A review of neuroimaging studies of stressor-evoked blood pressure reactivity: emerging evidence for a brain-body pathway to coronary heart disease risk.

A review of neuroimaging studies of stressor-evoked blood pressure reactivity: emerging evidence for a brain-body pathway to coronary heart disease risk.
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压力源诱发的血压反应性神经影像学研究综述:脑-体途径与冠心病风险的新证据。

DOI:
10.1016/j.neuroimage.2009.04.073
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发表时间:
2009-09
期刊:
影响因子:
5.7
通讯作者:
Sheu, Lei K.
Sheu, Lei K.
中科院分区:
医学1区
文献类型:
--
作者:
Gianaros, Peter J.;Sheu, Lei K.

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长期以来,个体对急性应激源表现出夸大或失调的心血管反应的倾向与冠心病(CHD)临床和临床前终点的风险增加有关。然而,将压力诱发的心血管反应与冠心病风险联系起来的“脑-体”途径仍不确定。这篇综述总结了新兴的神经影像学研究,表明应激源诱发的血压反应(心血管反应的一种特殊形式)的个体差异与皮质边缘大脑区域的激活模式有关,皮质边缘大脑区域共同参与处理应激源和调节心血管系统。根据meta分析得出的激活可能性估计的经验支持,这些皮质边缘区域包括扣带皮层、脑岛和杏仁核的分裂,以及参与动员血流动力学和代谢支持应激相关行为反应的网络皮层和皮层下区域。在此背景下,本文回顾的研究说明了如何将行为医学和健康神经科学方法相结合,以帮助描述将压力经历与冠心病风险机械地联系起来的“脑-体”途径。
An individual's tendency to show exaggerated or otherwise dysregulated cardiovascular reactions to acute stressors has long been associated with increased risk for clinical and preclinical endpoints of coronary heart disease (CHD). However, the ‘brain-body’ pathways that link stressor-evoked cardiovascular reactions to CHD risk remain uncertain. This review summarizes emerging neuroimaging research indicating that individual differences in stressor-evoked blood pressure reactivity (a particular form of cardiovascular reactivity) are associated with activation patterns in corticolimbic brain areas that are jointly involved in processing stressors and regulating the cardiovascular system. As supported empirically by activation likelihood estimates derived from a meta-analysis, these corticolimbic areas include divisions of the cingulate cortex, insula, and amygdala—as well as networked cortical and subcortical areas involved in mobilizing hemodynamic and metabolic support for stress-related behavioral responding. Contextually, the research reviewed here illustrates how behavioral medicine and health neuroscience methods can be integrated to help characterize the ‘brain-body’ pathways that mechanistically link stressful experiences with CHD risk.
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