Levine S P, Towell B L, Suarez A M, Knieriem L K, Harris M M, George J N
Circulation. 1985 Jun;71(6):1129-34. doi: 10.1161/01.cir.71.6.1129.
Platelets are believed to play a role in the pathogenesis of atherosclerosis and of the vascular obstruction that causes the acute complications of coronary artery disease. Since specific behavioral patterns appear to be related to the development of coronary artery disease and since emotional stress may predispose an individual to acute cardiovascular ischemia, it was hypothesized that platelet activation by catecholamines might be involved in these events. To study emotional stress, plasma samples were obtained from 61 senior medical residents immediately before they were to speak in public. There were significant increases in the plasma concentrations of the platelet-secreted proteins platelet factor 4 and beta-thromboglobulin and epinephrine and norepinephrine immediately before speaking, which demonstrates that platelet activation and secretion occur in association with this type of emotional stress. Four trials were carried out to study the mechanism for this observed platelet secretion: (1) phenoxybenzamine, (2) propranolol, (3) 650 mg aspirin, and (4) 80 mg aspirin were given several hours before the public speaking engagement. Neither phenoxybenzamine nor propranolol in doses that blocked the hemodynamic effects of alpha 1- and beta 1-adrenergic stimulation modified platelet secretion. Aspirin also did not block platelet secretion, which suggests that platelets were not being stimulated through a cyclooxygenase-dependent pathway. This study provides direct evidence of platelet secretion in vivo in association with emotional stress, and underscores the potential importance of platelet activation and secretion in the acute events that occur in patients with vascular disease.
血小板被认为在动脉粥样硬化的发病机制以及导致冠心病急性并发症的血管阻塞中发挥作用。由于特定行为模式似乎与冠心病的发展有关,并且由于情绪应激可能使个体易患急性心血管缺血,因此有人推测儿茶酚胺引起的血小板激活可能参与了这些事件。为了研究情绪应激,在61名高级住院医师即将进行公开演讲之前采集了他们的血浆样本。就在演讲前,血小板分泌蛋白血小板因子4和β-血小板球蛋白以及肾上腺素和去甲肾上腺素的血浆浓度显著升高,这表明血小板激活和分泌与这种情绪应激相关。进行了四项试验来研究这种观察到的血小板分泌的机制:(1)苯氧苄胺,(2)普萘洛尔,(3)650毫克阿司匹林,以及(4)80毫克阿司匹林在公开演讲前数小时给予。阻断α1和β1肾上腺素能刺激的血流动力学效应的剂量的苯氧苄胺和普萘洛尔均未改变血小板分泌。阿司匹林也未阻断血小板分泌,这表明血小板不是通过环氧化酶依赖性途径被刺激的。这项研究提供了与情绪应激相关的体内血小板分泌的直接证据,并强调了血小板激活和分泌在血管疾病患者发生的急性事件中的潜在重要性。