Hamer Mark, Gibson E Leigh, Vuononvirta Raisa, Williams Emily, Steptoe Andrew
Psychobiology Group, Department of Epidemiology and Public Health, University College London, London, UK.
Brain Behav Immun. 2006 Sep;20(5):456-9. doi: 10.1016/j.bbi.2006.01.001. Epub 2006 Feb 20.
An important assumption underlying psychobiological studies relating stress reactivity with disease risk is that individuals are characterized by stable response profiles that can be reliably assessed using acute psychophysiological stress testing. Previous research has mainly focused on the stability of cardiovascular, neuroendocrine, and cellular immune responses to repeated stressors, and less attention has been given to inflammatory and platelet responses. We therefore examined both average stability and individual test-retest stability of cardiovascular, neuroendocrine, hemostatic, inflammatory, and subjective responses to mental stress over two repeated stress sessions, four weeks apart. Ninety-one healthy, non-smoking men (mean age 33.2 years) completed a 3-min speech task followed by a 5-min mirror tracing task on two separate occasions. Blood samples were taken at baseline and 10 min after the stress tasks while cardiovascular activity, saliva samples, and subjective ratings were measured repeatedly. There was significant cardiovascular and cortisol activation to the stressors and stress-induced increases in plasma C-reactive protein, von Willebrand factor antigen, and platelet activation indexed by leukocyte-platelet aggregates. The magnitude of stress responses did not differ between sessions in any variable. Significant test-retest correlations between sessions were observed for baseline and stress values of all variables (r=0.47-0.74, p<.001), but reactivity (change scores) for C-reactive protein, von Willebrand factor, cortisol, and platelet activation were not significantly correlated. Our results demonstrate that the stress-induced responses did not habituate between sessions, though the small magnitude of acute inflammatory, cortisol, and platelet responses limits the test-retest reliability of stress reactivity assessments.
心理生物学研究中将应激反应性与疾病风险相关联的一个重要假设是，个体具有稳定的反应特征，可通过急性心理生理应激测试进行可靠评估。以往研究主要关注心血管、神经内分泌和细胞免疫对重复应激源反应的稳定性，而对炎症和血小板反应关注较少。因此，我们在相隔四周的两次重复应激试验中，考察了心血管、神经内分泌、止血、炎症和心理应激主观反应的平均稳定性和个体重测稳定性。91名健康、不吸烟男性（平均年龄33.2岁）在两个不同场合完成了一项3分钟的演讲任务，随后进行了一项5分钟的镜像追踪任务。在基线和应激任务后10分钟采集血样，同时多次测量心血管活动、唾液样本和主观评分。应激源导致心血管和皮质醇显著激活，应激诱导血浆C反应蛋白、血管性血友病因子抗原增加，以及白细胞-血小板聚集体所指示的血小板激活。各变量在两次试验中的应激反应强度无差异。所有变量的基线值和应激值在两次试验间均观察到显著的重测相关性（r=0.47-0.74，p<0.001），但C反应蛋白、血管性血友病因子、皮质醇和血小板激活的反应性（变化分数）无显著相关性。我们的结果表明，尽管急性炎症、皮质醇和血小板反应的幅度较小，限制了应激反应性评估的重测可靠性，但应激诱导的反应在两次试验间并未产生习惯化。
