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一氧化氮及内皮型一氧化氮合酶与血管迷走性晕厥发病机制的关联

[Association of nitric oxide and eNOS with the pathogenesis of vasovagal syncope].

作者信息

Shi Yun, Tian Hong, Gui Yong-Hao, He Lan

机构信息

Children's Hospital, Fudan University, Shanghai 200032, China.

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2008 Aug;10(4):478-80.

PMID:18706166
Abstract

OBJECTIVE

To investigate the roles of nitric oxide (NO) and eNOS in the pathogenesis of vasovagal syncope (VVS).

METHODS

Fourteen 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.

RESULTS

Plasma NO levels in group A increased significantly when syncope attacked from 76.7+/-9.6 micromol/L (before HUT) to 90.0+/-11.4 micromol/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).

CONCLUSIONS

Plasma 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.

摘要

目的

探讨一氧化氮(NO)和内皮型一氧化氮合酶(eNOS)在血管迷走性晕厥(VVS)发病机制中的作用。

方法

纳入14例VVS患儿(A组)、10例非血管迷走性晕厥患儿(B组)和20名健康志愿者(C组)。在A组和B组中,于头高位倾斜试验(HUT)前及试验结束时测定血浆NO水平。对三组进行eNOS基因G894T多态性检测。

结果

A组晕厥发作时血浆NO水平从76.7±9.6微摩尔/升(HUT前)显著升高至90.0±11.4微摩尔/升(P<0.05)。晕厥发作改善后,A组血浆NO水平显著降低。B组HUT前后血浆NO水平无统计学差异。eNOS基因G894T多态性检测显示,与B组和C组相比,A组GT基因型发生率更高(42.9%对10%;P<0.05)。

结论

血浆NO可能参与VVS的发病机制。血浆NO水平升高可能与eNOS基因的G894T多态性有关。

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