DOES THE RELAXATION RESPONSE INHIBIT ACUTE STRESS?

放松反应是否可以抑制急性压力？

• 批准号: 7606915
• 负责人: HERBERT BENSON
• 金额: $ 3.64万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-04-01 至 2008-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7606915
• 关键词: Acute; Adrenergic Agents; Adult; Age; Biochemical; Blood Platelets; Blood Vessels; Brain Part; Catecholamines; Clinical Trials Design; Computer Retrieval of Information on Scientific Projects Database; Dilatation - action; Education; Free Radicals; Functional Magnetic Resonance Imaging; Funding; General Hospitals; Goals; Grant; Institution; Leukocytes; Life; Lymphocyte; Massachusetts; Mediating; Mediator of activation protein; Molecular; Nervous system structure; Nitric Oxide; Pathological Dilatation; Physiological; Placebo Control; Psychosocial Stress; Randomized; Relaxation; Research; Research Personnel; Resources; Source; Techniques; Testing; Training; United States National Institutes of Health; Variant; acute stress; adrenergic; blind; hypothalamic-pituitary-adrenal axis; in vivo; response

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. This study will examine how the relaxation response inhibits the physiologic changes of acute stress. It will test the hypothesis that molecular mediators of the relaxation response will counteract the biochemical and cellular changes associated with acute psychosocial stress. Nitric oxide, a short-lived nitrogenous free radical, mediates diverse physiologic activities including a) vascular dilatation, b) decreased hypothalamic-pituitary-adrenal (HPA) axis activation and c) decreased proinflammatory response by leukocytes, findings that are also observed with the relaxation response. We will investigate whether NO is generated outside the CNS during the relaxation response. In addition, we will determine whether the relaxation response 1) differentially inhibits activation of the adrenergic nervous system and HPA axis during acute stress and 2) decreases catecholamine-mediated activities of platelets and lymphocytes in vivo. An additional study will be conducted using functional Magnetic Resonance Imaging, using facilities at Massachusetts General Hospital. The goal of this sub-study is to understand which parts of the brain are involved when the relaxation response is practiced and to develop techniques for studying the effects of normal physiologic variation using functional magnetic resonance images. This study is a randomized, controlled, single blind clinical trial designed to test how the relaxation response inhibits the physiologic changes of acute stress in normal, healthy adults, age 18-45 years. By including an active relaxation response training group, and a relaxation response education placebo control treatment group, we will be able to test the overall effect of relaxation response training.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 这项研究将探讨放松反应如何抑制急性应激的生理变化。 它将检验这样的假设：放松反应的分子介质会抵消与急性社会心理压力相关的生化和细胞变化。 一氧化氮是一种短命的含氮自由基，介导多种生理活动，包括a）血管扩张，b）下丘脑-垂体-肾上腺（HPA）轴激活减少，c）白细胞促炎反应减少，这些结果在松弛反应中也观察到。 我们将研究在松弛反应期间中枢神经系统外部是否产生一氧化氮。 此外，我们将确定松弛反应是否 1) 在急性应激期间差异性地抑制肾上腺素能神经系统和 HPA 轴的激活，2) 降低儿茶酚胺介导的体内血小板和淋巴细胞的活性。 另一项研究将利用马萨诸塞州总医院的设施，利用功能性磁共振成像进行。 这项子研究的目的是了解练习放松反应时涉及大脑的哪些部分，并开发使用功能磁共振图像研究正常生理变化影响的技术。 本研究是一项随机、对照、单盲临床试验，旨在测试放松反应如何抑制 18-45 岁正常健康成年人的急性应激生理变化。 通过包括主动放松反应训练组和放松反应教育安慰剂对照治疗组，我们将能够测试放松反应训练的整体效果。