【摘要】 目的探讨左旋多巴治疗帕金森病诱发羟自由基增高的机制与防治的药物。方法使用脑微透析方法在帕金森病大鼠模型的活体内，用高压液相电化学检测法测定羟自由基和多巴胺的水平。结果发现在注射左旋多巴后，帕金森病动物模型的纹状体细胞外液多巴胺和羟自由基同步地明显增高，而同样的治疗在正常的动物没有引起任何的明显增高。在使用多巴胺高亲和力重摄取位点的阻断剂ＧＢＲ１２９０９后，左旋多巴治疗正常动物也引起了类似于帕金森病动物的变化。实验结果没有发现使用单胺氧化酶Ｂ的抑制剂能防止左旋多巴治疗后引起的羟自由基的增高。结论左旋多巴治疗可能仅在帕金森病人的脑内相应部位造成羟自由基的增高，而帕金森病多巴胺高亲和力重摄取位点的丧失可能是造成羟自由基增高的原因更多还原

【Abstract】 Objective To investigate the mechanism and prevention of increasing hydroxyl radical induced by LDOPA treatment in Parkinson’s disease. Method The levels of dopamine and hydroxyl radical in the dialysates were examined with a microdialysis technique and a high pressure liquid chromatography in the parkinsonian rats. Results The results showed that both hydroxyl radical and dopamine levels were increased in the dialysates of the striata of the parkinsonian animals, but no significant increase was found in those of the intact animals after LDOPA (100 mg/kg, i.p.) treatment. A similar increase was shown in those of the intact animals given an inhibitor of high affinity dopamine uptake, GBR 12909 (20 mg/kg, i.p.), in response to DOPA. No evidence was found to show monoamine oxidase B inhibitor, selegiline (50 mg/kg, i.p.), attenuating hydroxyl radical formation. Conclusion LDOPA treatment may be toxic to the neurons with producing hydroxyl radical in parkinsonian animals, but may not be toxic to the intact animals. The loss of dopamine high affinity uptake site is critical for the enhancement of extracellular dopamine and hydroxyl radical after L-DOPA treatment更多还原