目的：探讨一氧化氮和内皮型一氧化氮合成酶与儿童血管迷走性晕厥发病的关系。方法：血管迷走性晕厥患儿14例（A组），其他原因引起晕厥患儿10例（B组），健康志愿者20例（C组）。于倾斜试验（HUT）前和倾斜不同时间测定A组与B组患儿的血浆一氧化氮（NO）水平，同时对3组儿童进行内皮型一氧化氮合成酶（eNOS）基因G894T多态性检测。结果：①A组患儿出现阳性反应时血浆NO水平较平卧时显著升高（76.7±9.6 vs 90.0±11.4 μmol/L, P<0.05）；②A组患儿在症状好转后血浆NO水平较试验前显著降低（82.7±9.2 vs 61.5±6.9 μmol/L，P<0.01）；③B组患儿倾斜时血浆NO水平较平卧时差异无显著性；④A，B两组患儿的血压、心率变化与NO水平无显著相关性；⑤A组患儿eNOS基因G894T突变型基因频率显著高于B组与C组(42.9% vs 10%, P<0.05)。结论： 倾斜体位时血浆NO水平异常升高可能参与了血浆血管迷走性晕厥的发病机制，而其升高水平可能与eNOS基因G894T多态性表达有关。

ObjectiveTo investigate the roles of nitric oxide (NO) and eNOS in the pathogenesis of vasovagal syncope (VVS). MethodsFourteen children with VVS (group A), 10 children with syncope other than vasovagal (group B) and 20 healthy volunteers (group C) were enrolled. Plasma NO levels in groups A and B were determined before and at the termination of the head-up tilt table test (HUT). The G894T polymorphism within the eNOS gene was determined in the three groups. ResultsPlasma NO levels in group A increased significantly when syncope attacked from 76.7±9.6 μmol/L (before HUT) to 90.0±11.4 μmol/L (P<0.05). After the syncope attack was improved, plasma NO level in group A was significantly reduced. There were no statistical differences in plasma NO levels before and after the HUT in group B. Determining the G894T polymorphism within the eNOS gene showed that group A was associated with a higher incidence of the GT gene type as compared to groups B and C (42.9% vs 10%; P<0.05). ConclusionsPlasma NO may be involved in the pathogenesis of VVS. The increased plasma NO level may be associated with the G894T polymorphism of the eNOS gene.