal ischemia and at 48 hours postoperatively. Spinal cords were harvested for histopathologic examination with hematoxylin-eosin staining and biochemical analysis for tissue malondialdehyde, superoxide dismutase, and glutathione peroxidase levels. RESULTS: Decreased spinal cord tissue malondialdehyde levels (p = .01) and increased tissue superoxide dismutase (p = .01) and glutathione peroxidase (p = .09) levels were observed in the RSV-treated group, as compared with the ischemia group. Histopathologic analyses demonstrated typical changes of ischemic necrosis in the ischemia group; however, RSV attenuated tissue necrosis. Total injury score in the RSV-treated group was significantly decreased, as compared with the ischemia group (p < .05). The Tarlov scores at 48 hours postoperatively were higher in the RSV group as compared with the ischemia group. CONCLUSION:RSV administration before spinal cord ischemia reduces spinal cord tissue injury by increasing antioxidant enzyme levels and may reduce the incidence of associated neurological dysfunction.