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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。
As a nitric oxide isoenzyme, changes in the activity of native nitric oxide synthase (ceNOS) and inducible nitric oxide synthase (iNOS) directly affect the development of cardiovascular disease. Preliminary studies have shown that ceNOS maintain normal cardiovascular physiological function, restrict the pathological remodeling of the heart and blood vessels, play a protective role on the cardiovascular system; iNOS expression in ischemia, injury and other states, NO pathological formation, and superoxide Material effects increase endothelial and myocardial injury. Heart Failure eNOS ↓ iNOS ↑. Line eNOS vessels, intracardiac transgene, to improve the bioavailability of eNOS can reverse the pathological changes of cardiovascular disease.