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2
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Atorvastatin inhibition of cytokine-inducible nitric oxide synthase expression in native endothelial cells in situ.阿托伐他汀对原位天然内皮细胞中细胞因子诱导型一氧化氮合酶表达的抑制作用。
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本文引用的文献

1
Monocyte-vascular smooth muscle cell interaction enhances nitric oxide production.单核细胞与血管平滑肌细胞的相互作用可增强一氧化氮的生成。
Cardiovasc Res. 1998 Mar;37(3):820-5. doi: 10.1016/s0008-6363(97)00265-4.
2
Nitric oxide and cardiovascular disease.一氧化氮与心血管疾病
Postgrad Med J. 1997 Oct;73(864):630-4. doi: 10.1136/pgmj.73.864.630.
3
Expression and function of a recombinant endothelial nitric oxide synthase gene in porcine coronary arteries.重组内皮型一氧化氮合酶基因在猪冠状动脉中的表达及功能
Cardiovasc Res. 1997 Sep;35(3):553-9. doi: 10.1016/s0008-6363(97)00161-2.
4
Expression of multiple isoforms of nitric oxide synthase in normal and atherosclerotic vessels.一氧化氮合酶多种同工型在正常血管和动脉粥样硬化血管中的表达
Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2479-88. doi: 10.1161/01.atv.17.11.2479.
5
Expression and function of recombinant endothelial NO synthase in coronary artery smooth muscle cells.重组内皮型一氧化氮合酶在冠状动脉平滑肌细胞中的表达及功能
Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2405-12. doi: 10.1161/01.atv.17.11.2405.
6
Recombinant endothelial nitric oxide synthase-transduced human saphenous veins: gene therapy to augment nitric oxide production in bypass conduits.重组内皮型一氧化氮合酶转导的人隐静脉：用于增强旁路血管中一氧化氮生成的基因治疗。
Circulation. 1997 Nov 4;96(9 Suppl):II-173-8.
7
Adventitial gene transfer of recombinant endothelial nitric oxide synthase to rabbit carotid arteries alters vascular reactivity.将重组内皮型一氧化氮合酶进行兔颈动脉外膜基因转移可改变血管反应性。
Circulation. 1997 Oct 7;96(7):2254-61. doi: 10.1161/01.cir.96.7.2254.
8
The antiadhesive and antithrombotic effects of the nitric oxide donor SIN-1 are combined with a decreased vasoconstriction in a porcine model of balloon angioplasty.在猪气囊血管成形术模型中，一氧化氮供体SIN - 1的抗黏附、抗血栓形成作用与血管收缩减弱相结合。
Arterioscler Thromb Vasc Biol. 1997 Sep;17(9):1806-12. doi: 10.1161/01.atv.17.9.1806.
9
Adenosine stimulates nitric oxide synthesis in vascular smooth muscle cells.腺苷刺激血管平滑肌细胞中一氧化氮的合成。
Cardiovasc Res. 1997 Jul;35(1):168-74. doi: 10.1016/s0008-6363(97)00068-0.
10
Interleukin-1beta-induced, nitric oxide-dependent and -independent inhibition of vascular smooth muscle contraction.白细胞介素-1β诱导的、一氧化氮依赖性和非依赖性的血管平滑肌收缩抑制
Eur J Pharmacol. 1997 Jul 9;330(2-3):143-50. doi: 10.1016/s0014-2999(97)00164-7.

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.

DOI:10.1002/clc.4960210705
PMID:9669055
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6655488/
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。