CARDIOVASCULAR REACTIVITY AND THE COURSE OF IMMUNE-RESPONSE TO AN ACUTE PSYCHOLOGICAL STRESSOR
CARDIOVASCULAR REACTIVITY AND THE COURSE OF IMMUNE-RESPONSE TO AN ACUTE PSYCHOLOGICAL STRESSOR
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DOI：
10.1097/00006842-199407000-00009
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发表时间：
1994-07-01
影响因子：
3.3
通讯作者：
MANUCK, SB
中科院分区：
文献类型：
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作者：
HERBERT, TB;COHEN, S;MANUCK, SB
本研究评估了细胞免疫反应的时间性质，以及暴露于急性心理应激源后心血管反应对免疫反应的影响。淋巴细胞亚群和淋巴细胞增殖反应的植物血凝素进行了评估，在基线和5和21分钟后的应激源发作的实验组和在同一时间点在非应激对照组。应激源发作后5分钟，CD 8抑制/细胞毒性T细胞和CD 16/56自然杀伤细胞的数量增加，对植物血凝素的增殖反应下降。这些变化保持在21分钟。那些表现出最大心血管反应性的受试者具有最大的免疫改变。这些数据并没有表明性别显著调节免疫反应。结果是一致的假设，交感神经激活介导的压力诱导的外周血淋巴细胞亚群和非特异性有丝分裂原刺激增殖的数量变化。
This study evaluated the temporal nature of cellular immune responses, as well as the effects of cardiovascular reactivity on immune responses after exposure to an acute psychological stressor. Lymphocyte subsets and lymphocyte proliferative response to phytohemagglutinin were assessed at baseline and at 5 and 21 minutes after stressor onset in the experimental group and at the same time points in a nonstressor control group. By 5 minutes after stressor onset, the number of CD8 suppressor/cytotoxic T and CD16/56 natural killer cells increased and proliferative response to phytohemagglutinin decreased. These changes were maintained at 21 minutes. Those subjects showing the greatest cardiovascular reactivity had the largest immune alterations. These data did not indicate that gender significantly moderated immune responses. Results are consistent with the hypothesis that sympathetic activation mediates stressor-induced quantitative alterations of peripheral blood lymphocyte subpopulations and nonspecific mitogen stimulated proliferation.