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Psychosomatic Medicine, Vol 57, Issue 6 592-599, Copyright © 1995 by American Psychosomatic Society
ORIGINAL ARTICLES |
SM Patterson, DS Krantz, JS Gottdiener, G Hecht, S Vargot and DS Goldstein
Georgetown University Medical Center, Washington, DC, USA.
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.
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