诱导型一氧化氮合酶与动脉粥样硬化。
Inducible nitric oxide synthase and atherosclerosis.
作者信息
Ikeda U, Maeda Y, Shimada K
机构信息
Department of Cardiology, Jichi Medical School, Tochigi, Japan.
出版信息
Clin Cardiol. 1998 Jul;21(7):473-6. doi: 10.1002/clc.4960210705.
Abstract
Nitric oxide (NO) synthase induction in vascular smooth muscle cells may play a role in local vascular injury associated with atherosclerosis or postangioplasty restenosis by inhibiting smooth muscle cell proliferation and contraction, as well as by preventing leukocyte and platelet adhesion. The expression of inducible NO synthase is increased in balloon-injured arteries of experimental animals or in human atherosclerotic lesions. Replacement therapy with NO donors or NO synthase gene transfer may improve the clinical course of atherosclerosis or restenosis.
摘要
血管平滑肌细胞中一氧化氮（NO）合酶的诱导可能通过抑制平滑肌细胞增殖和收缩以及防止白细胞和血小板黏附，在与动脉粥样硬化或血管成形术后再狭窄相关的局部血管损伤中发挥作用。在实验动物的球囊损伤动脉或人类动脉粥样硬化病变中，诱导型NO合酶的表达增加。用NO供体进行替代治疗或进行NO合酶基因转移可能会改善动脉粥样硬化或再狭窄的临床病程。
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