Article

Platelet activation and secretion associated with emotional stress.

Circulation (Impact Factor: 14.95). 07/1985; 71(6):1129-34. DOI: 10.1161/01.CIR.71.6.1129
Source: PubMed

ABSTRACT 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.

0 Followers
 · 
54 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Electric-foot-shock was given to rats to initiate constant mental stress and its effect on fibrinolytic activity was analyzed. After the termination of electric-foot-shock which was given for an hour, euglobulin clot lysis time in the stressed group significantly prolonged than those in the control group. tissue plasminogen activator activity was also significantly lower in the stressed group. These effects lasted at least for an hour and returned to the control values 24 hours after the stress. Whole blood serotonin levels, which mainly show serotonin contents in platelets, were higher in the stressed group. A negative correlation between whole blood serotonin and tPA activity in the stressed group was obtained. These results suggest that prolonged mental stress impairs fibrinolysis by decreasing tPA activity with a concomitant increase of serotonin contents in platelets.
    Thrombosis Research 07/1994; 74(6):595-603. DOI:10.1016/0049-3848(94)90216-X · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Blood cell aggregates are thought to be the cause of spontaneous echo contrast (SEC), although there is disagreement as to whether red cell or platelet aggregates produce this effect. One way to differentiate between these 2 possibilities is to evaluate the effect of aspirin on SEC because aspirin would not be expected to affect red cell aggregates. To eliminate the need to perform repetitive transesophageal echocardiographic studies, and the possible effect of the underlying disease process on SEC, the effect of aspirin on SEC in the brachial vein was studied in normal volunteers using a single-blind, before-and-after study design. Other factors known to affect blood echogenicity including hematocrit, sedimentation rate, and the presence of platelet aggregates by microscopy were also studied. The amount of SEC was quantitated by image analysis and expressed as the aggregate score. The results in 10 volunteers showed that all had SEC in brachial veins before aspirin, but there was no significant day-to-day variation in the amount of SEC during the control period (mean +/- SEM 104,248 +/- 23,088, 153,722 +/- 35,664, and 124,568 +/- 22,827 for days 1, 3, and 5, respectively). A significant decrease in the aggregate score occurred after 7 days of aspirin, 650 mg twice a day (51,690 vs 127,513, p = 0.002); this was accompanied by a striking decrement in the size of the largest platelet aggregate found in venous blood. Aspirin caused no significant change in the hematocrit or sedimentation rate. These results indicate that there is a component of SEC that is aspirin-sensitive and is likely to represent platelet aggregates.
    The American Journal of Cardiology 06/1995; 75(14):924-8. DOI:10.1016/S0002-9149(99)80688-2 · 3.43 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Es ist weithin akzeptiert, dass Stress die Anfälligkeit für gewisse Krankheiten steigert. Stress bezieht sich nicht nur auf die körperliche sondern auch auf psychologische Anstrengungen. Besonders relevant ist dies für Krankheiten in der psychosomatischem Medizin (z.B. Hypertonie, Herzinfarkt). So gibt es schon mehrere Studien die sich auf die Auswirkungen von Stress, auf den Krankheitseinbruch und/oder dem Krankheitsverlauf, beziehen. Bislang sind die Mechanismen noch nicht vollständig geklärt. Die gegenwärtige Studie wurde durchgeführt, um zu Untersuchungen, ob der akute psychologische Stress von Public Speaking die endokrinen Reaktionen (Cortisol- und Catecholaminausschüttung) und die Thrombozytenanzahl beeinflusst. Zudem wurde in dieser Studie eine neue Methode zu der Thrombozytenadhäsionsmessung eingeführt (Retentionstest Homburg). Es wurden 32 gesunden männlichen Nichtraucher unter dem Paradigma Public speaking (N=16) oder in einer Kontrollbedingung untersucht (kein Stress). In diesem Versuch wurden Cortisol, Adrenalin, Noradrenalin, Herzrate, Thrombozytenanzahl und die Thrombozytenadhäsion zu unterschiedlichen Zeitpunkten gemessen. Die Versuche dauerten ca. 2.5 Stunden. Des Weiteren wurde die emotionale Befindlichkeit ermittelt. Die Ergebnisse demonstrieren deutlich, dass durch Public Speaking, in Bezug auf die endokrinen und psychologischen Variablen, Stressantworten resultierten. Zudem konnte ebenso eine Zunahme der Thrombozytenanzahl unter dem Einfluss von Stress beobachtet werden. Allerdings war die Thrombozytenadhäsion, die mit dem Retentionstest Homburg gemessen wurde, nicht signifikant. Die Hypothese, dass Catecholamine für die Veränderung der Thrombozytenfunktion verantwortlich seien und es somit eine Korrelation zwischen den Änderungen der Catecholamine und den Änderungen der Thrombozytenparametern gäbe, bestätigte sich nicht. Diese Ergebnisse wurden in Bezug auf das Regelungsmuster der Thrombozyten sowie auf den methodischen Beschränkungen, die sich auf den Retentionstest beziehen, diskutiert. It is widely accepted that stress increases the vulnerability for certain diseases. This is not only true for physical but also for psychological strain. Especially with respect to diseases relevant in psychosomatic medicine (e.g. hypertension, cardiac infarction) several studies tried to relate stress to disease onset and/or progression. However, mechanisms are quite unknown. The present study was conducted to investigate whether the acute psychological stress of public speaking influences endocrine reactions (cortisol and catecholamine release) and the number of platelets. Moreover, a new method for measuring platelet adhesion has been introduced in this study (Retentionstest Homburg). A number of 32 healthy male non-smoking participants were investigated in a public speaking paradigm (N=16) or in a control condition (no stress). Levels of cortisol, adrenaline, noradrenalin, heart rate, number of platelets as well platelet adhesion were measured at different time points throughout the experiment which lasted for about 2.5 hours. In addition ratings of emotional states were measured. The results clearly demonstrate that public speaking resulted in marked stress responses with respect to the endocrine and psychological variables. Moreover, a stress induced increase in platelet number could be observed as well. However, the platelet adhesion as measured by the retention test was not affected significantly. A concomitant correlation between changes in catecholamines and changes in platelet parameters did not confirm the hypothesis that catecholamines are responsible for changes in platelet function. Results are discussed with respect to the stress reactions found after public speaking and with regard to methodological restrictions related to the retention test.

Preview

Download
0 Downloads
Available from