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一氧化氮的影响依赖于微环境,是由于与氧、血红蛋白和疏基相互作用所致。一氧化氮通过控制血管张力、血压、细胞间相互作用和增殖调节血管自身稳定。动脉粥样化形成会引起一氧化氮生物活性降低,这样就促进了细胞粘附、增殖、血管收缩和加速了动脉粥样硬化病变产生。动脉粥样硬化对一氧化氮通路的有害影响是由于继发性氧化物如过氧亚硝酸盐即一氧化氮与超氧化物反应的一种产物所致。通过刺激内源性一氧化氮产生,一氧化氮替代治疗和降低氧化作用等措施可有利于改善动脉粥样硬化的临床过程。
The effects of nitric oxide depend on the microenvironment due to the interaction with oxygen, hemoglobin and sparse base. Nitric oxide regulates the stability of blood vessels by controlling vascular tone, blood pressure, cell-cell interactions and proliferation. The formation of atherosclerosis leads to a decrease in the biological activity of nitric oxide, thus promoting cell adhesion, proliferation, vasoconstriction and accelerating atherosclerotic lesions. The detrimental effects of atherosclerosis on the nitric oxide pathway are due to the secondary oxides such as peroxynitrite, a product of the reaction of nitric oxide with superoxide. By stimulating endogenous nitric oxide production, nitric oxide replacement therapy and reduce oxidative effects and other measures can help to improve the clinical process of atherosclerosis.