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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。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。列出的机构是 对于中心，这不一定是调查员的机构。 这项研究将研究松弛反应如何抑制急性应激的生理变化。 它将检验以下假设：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。 一氧化物是一种短暂的氮自由基，介导了多种生理活性，包括a）血管扩张，b）下丘脑 - 垂体 - 肾上腺肾上腺（HPA）轴激活和c）降低了白细胞促进的促炎反应，这些发现也与宽松响应一起观察到。 我们将在放松响应期间调查是否在中枢神经系统之外产生NO。 此外，我们将确定弛豫反应1）在急性应激期间差异抑制肾上腺素能神经系统和HPA轴的激活以及2）降低了体内血小板和淋巴细胞的儿茶酚胺介导的活性。 使用马萨诸塞州综合医院的设施，将使用功能磁共振成像进行其他研究。 该子研究的目的是了解实践放松反应时涉及哪些大脑的部分，并开发使用功能磁共振图像来研究正常生理变异的影响的技术。 这项研究是一项随机，受控的单盲临床试验，旨在测试弛豫反应如何抑制正常，健康成年人（18-45岁）急性应激的生理变化。 通过包括一个积极的放松反应训练组和放松响应教育安慰剂控制治疗组，我们将能够测试放松响应训练的整体效果。