• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Vascular effects of a common gene variant of extracellular superoxide dismutase in heart failure.
【24h】

Vascular effects of a common gene variant of extracellular superoxide dismutase in heart failure.

机译：细胞外超氧化物歧化酶的常见基因变异对心力衰竭的血管作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

A common gene variant of human extracellular superoxide dismutase (ecSOD), in approximately 5% of humans, is associated with increased risk of ischemic heart disease. The purpose of this study was to examine vascular effects of ecSOD with effects of the ecSOD variant (ecSOD(R213G)) in rats with heart failure. Seven weeks after coronary artery ligation, we studied rats with heart failure and sham-operated rats. Adenoviral vectors expressing human ecSOD, ecSOD(R213G), or a control virus were injected intravenously. In the aorta from rats with heart failure, responses to acetylcholine (69 +/- 4% relaxation, means +/- SE) and basal levels of nitric oxide (NO) (vasoconstrictor responses to a NO synthase inhibitor) were greatly impaired, and levels of superoxide and peroxynitrite were increased. Gene transfer of ecSOD restored responses to acetylcholine (92 +/- 2% relaxation) and basal levels of NO to normal and reduced levels of superoxide [from 2.3 +/- 0.2 to 0.9 +/- 0.2 relative light units per second permillimeter squared (RLU x s(-1) x mm(-2))] and peroxynitrite (from 2.4 +/- 0.2 to 0.9 +/- 0.1 RLU x s(-1) x mm(-2)) in the aorta from rats with heart failure. Gene transfer of ecSOD(R213G) produced little or no improvement. Responses to nitroprusside were not different among the groups. Expression of endogenous mRNA for SODs (CuZnSOD, MnSOD, and ecSOD) and endothelial NOS in the aorta was not different among the groups. In contrast to ecSOD, gene transfer of ecSOD(R213G) in rats with heart failure has minimal beneficial effect on oxidative stress, endothelial function, or basal bioavailability of NO. We speculate that greatly diminished efficacy of ecSOD(R213G) in protection against oxidative stress and endothelial dysfunction may contribute to increased risk of cardiovascular disease in humans with ecSOD(R213G).
机译：在大约5％的人类中，人类细胞外超氧化物歧化酶（ecSOD）的常见基因变异与缺血性心脏病的风险增加相关。这项研究的目的是检查ecSOD对心力衰竭大鼠的血管作用以及ecSOD变体（ecSOD（R213G））的作用。冠状动脉结扎后七周，我们研究了心力衰竭大鼠和假手术大鼠。静脉注射表达人ecSOD，ecSOD（R213G）或对照病毒的腺病毒载体。在患有心力衰竭的大鼠的主动脉中，对乙酰胆碱的反应（69 +/- 4％松弛，意味着+/- SE）和一氧化氮（NO）的基础水平（对NO合酶抑制剂的血管收缩反应）大大受损，并且超氧化物和过氧亚硝酸盐的水平增加。 ecSOD的基因转移恢复了对乙酰胆碱的响应（92 +/- 2％的弛豫）和基础水平的NO还原为正常水平，而超氧化物水平降低了（从每秒2.3 +/- 0.2到0.9 +/- 0.2相对光单位平方毫米平方（ RLU xs（-1）x mm（-2））]和过氧亚硝酸盐（从2.4 +/- 0.2到0.9 +/- 0.1 RLU xs（-1）x mm（-2））在心衰大鼠的主动脉中。 ecSOD（R213G）的基因转移几乎没有改善。各组对硝普钠的反应无差异。各组中主动脉SOD（CuZnSOD，MnSOD和ecSOD）和内皮NOS的内源性mRNA表达没有差异。与ecSOD相比，心力衰竭大鼠中ecSOD（R213G）的基因转移对NO的氧化应激，内皮功能或基础生物利用度具有最小的有益作用。我们推测ecSOD（R213G）抵抗氧化应激和内皮功能障碍的功效大大降低，可能导致ecSOD（R213G）患心血管疾病的风险增加。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号