Anxiety and Delayed Type Hypersensitivity Responses

描述（由申请人提供）：虽然实验室之间的关系 对急性心理社会应激源和心血管功能的反应一直是 探索了几十年，直到最近，研究人员才对 研究这些压力源对免疫功能的额外影响。简要 实验室压力源已被证明会导致某些 细胞介导免疫的参数。有趣的是，这些与压力有关的 免疫学变化似乎在身体强壮的个体中得到加强， 心血管对压力的反应换句话说，那些表现出 对短暂心理压力的最大心血管反应也 表现出增强的功能，有助于细胞介导的 免疫反应尽管有这些有趣的发现，急性实验室诱导的 压力源尚未与临床相关的 细胞介导的免疫反应的变化。这是我们的首要目标。 拟议的研究项目，这将是利用延迟型 超敏反应（DTH）作为细胞介导的临床相关模型 免疫力受试者将被要求完成两个独立的实验 会议（基线与急性压力），间隔两周，这将是 平衡。在每次治疗结束时注射破伤风类毒素， ，以启动DTH反应，受试者将被要求返回48 在每次实验后的几个小时， 可以评估DTH反应。急性应激源是一个模拟的公众 说话的任务。心率、每搏输出量、射血前期和左心室 心室射血时间将被连续且无创地测量 在使用阻抗心动描记术技术的两个实验期间， 血压将定期监测，使用自动 血压监测仪据推测，DTH反应， 在压力性任务后立即启动的任务， 比基线条件下启动的DTH响应幅度更大，以及 压力引起的DTH反应增强将直接与 压力引起的心血管反应

DESCRIPTION (provided by applicant): While the relationship between laboratory responses to acute psychosocial stressors and cardiovascular function has been explored for decades, only recently have researchers become interested in examining the additional impact of such stressors on immune function. Brief laboratory stressors have been shown to induce significant increases in some parameters of cell-mediated immunity. Interestingly, these stress-related immunologic changes appear to be potentiated in individuals who are also strong cardiovascular reactors to stress. In other words, those individuals who show the greatest cardiovascular response to brief psychological stressors also exhibit increased enhancement of functions that contribute to the cell-mediated immune response. Despite these interesting findings, acute laboratory-induced stressors have yet to be correlated significantly with clinically relevant shifts in the cell-mediated immune response. This is the primary objective of the proposed research project, which would be undertaken using the delayed-type hypersensitivity (DTH) response as a clinically relevant model of cell-mediated immunity. Subjects would be required to complete two separate experimental sessions (baseline vs. acute stress), spaced two weeks apart, which would be counterbalanced. Injection of tetanus toxoid at the end of each session would serve to initiate the DTH response, and subjects would be required to return 48 hours after each of the experimental sessions so that the magnitude of these DTH responses could be assessed. The acute stressor would be a simulated public speaking task. Heart rate, stroke volume, pre-ejection period and left ventricular ejection time would be measured continuously and non-invasively during the two experimental sessions using impedance cardiographic techniques, and blood pressure would be monitored at regular intervals using an automated blood pressure monitor. It is hypothesized that DTH responses that are initiated immediately following the stressful task will be significantly larger in magnitude than DTH responses initiated during the baseline condition, and that stress-induced enhancement of the DTH response will be directly related to stress-induced cardiovascular reactivity.