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心血管疾病患者应激引起的外周血管收缩的大脑相关因素。

Brain correlates of stress-induced peripheral vasoconstriction in patients with cardiovascular disease.

机构信息

Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia.

Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.

出版信息

Psychophysiology. 2019 Feb;56(2):e13291. doi: 10.1111/psyp.13291. Epub 2018 Oct 1.

Abstract

The influence of acute psychological stress on cardiovascular disease is an emerging public health concern. Identification of brain mechanisms underlying this may aid in the discovery of possible treatments. Acute psychological stress may induce arteriolar vasoconstriction and reduce blood flow to vital organs. We hypothesized that functional changes in brain regions involved with memory and autonomic/emotional regulation are implicated in the vasoconstrictive stress response, including the medial prefrontal cortex (anterior cingulate), insula, and dorsolateral prefrontal cortex. Subjects with a history of coronary artery disease (N = 59) underwent measurement of microvascular vasomotor tone with the EndoPAT device and O-15 positron emission tomography (PET) imaging of the brain during exposure to mental stress and control conditions. The peripheral arterial tonometry (PAT) ratio was calculated as the mean peripheral vasomotor tone during stress divided by the mean tone during rest. Whole brain contrasts were performed between groups above and below the median PAT ratio, and significant contrasts were defined with cutoff p < 0.005. Stress-induced peripheral vasoconstriction (below median PAT ratio) was associated with increased stress activation in insula and parietal cortex, and decreased activation in the medial prefrontal cortex with stress tasks compared to control tasks. These findings demonstrate that stress-induced vasoreactivity is associated with changes in brain responses to stress in areas involved in emotion and autonomic regulation. These findings have important implications on possible treatments for mental stress-induced vascular toxicity.

摘要

急性心理应激对心血管疾病的影响是一个新出现的公共卫生问题。确定其潜在的大脑机制可能有助于发现可能的治疗方法。急性心理应激可引起小动脉血管收缩,减少重要器官的血流。我们假设,与记忆和自主/情绪调节相关的大脑区域的功能变化与血管收缩应激反应有关,包括内侧前额叶皮层(前扣带回)、岛叶和背外侧前额叶皮层。有冠心病病史的受试者(N=59)在经历心理应激和对照条件时,使用 EndoPAT 设备测量微血管血管舒缩张力,并使用 O-15 正电子发射断层扫描(PET)成像测量大脑。外周动脉张力(PAT)比计算为应激期间的平均外周血管张力除以休息期间的平均张力。在 PAT 比中位数以上和以下的组之间进行全脑对比,具有截定点 p<0.005 的显著对比被定义。与对照任务相比,与应激任务相比,外周血管收缩(低于 PAT 比中位数)与岛叶和顶叶皮层的应激激活增加以及内侧前额叶皮层的激活减少有关。这些发现表明,应激诱导的血管反应性与涉及情绪和自主调节的大脑对应激的反应变化有关。这些发现对可能治疗精神应激引起的血管毒性具有重要意义。

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