内皮功能和冠状动脉风险降低:一氧化氮的机制和影响。

Cardio-vascular nursing Pub Date : 1996-05-01
J M Fair, K Berra
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引用次数: 0

摘要

与CAD进展和消退相关的生物学机制确实很复杂。虽然内皮损伤和脂质积累在CAD的进展/消退中起着重要作用,但血管功能的机制,特别是内皮调节血管舒张的机制,也不容忽视。关于内皮功能对冠心病进展/消退和稳定的影响,我们还需要了解很多。初步证据表明,降低风险的干预措施有利于血管功能,这一作用值得进一步研究。迄今为止,许多关于降低风险的研究都集中在降脂和动脉斑块的消退上,重点是动脉结构。对功能和结构的关注可能会扩大我们对降低风险干预的影响的理解,而不仅仅是降脂。考虑到与CAD发展相关的多因素原因,这种方法是必要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endothelial function and coronary risk reduction: mechanisms and influences of nitric oxide.

The biological mechanisms related to progression and regression of CAD are indeed complex. While endothelial injury and lipid accumulation play an important role in the progression/regression of CAD, mechanisms of vascular function, particularly that of the endothelial modulation of vasodilation, cannot be ignored. Much is yet to be learned about the influences of endothelial function on the progression/regression and stabilization of CAD. Initial evidence suggesting that risk reduction interventions favorably influence vascular function argues for further investigation of this role. To date, much of the research on risk reduction has focused on lipid lowering and regression of artery plaque, a focus on artery structure. A focus on both function and structure is likely to expand our understanding of the effect of risk reduction interventions beyond lipid lowering. Given the multifactorial causes associated with development of CAD, such an approach is necessary.

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