DOES RELAXATION RESPONSE INHIBIT ACUTE STRESS?

放松反应可以抑制急性压力吗？

• 批准号: 7366512
• 负责人: HERBERT BENSON
• 金额: $ 0.81万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-03-01 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7366512
• 关键词: DOES; RELAXATION; RESPONSE; INHIBIT; ACUTE

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The relaxation response designates a set of integrated physiologic changes that includes states of perceived well-being with reduced cortical activation on electroencephalograms (EEG) and reductions in respiratory rate, blood pressure, oxygen consumption and arterial blood lactate. This Centers for Disease Control and Prevention supported study examines how the relaxation response inhibits the physiologic changes of acute stress. It tests the hypothesis that molecular mediators of the relaxation response will counteract the biochemical and cellular changes associated with acute psychosocial stress. An additional goal is to develop techniques for studying the effects of normal physiologic variation, such as changes in breathing rate and heart rate, on functional magnetic resonance images. The hypothesis is that in a subset of structures namely the medulla, hypothalamus, amygdala and rostral anterior cingulate cortex) the fMRI signal changes will strongly correlate temporally with changes in respiratory function. Another hypothesis is that activation in the insula and lateral hypothalamus will correlate with non-linear heart rate and respiration rate complexity. The effects of decreased respiratory rate without focused attention or mantra will activate only a subset of the regions activated by the relaxation response. Specifically, the prediction is that limbic structures will not be significantly activated by this task in either group, but that primary and secondary motor cortex regions involved in volitional control of breathing will be activated.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。松弛响应指定了一组综合的生理变化，其中包括感知幸福感的状态，并降低了脑电图（EEG）的皮质激活（EEG）以及呼吸频率，血压，氧气消耗和动脉血液乳酸的降低。该疾病控制和预防中心支持的研究研究了弛豫反应如何抑制急性应激的生理变化。它检验了以下假设：弛豫反应的分子介体将抵消与急性社会心理应激相关的生化和细胞变化。另一个目标是开发用于研究正常生理变异的影响的技术，例如呼吸率和心率变化对功能磁共振图像的影响。假设是，在结构的子集中，即延髓，下丘脑，杏仁核和前扣带回皮层）fMRI信号变化将与呼吸功能的变化紧密相关。另一个假设是，绝缘和下丘脑侧的激活将与非线性心率和呼吸率复杂性相关。没有集中注意力或咒语的呼吸率降低的影响只会激活弛豫反应激活的区域的一部分。具体而言，预测是，在这两组中，该任务不会显着激活边缘结构，但是将激活参与呼吸自愿控制的主要和次级运动皮层区域。