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[一氧化氮(NO),血管保护因子。与NO相关的心血管疾病]

[Nitric oxide (NO), vascular protection factor. NO related cardiovascular diseases].

作者信息

Tiritilli A

机构信息

Laboratoire de Physiologie et Pharmacologie cardiovasculaire, Centre Hospitalier, Saint-Germain-en-Laye.

出版信息

Presse Med. 1998 Jun 13;27(21):1065-70.

PMID:9767831
Abstract

ALTERATIONS OF THE ENDOTHELIUM

Because of its anatomic position between circulating blood and smooth muscle cells, the vascular endothelium is a prime target for cardiovascular diseases such as hypertension, hypercholesterolemia, diabetes or ischemia. The morphological changes occurring in the endothelium have been known for many years, but it was only recently that the functional alterations have been described. IMPACT OF NO: Under physiological conditions, the vascular endothelium plays a protective role by secreting relaxation factors. In the disease state, the synthesis and release of NO may be reduced or even abolished. The exact significance of endothelium-dependent vasodilatation disorders remains a topic of research, but the properties of NO strongly suggest it is involved in several diseases. For some diseases it is still a question as to whether the observed anomalies are the cause or the consequence of the underlying disease. DISEASE-SPECIFIC CHANGES: NO is known to be reduced in atherosclerosis, either because of less synthesis or accelerated degradation. In different experimental modules of hypertension, the baseline level of NO release appears to be decreased. Conversely, NO release can be normal, reduced or increased in diabetes. In heart failure, there appears to be not only a permanent alteration in NO secretion, but also an increase in factors stimulating vascular contraction, contributing to an altered capacity for vascular adaptation in these patients.

摘要

内皮的改变

由于其在循环血液和平滑肌细胞之间的解剖位置,血管内皮是高血压、高胆固醇血症、糖尿病或局部缺血等心血管疾病的主要靶点。内皮发生的形态学变化已为人所知多年,但直到最近才描述了其功能改变。一氧化氮的影响:在生理条件下,血管内皮通过分泌舒张因子发挥保护作用。在疾病状态下,一氧化氮的合成和释放可能会减少甚至停止。内皮依赖性血管舒张障碍的确切意义仍是一个研究课题,但一氧化氮的特性强烈表明它与多种疾病有关。对于某些疾病,观察到的异常是潜在疾病的原因还是结果仍是一个问题。疾病特异性变化:已知在动脉粥样硬化中一氧化氮减少,这要么是由于合成减少,要么是由于降解加速。在不同的高血压实验模型中,一氧化氮释放的基线水平似乎降低。相反,在糖尿病中一氧化氮释放可能正常、减少或增加。在心力衰竭中,似乎不仅一氧化氮分泌存在永久性改变,而且刺激血管收缩的因子增加,导致这些患者血管适应能力改变。

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Presse Med. 1998 Jun 13;27(21):1065-70.
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