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工作压力与代谢及止血风险因素

Work stress and metabolic and hemostatic risk factors.

作者信息

Vrijkotte T G, van Doornen L J, de Geus E J

机构信息

Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands.

出版信息

Psychosom Med. 1999 Nov-Dec;61(6):796-805. doi: 10.1097/00006842-199911000-00012.

Abstract

OBJECTIVE

A high level of work stress has been associated with cardiovascular disease. However, the pathophysiological mechanisms underlying this association remain unclear. This study examined the effect of work stress on a cluster of metabolic and hemostatic risk factors.

METHODS

Blood was collected three times, on the first, third, and fifth day of a work week, from 124 middle-aged, white-collar workers. Metabolic measures were insulin, glucose, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and total cholesterol. Hemostatic measures were fibrinogen, tissue-type plasminogen activator activity, tissue-type plasminogen activator antigen, and type 1 plasminogen activator inhibitor antigen. Chronic work stress was defined according to Siegrist's model as 1) a combination of high effort and low reward at work (effort-reward imbalance) or 2) high overcommitment (an exhaustive work-related coping style).

RESULTS

Overcommitment, but not imbalance or the imbalance-overcommitment interaction, was associated with an impaired fibrinolytic system, as reflected in decreased tissue-type plasminogen activator activity levels and increased type 1 plasminogen activator inhibitor antigen levels on all three measurement occasions. After controlling for body mass index, total cholesterol, triglycerides, high-density lipoprotein/low-density lipoprotein cholesterol ratio, glucose, and insulin, the relation between overcom-mitment and the fibrinolytic factors was attenuated but remained significant.

CONCLUSIONS

The results suggest that individuals with an exhaustive coping style at work have an impaired fibrinolytic capacity that is possibly due to the effects of chronic stress on insulin resistance.

摘要

目的

高水平的工作压力与心血管疾病相关。然而,这种关联背后的病理生理机制仍不清楚。本研究探讨了工作压力对一系列代谢和止血危险因素的影响。

方法

在工作周的第一天、第三天和第五天,对124名中年白领工人进行了三次血液采集。代谢指标包括胰岛素、葡萄糖、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇和总胆固醇。止血指标包括纤维蛋白原、组织型纤溶酶原激活物活性、组织型纤溶酶原激活物抗原和1型纤溶酶原激活物抑制剂抗原。根据西格里斯特模型,慢性工作压力定义为:1)工作中高努力与低回报的组合(努力-回报失衡)或2)高过度投入(一种过度的与工作相关的应对方式)。

结果

过度投入与纤溶系统受损相关,而失衡或失衡-过度投入的相互作用则不然,这体现在所有三次测量中组织型纤溶酶原激活物活性水平降低和1型纤溶酶原激活物抑制剂抗原水平升高。在控制了体重指数、总胆固醇、甘油三酯、高密度脂蛋白/低密度脂蛋白胆固醇比值、葡萄糖和胰岛素后,过度投入与纤溶因子之间的关系减弱但仍显著。

结论

结果表明,工作中采用过度应对方式的个体纤溶能力受损,这可能是由于慢性应激对胰岛素抵抗的影响。

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