Reactive Oxygen Species Mediate Nicorandil-induced Metabolic Tolerance to Spinal Cord Injury

BackgroundSpinal cord injury remains a devastating complication of thoracoabdominal aortic surgery. We previously demonstrated that pretreatment with nicorandil preserved motor function in murine spinal model through mitochondrial adenosine triphosphate-sensitive potassium channel activation. hypothesized the neuroprotective effect is mediated by downstream generation reactive oxygen species.MethodsSpinal was induced 7 minutes thoracic cross-clamping adult male C57BL/6 mice. Five groups were evaluated: ischemic control (n = 19); 1.0 mg/kg 17); plus N acetyl L-cysteine (NAC [reactive species scavenger, n 18)]) 150 mg/kg; NAC 13); and sham 10). Limb number viable neurons within anterior horn evaluated.ResultsMice group showed no functional deficits after Compared control, significantly at every timepoint ischemia. In group, motor-preserving completely abolished (P < .001). Viable neuron quantification significant preservation (29.± 2.6) compared (18.5 ± 2.1, P .024) (14 8.3, .001); difference observed between 0.768).ConclusionsReactive plays key role nicorandil-induced metabolic tolerance to injury. Manipulation channels may lead improvement preventing interventions. Spinal species. evaluated. Mice 0.768). Reactive