Malkoff S B, Muldoon M F, Zeigler Z R, Manuck S B
Department of Psychology, University of Pittsburgh, PA 15260.
Psychosom Med. 1993 Nov-Dec;55(6):477-82. doi: 10.1097/00006842-199311000-00001.
To evaluate the effects of mental stress on blood platelet activity, platelet secretion and aggregation were measured in 40 healthy young men, assigned in a 3:1 ratio to an experimental and control condition. After a baseline period, experimental subjects participated in a 21-minute, frustrating computer task (the Stroop test), while control subjects remained seated quietly for the same duration. Blood was drawn from all subjects immediately before and after the task period for assessment of platelet activity (secretion of ATP and aggregation in response to 5 and 20 microM ADP). Heart rate and blood pressure were also assessed at baseline and throughout the task period. Results indicated that measures of platelet secretion, heart rate, and blood pressure rose significantly from baseline to posttask assessments in subjects exposed to the experimental stressor (p < .05), but not among controls. These findings are consistent with the hypothesis that stress may potentiate coronary disease pathogenesis, in part, via activation of blood platelets and their associated effects on coronary artery occlusion and/or constriction.
为评估精神压力对血小板活性的影响，对40名健康青年男性进行了血小板分泌和聚集的测量，这些男性按3:1的比例被分配到实验条件和对照条件。在基线期之后，实验对象参与一项持续21分钟的令人沮丧的计算机任务（斯特鲁普测验），而对照对象在相同时间段内安静地坐着。在任务期前后立即从所有对象抽取血液，以评估血小板活性（ATP分泌以及对5和20微摩尔ADP的聚集反应）。在基线期以及整个任务期还评估了心率和血压。结果表明，暴露于实验性应激源的对象中，从基线期到任务后评估，血小板分泌、心率和血压的测量值显著升高（p <.05），但对照组中未出现这种情况。这些发现与以下假设一致，即压力可能部分通过激活血小板及其对冠状动脉阻塞和/或收缩的相关影响来增强冠心病的发病机制。
