Patterson S M, Krantz D S, Gottdiener J S, Hecht G, Vargot S, Goldstein D S
Georgetown University Medical Center, Washington, DC, USA.
Psychosom Med. 1995 Nov-Dec;57(6):592-9. doi: 10.1097/00006842-199511000-00012.
Mental stress can affect a range of variables relevant to hemostasis and thrombosis. However, research has not clarified whether these effects occur as part of a generalized sympathoadrenal response or whether stress-induced increases in catecholamines and blood pressure have selective and independent effects on hematologic variables. This study assessed the effects of mental and cold pressor stress on platelet activation, hematocrit, and total plasma protein and the relationship of these changes to sympathoadrenal and hemodynamic mechanisms. Platelet factor 4, beta-thromboglobulin, total plasma protein, hematocrit values, and hemoglobin were measured in 22 healthy men (32 +/- 7 years) during rest, mental arithmetic, and cold pressor task. A no-stress control group of five male subjects was used to rule out the possible effects of blood withdrawal in producing these changes. Significant increases to mental arithmetic and cold pressor (p < .001) were observed in platelet factor 4 and beta-thromboglobulin. Increases (p < .002) in hematocrit values and total plasma protein also occurred with mental arithmetic and cold pressor. Correlational analyses revealed that changes in hematocrit and total plasma protein concentrations were related to increased mean arterial pressure during stress, and platelet activation correlated positively with norepinephrine and negatively with epinephrine. The present results indicate that acute psychologic and cold stress cause concurrent changes in several hemostatic factors (increased platelet activation, hematocrit, and total plasma protein) that may play key roles in thrombosis and ischemia. The relationships of hematocrit and total plasma protein to blood pressure increases and the associations between platelet activation and catecholamines support the notion that stress-induced increases in catecholamines and blood pressure have selective effects on specific hemostatic variables.
精神压力会影响一系列与止血和血栓形成相关的变量。然而，研究尚未阐明这些影响是作为全身性交感肾上腺反应的一部分出现，还是压力诱导的儿茶酚胺和血压升高对血液学变量具有选择性和独立的影响。本研究评估了精神压力和冷加压应激对血小板活化、血细胞比容和总血浆蛋白的影响，以及这些变化与交感肾上腺和血流动力学机制的关系。在22名健康男性（32±7岁）休息、进行心算和冷加压任务期间，测量了血小板因子4、β-血小板球蛋白、总血浆蛋白、血细胞比容值和血红蛋白。使用由五名男性受试者组成的无应激对照组来排除采血在产生这些变化方面可能的影响。在心算和冷加压试验中，血小板因子4和β-血小板球蛋白显著增加（p<.001）。心算和冷加压试验时，血细胞比容值和总血浆蛋白也增加（p<.002）。相关性分析显示，应激期间血细胞比容和总血浆蛋白浓度的变化与平均动脉压升高有关，血小板活化与去甲肾上腺素呈正相关，与肾上腺素呈负相关。目前的结果表明，急性心理应激和冷应激会导致几种止血因子同时发生变化（血小板活化、血细胞比容和总血浆蛋白增加），这些变化可能在血栓形成和局部缺血中起关键作用。血细胞比容和总血浆蛋白与血压升高的关系以及血小板活化与儿茶酚胺之间的关联支持了以下观点：压力诱导的儿茶酚胺和血压升高对特定的止血变量具有选择性影响。
