Anxiety and Delayed Type Hypersensitivity Responses

描述(由申请人提供)：虽然实验室对急性心理社会应激源的反应与心血管功能之间的关系 经过几十年的探索，研究人员直到最近才开始对 研究这些应激源对免疫功能的额外影响。简介 实验室应激源已被证明在某些情况下会导致显著增加 细胞免疫参数。有趣的是，这些与压力有关的 在身体强壮的个体中，免疫变化似乎得到加强。 心血管反应物来应对压力。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是 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 应激源尚未与临床相关性显著相关。 细胞介导的免疫反应的变化。这是 拟议的研究项目，将使用延迟型 超敏反应(DTH)作为细胞介导的临床相关模型 豁免权。受试者将被要求完成两个独立的实验 会议(基线与急性应激)，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将 用于启动DTH响应，受试者将被要求返回48 在每一次实验后的几个小时内， 可以评估潜伏期反应。急性应激源将是模拟的公众 口语任务。心率、每搏量、射血前期和左 将连续、无创地测量心脏射血时间。 在使用阻抗心动图技术的两个实验过程中， 血压将定期监测，使用自动化的 血压监测仪。假设DTH响应是 紧跟在紧张任务之后立即发起的任务将显著更大 比在基线条件下发起的潜伏期反应的幅度更大，以及 应激诱导的潜伏期反应增强将直接与 应激诱导的心血管反应性。

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.