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心理压力如何影响血管内皮功能。

How mental stress affects endothelial function.

机构信息

Toyama Institute for Cardiovascular Pharmacology Research, 7-13, 1-Chome, Azuchi-machi, Chuo-ku, Osaka 541-0052, Japan.

出版信息

Pflugers Arch. 2011 Dec;462(6):779-94. doi: 10.1007/s00424-011-1022-6. Epub 2011 Sep 23.

DOI:10.1007/s00424-011-1022-6
PMID:21947555
Abstract

Mental stress is an important factor contributing to recognized mechanisms underlying cardiovascular events. Among these, stress-related endothelial dysfunction is an early risk factor that predicts future development of severe cardiovascular disorders. Acute mental stress by a variety of tests impairs endothelial function in humans, although the opposite results have been reported by some investigators. Chronic stress always deteriorates endothelial function in humans and experimental animals. Stress hormones, such as glucocorticoids and pro-inflammatory cytokines, and endothelin-1 liberated in response to mental stress participate in endothelial dysfunction possibly via downregulation of endothelial nitric oxide synthase (eNOS) expression, eNOS inactivation, decreased nitric oxide (NO) actions, and increased NO degradation, together with vasoconstriction counteracting against NO-induced vasodilatation. Catecholamines do not directly affect endothelial function but impair its function when blood pressure elevation by the amines is sustained. Endogenous opioids favorably affect endothelial function, which counteract deteriorating effects of other stress hormones and mediators. Inhibition of cortisol and endothelin-1 production, prevention of pro-inflammatory mediator accumulation, hypnotics, mirthful laughter, humor orientation, and lifestyle modification would contribute to the prevention and treatment for stress-related endothelial dysfunction and future serious cardiovascular disease.

摘要

精神压力是导致心血管事件公认机制的一个重要因素。其中,与应激相关的内皮功能障碍是一个早期的风险因素,可预测未来严重心血管疾病的发展。各种测试引起的急性精神压力会损害人类的内皮功能,但一些研究人员报告了相反的结果。慢性应激总是会损害人类和实验动物的内皮功能。应激激素,如糖皮质激素和促炎细胞因子,以及内皮素-1在精神应激下释放,可能通过下调内皮型一氧化氮合酶(eNOS)表达、eNOS 失活、减少一氧化氮(NO)作用和增加 NO 降解,以及与 NO 诱导的血管舒张作用相反的血管收缩,参与内皮功能障碍。儿茶酚胺不会直接影响内皮功能,但当胺类物质引起的血压升高持续存在时,会损害其功能。内啡肽有利于内皮功能,可抵消其他应激激素和介质的恶化作用。抑制皮质醇和内皮素-1的产生、预防促炎介质的积累、催眠、欢笑、幽默取向和生活方式的改变,有助于预防和治疗与应激相关的内皮功能障碍和未来严重的心血管疾病。

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