Stress Responses, Psychosocial Stress and Pain Perception in African Americans

非裔美国人的压力反应、心理社会压力和疼痛感知

基本信息

批准号：
7590688
负责人：
SUSAN S. GIRDLER
金额：
$ 35.56万
依托单位：
UNIV OF NORTH CAROLINA CHAPEL HILL
依托单位国家：
美国
项目类别：
财政年份：
2001
资助国家：
美国
起止时间：
2001-08-01 至 2011-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7590688
关键词：
Absence of pain sensation Address Adrenal Glands African American Age-Years Allopregnanolone American Baroreflex Behavior Therapy Behavioral Behavioral Model Biological Blood Pressure Cardiac Output Caucasians Caucasoid Race Child Abuse Chronic Chronic stress Clinical Control Groups Corticotropin Data Development Discrimination Electrocardiogram Endogenous Factors Endorphins Equation Ethnic Origin Ethnic group Event Face Gender Gender Role Goals Hand Heart Rate Heating Hormones Hydrocortisone Hypothalamic structure Intervention Studies Interview Ischemia Knowledge Laboratories Life Light Literature Measurement Measures Mediating Modeling New Territories Not Hispanic or Latino Oxytocin Pain Pain Threshold Pain-Free Perception Peripheral Physiologic pulse Pituitary Gland Plasma Pressoreceptors Process Psyche structure Psychosocial Stress Reaction Recovery Recruitment Activity Relative (related person)Research Research Design Rest Risk Role Sampling Social support Speech Stimulus Stress Sympathetic Nervous System System Techniques Testing Time Tourniquets Training Trauma Treatment/Psychosocial Effects Trier Social Stress Test Violence Woman Work acute stress base biological adaptation to stress biopsychosocial central pain central sensitization design diffuse noxious inhibitory control ethnic difference ethnic discrimination experience forging heat stimulus hypothalamic-pituitary-adrenal axis indexing men neglect pain inhibition psychosocial response stress management stressor

项目摘要

African Americans (AA) are at risk for clinical pain, though the biopsychosocial mechanisms underlying enhanced pain in AAs are unknown. Relative to Caucasians, our prior work found that AAs show blunted responses of the hypothalamic-pituitary-adrenal (HPA) and sympathetic nervous system axes (SNS), and also lower oxytocin (OT) and allopregnanolone (AP), and the absence of relationship to pain sensitivity during activation of these stress-responsive systems. The relationship of these stress-responsive factors to pain sensitivity is thought to reflect an integrated response during the defense reaction. Blunted stress responses and an uncoupling of the relationship between stress responses and pain sensitivity in AAs are hypothesized to result from excessive activation of these stress systems resulting from chronic psychosocial stress in AAs. A total of 280 medically healthy AA men and women (18 – 45 years of age) will be recruited to reflect the entire SES spectrum. Interviews will access psychosocial stress, including cumulative trauma exposure, chronic stress (i.e., discrimination and difficulties), and recent negative life events. Also, potential stress buffers (e.g. religiosity, social support) will be assessed. Subjects will undergo one laboratory test session to assess pain sensitivity and endogenous pain regulatory mechanisms. Subjects will be tested while supine for baroreceptor reflex sensitivity, involving EKG measurement of heart rate and beat-to-beat changes in BP. Each subject will be tested for an index of central sensitization of pain processing by administration of a repetitive application of transient heat pulses for a maximum of 40 trials or until the subject rates the intensity of the stimulus at 100 (0-100 scale). The assessment of centrally-mediated pain inhibition will be conducted by repeating the application of transient heat pulses during concurrent hand cold presser stimulation to assess for diffuse noxious inhibitory controls (DNIC). Voluntary pain tolerance to tourniquet-induced ischemia will also be assessed. Each subject will also be exposed to the Trier Social Stress Test in order to assess stress-induced HPA and SNS reactivity. The relationship of psychosocial stress to endogenous pain regulatory mechanisms, central pain processing and peripheral pain sensitivity, and the role of stress buffers will be examined using structural equation modeling. This proposal is intended to forge new territory in the development of a bio-behavioral model relating to the development of clinical pain in African Americans. Project Description

非洲裔美国人 (AA) 面临临床疼痛的风险，尽管与白种人相比，非洲裔美国人 (AA) 疼痛加剧的生物心理社会机制尚不清楚，但我们之前的研究发现，非洲裔美国人 (AA) 的下丘脑 - 垂体 - 肾上腺 (HPA) 和交感神经反应迟钝。系统轴（SNS），以及较低的催产素（OT）和四氢孕酮（AP），并且在这些压力反应系统激活期间与疼痛敏感性不存在关系。这些应激反应因子与疼痛敏感性的关系被认为反映了防御反应过程中的综合反应，而应激反应和疼痛敏感性之间关系的脱钩是由于这些应激的过度激活而导致的。总共 280 名身体健康的 AA 男性和女性（18 至 45 岁）将被招募，以反映整个 SES 谱系，包括心理社会压力。此外，还将评估潜在的压力缓冲（例如宗教信仰、社会支持），以评估疼痛敏感性和内源性疼痛。受试者将在仰卧时接受压力感受器反射敏感性测试，包括心电图测量心率和逐次血压变化，测试每个受试者的疼痛处理中枢敏感度指数。通过重复施加瞬时热脉冲最多 40 次试验或直到受试者将刺激强度评分为 100（0-100 等级）。通过重复施加来进行中枢介导的疼痛抑制的评估。同时进行手部冷压刺激期间的瞬时热脉冲，以评估对止血带引起的缺血的自愿疼痛耐受性。社会压力测试旨在评估压力引起的 HPA 和 SNS 反应性，该提案将使用结构方程模型来检查社会心理压力与内源性疼痛调节机制、中枢疼痛处理和外周疼痛敏感性的关系以及压力缓冲的作用。旨在开发与非裔美国人临床疼痛发展相关的生物行为模型的新领域。