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对言语应激源的心理生理反应:冠心病患者静息时及心理应激后血浆β-内啡肽水平与热测量疼痛阈值的相关性。

Psychophysical responses to a speech stressor: correlation of plasma beta-endorphin levels at rest and after psychological stress with thermally measured pain threshold in patients with coronary artery disease.

作者信息

Sheps D S, Ballenger M N, De Gent G E, Krittayaphong R, Dittman E, Maixner W, McCartney W, Golden R N, Koch G, Light K C

机构信息

Department of Cardiology, University of North Carolina School of Medicine, Chapel Hill, USA.

出版信息

J Am Coll Cardiol. 1995 Jun;25(7):1499-503. doi: 10.1016/0735-1097(95)00045-6.

Abstract

OBJECTIVES

We tested the hypothesis that psychological stress alters plasma levels of opioid peptides and that these plasma levels are related to pain perception in patients with coronary artery disease.

BACKGROUND

Public speaking psychological stress has previously been shown to be associated with silent ischemia.

METHODS

After instrumentation and a 30-min rest period, venous blood samples for beta-endorphin were obtained before and immediately after psychological stress in 20 patients with coronary artery disease. Pain threshold was then assessed using a thermal probe technique at baseline and immediately after stress. Patients gave three brief speeches lasting a total of 15 min about real-life hassle situations.

RESULTS

Psychological stress significantly increases plasma beta-endorphin levels (4.3 +/- 0.9 pmol/liter [mean +/- SE] at rest to 8.3 +/- 2 pmol/liter after stress, p < 0.05). There was a significant positive correlation between pain threshold and beta-endorphin levels after stress (r = 0.577, p = 0.008). This significant positive correlation was still present while rest blood pressure and change in blood pressure during stress were controlled for by analysis of covariance techniques.

CONCLUSIONS

In patients with coronary artery disease and exercise-induced ischemia, public speaking produces psychological stress manifested by increased cardiovascular reactivity and causes an increase in plasma beta-endorphin levels that is significantly correlated with pain thresholds. These findings may explain the predominance of silent ischemia during psychological stress in patients with coronary artery disease.

摘要

目的

我们检验了以下假设,即心理应激会改变阿片肽的血浆水平,且这些血浆水平与冠状动脉疾病患者的疼痛感知有关。

背景

先前已表明公开演讲心理应激与无症状性缺血有关。

方法

在安装仪器并经过30分钟的休息期后,对20例冠状动脉疾病患者在心理应激前和应激后立即采集静脉血样本以检测β-内啡肽。然后在基线和应激后立即使用热探针技术评估疼痛阈值。患者就现实生活中的麻烦情况进行了三次共持续15分钟的简短演讲。

结果

心理应激显著增加血浆β-内啡肽水平(静息时为4.3±0.9 pmol/升[均值±标准误],应激后为8.3±2 pmol/升,p<0.05)。应激后疼痛阈值与β-内啡肽水平之间存在显著正相关(r = 0.577,p = 0.008)。通过协方差分析技术控制静息血压和应激期间血压变化后,这种显著正相关仍然存在。

结论

在患有冠状动脉疾病和运动诱发缺血的患者中,公开演讲会产生心理应激,表现为心血管反应性增加,并导致血浆β-内啡肽水平升高,且与疼痛阈值显著相关。这些发现可能解释了冠状动脉疾病患者在心理应激期间无症状性缺血占主导的原因。

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