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作为一氧化氮的同功酶 ,原生型一氧化氮合酶 (ceNOS)和诱生型一氧化氮合酶 (iNOS)活性的变化直接影响到心血管疾病的发生发展。研究初步显示 ,ceNOS维持心血管的正常生理机能 ,限制心脏和血管的病理性重构 ,对心血管系统起保护作用 ;iNOS在缺血、损伤等状态下表达 ,NO病理性生成 ,与超氧化物作用加重内皮和心肌损伤。心衰时eNOS↓iNOS↑。行eNOS血管、心脏内转基因 ,提高eNOS的生物利用度可逆转心血管疾病的病理改变。
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基本信息:
中图分类号:R54
引用信息:
[1]石姝梅,陆东风.一氧化氮合酶在心血管系统中的作用和治疗应用[J].广州医学院学报,2003(03):88-90.