Effect of Emotional Stress on Platelet Aggregation in Humans

Haft, Jacob I.; Arkel, Yale S.

doi:10.1378/chest.70.4.501

Cited by 50 publications

(22 citation statements)

References 13 publications

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“…There was a significant difference between the MDA concentrations in the placebo-and aspirin-treated groups immediately before stress. In spite of this effect on MDA concentration, which is a measure of prostaglandin production, there were no differences in PF4 secretion when the data for the placebo-and aspirin- (11) 59 (14) Epinephrine (pg/ml) 73 (23) 127 (30) 54 (13) 51 (17) 123 (23) 36 (11) Norepinephrine (pg/ml) 397 (48) 491 (108) 414 (65) 385 (39) 519 (94) 409 (47) Platelets ( x 103/gl) 255 (27) 290 (30) 288 (18) 313 (39) 317 (27) 326 ( The data are values from seven subjects in each group in the 650 mg aspirin study and six subjects in each group in the 80 mg aspirin study. Numbers in parentheses represent the SEM.…”

Section: Resultsmentioning

confidence: 99%

Platelet activation and secretion associated with emotional stress.

Levine¹,

Towell²,

Suárez³

et al. 1985

Circulation

189

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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 ,B-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 a,-and 3,1-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.

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Section: Resultsmentioning

confidence: 99%

Platelet activation and secretion associated with emotional stress.

Levine¹,

Towell²,

Suárez³

et al. 1985

Circulation

189

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“…They may be responsible for the increased aggregation seen wvith cigarette smoking and in animals and humans subjected to psychologic and physical stress (26)(27)(28). Platelets obtained from patients with hyperbetalipoproteinemia aggregate with very low doses of (-) epinephrine (29,30).…”

Section: Methodsmentioning

confidence: 99%

Characterization of the Human Platelet α-Adrenergic Receptor

Alexander¹,

Cooper²,

Handin³

1978

J. Clin. Invest.

126

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A B S T R A C T Human platelets aggregate and undergo a release reaction wvhen inetubated wvith catecholamines. Indirect evidence indicates that these events are mediated through a-adrenergic receptors. We used [3H]dihydroergocryptine, an a-adrenergic antagonist, to identify binding sites on platelets that have the characteristics of a-adrenergic receptors. Catecholamines compete for the binding sites in a stereo-specific manner with the potency series of (-) epinephrine > (-) norepinephrine > (+) phenylephrine > (-) isoproterenol. The dissociation constant (Kd) of (-) ,M. Phentolamine and dihydroergocyrptine blocked this response, whereas (±) propranolol had no effect. (-) Epinephrine and (-) norepiniephrine inhibited basal and prostaglandin El-stimulated adenylate cyclase in a dose-related manner. The conicentrationi of( -) epiinephrinie inhibiting adenvlate cyclase 50% was 0.7 ,uM. This inhibitioni was also blocked by phentolamiiine and dihydroergocryptine btut not by (±) propranolol. The specificity of binding and the close correlationi with a-adrenergic receptor-mediated biochemical and physiological responses suggest that the [3H]dihydroergocryptine binding site represents, or is closely related to, the human platelet a-adrenergic receptor. The ability to assay this receptor directly and to correlate these data with independently measured se(uelae of receptor activation should facilitate increased understandinig of the physiology and pathophysiology of the hulmlani platelet a-adrenergic receptor.

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“…Short-term exposure (1 h) seemed to have no influence on platelet aggregation. Stress is one o f the factors shown to change platelet aggre gation, although the data concerning stressinduced alterations in human platelet func tions have been inconsistent with both en hancement and suppression reported [3, [17][18][19]. Studies on platelet aggregation, particu larly in the whole blood in laboratory animals subjected to stress, are lacking.…”

Section: Discussionmentioning

confidence: 99%

Time-Dependent Changes in Platelet Aggregation, Fibrinolytic Activity, and Peripheral Serotonergic Measures in Rats Subjected to Water Immersion Restraint Stress

Małyszko¹,

Urano²,

Takada³

et al. 1994

Pathophysiol Haemos Thromb

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The effects of water immersion restraint stress on collagen-induced platelet aggregation in whole blood, and on the fibrinolytic and serotonergic systems in rats have been studied. One hour long stress caused a release of tissue plasminogen activator (tPA) into the blood and a shortening of euglobulin clot lysis time (ECLT), whereas restraint of longer duration was responsible for a reduction in platelet aggregation, an elevation in the activity of plasminogen activator inhibitor with a concomitant fall in tPA and a prolongation of ECLT relative to controls. Whole-blood and plasma serotonin and its metabolite 5-hydroxyindoleacetic acid were also higher in the stressed rats and whole-blood serotonin level showed a negative correlation with tPA in the stressed rats. Either stress and/ or its duration are responsible for changes in both fibrinolytic and serotonergic systems.

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Effect of Emotional Stress on Platelet Aggregation in Humans

Cited by 50 publications

References 13 publications

Platelet activation and secretion associated with emotional stress.

Platelet activation and secretion associated with emotional stress.

Characterization of the Human Platelet α-Adrenergic Receptor

Time-Dependent Changes in Platelet Aggregation, Fibrinolytic Activity, and Peripheral Serotonergic Measures in Rats Subjected to Water Immersion Restraint Stress

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