Roles of nitric oxide in compression injury of rat spinal cord
Roles of nitric oxide in compression injury of rat spinal cord
复制标题
DOI：
10.1016/0891-5849(95)02017-9
复制
发表时间：
1996-01-01
影响因子：
7.4
通讯作者：
Fukuzawa, K
中科院分区：
文献类型：
--
作者：
Hamada, Y;Ikata, T;Fukuzawa, K
在大鼠脊髓损伤 (SCI) 后，通过使用 Fe2+ 和二乙基二硫代氨基甲酸酯 (DETC) 的 ESR 自旋捕获技术直接测量一氧化氮 (NO)。 SCI 损伤区域和邻近中心区域的 NO 和以硫代巴比妥酸反应物质 (TEARS) 形式表达的脂质过氧化物水平升高。用30 mg/kg NO合酶抑制剂N-G-硝基-L-精氨酸甲酯（L-NAME）进行预处理，可加速损伤组织中TEARS水平和髓过氧化物酶（MPO）活性的增加，并导致SCI后后肢运动功能恶化，表明组成型NO合酶（i-NOS）形成的NO对SCI后缺血再灌注引起的细胞损伤具有保护作用。尽管 SCI 后 c-NOS mRNA 表达没有改变，但随着运动功能障碍的进展，诱导型 NO 合酶 (i-NOS) mRNA 表达在 SCI 后 24 小时增加至最大值。 SCI 后 6、24、48 和 72 小时静脉注射 L-NAME (0.1 mg/kg) 可减轻运动障碍。这些结果表明，I-NOS 诱导的 NO 在 SCI 后的亚急性期可能具有神经毒性。
Nitric oxide (NO) was measured directly after spinal cord injury (SCI) in rats by an ESR spin-trapping technique using Fe2+ and diethyldithiocarbamate (DETC). The levels of NO and lipid peroxides expressed as thiobarbituric acid reactive substances (TEARS) were increased by SCI in the injured region and the adjacent central region. Pretreatment with 30 mg/kg of N-G-nitro-L-arginine methylester (L-NAME), an inhibitor of NO synthase, accelerated increases of the TEARS level and myeloperoxidase (MPO) activity in the injured tissue and caused deterioration of hind limb motor function after SCI, suggesting that NO formation by constitutive NO synthase (i-NOS) has a protective effect against cellular damage resulting from ischemia-reperfusion after SCI. Though c-NOS mRNA expression was not altered after SCI, inducible NO synthase (i-NOS) mRNA expression increased to a maximum of 24 h after SCI with progress of motor dysfunction. Intravenous injection of L-NAME (0.1 mg/kg) 6, 24, 48, and 72 h after SCI reduced the motor disturbance. These results indicate that NO induced by I-NOS may be neurotoxic in the subacute phase after SCI.