Acute traumatic spinal cord injury (SCI) represents one of the most devastating injuries that afflict the human body. Ascorbic acid ( AA) plays an important role in mammalian central nervous system, especially in SCI. In this study, the change of AA concentration after SCI was investigated by using an on-line electrochemical method integrated with in vivo microdialysis. A microdialysis probe (2 mm in length) was implanted into the spinal cord of an anesthetized rat (Thoracic-10). Microdialysis perfusate (2 μL/ min) was collected in the sample loop of an on-line injector for direct injection onto a glassy carbon electrode which was modified with the heat-treated single-walled carbon nanotubes (SWNTs). Normal ascorbic acid concentration in the extracellular fluids of spinal cords was (26. 17 ± 1. 25) μmol/ L (n =8). The experimental spinal cord injury, induced by a lesion at T-10, significantly increased the extracellular ascorbic acid levels to (53. 24± 1. 95) μmol/ L (n =8). This study provides the experimental evidence on the essential roles of ascorbic acid in spinal cord injuries.%利用活体微透析技术结合在线高选择性抗坏血酸电化学检测技术,以实验性胸10节段脊髓钳夹损伤为动物模型,研究了脊髓损伤过程中胞外抗坏血酸的变化规律.结果表明,微透析探针植入及钳夹损伤瞬间,均存在脊髓抗坏血酸浓度高峰,随后浓度回到稳定水平,对照组大鼠脊髓细胞外液中抗坏血酸的平均基础浓度为(26.17±1.25)μmol/L(n=8).实验组脊髓钳夹损伤后,胞外抗坏血酸水平显著增加,达到(53.24±1.95)μmol/L(n=8),这种显著性升高可能与继发性脊髓损伤保护机制导致胞内抗坏血酸外流相关.本研究结果为抗坏血酸参与调节继发性脊髓损伤提供了直接的实验证据.
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