Publications by authors named "Daniel Preckel"

We hypothesized that the 2 cardiovascular drugs aspirin and propranolol attenuate the prothrombotic response to acute psychosocial stress relative to placebo medication. We randomized 56 healthy subjects, double-blind, to 5-day treatment with an oral dose of either 100 mg of aspirin plus 80 mg of propranolol combined, single aspirin, single propranolol, or placebo medication. Thereafter, subjects underwent a 13-minute psychosocial stressor.

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Background: The characterization of an individual's hypothalamic-pituitary-adrenal axis stress response is a main research topic in neuropsychobiology since alterations have been causally linked to several disease states. Over the last years, several studies focused on the identification of sources of inter- and intraindividual variability, but there is still a paucity of experimental data on the effect of different pharmaceuticals on cortisol responses to acute psychological stress. Therefore, in this randomized double-blind placebo-controlled study, we investigated the effect of treatment with two popular and clinically used pharmaceuticals on stress-related cortisol responses, namely acetylsalicylic acid (aspirin), a known prostaglandin synthesis inhibitor, and the beta-blocker propranolol (Inderal), a nonselective beta-receptor antagonist.

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Activity of clotting factor VIII has been shown to acutely increase with sympathetic nervous system stimulation. We investigated whether aspirin and propranolol affect the responsiveness of plasma clotting factor VIII activity levels to acute psychosocial stress. We randomized 54 healthy subjects double-blind to 5-day treatment with a single daily oral dosage of either 100 mg aspirin plus 80 mg propranolol combined, 100 mg of aspirin, 80 mg of propranolol, or placebo medication.

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Psychosocial stress might increase the risk of atherothrombotic events by setting off an elevation in circulating levels of the proinflammatory cytokine interleukin (IL)-6. We investigated the effect of aspirin and propranolol on the responsiveness of plasma IL-6 levels to acute psychosocial stress. For 5 days, 64 healthy subjects were randomized, double-blind, to daily oral aspirin 100mg plus long-acting propranolol 80 mg, aspirin 100mg plus placebo, long-acting propranolol 80 mg plus placebo, or placebo plus placebo.

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We investigated the association between exhaustion and the habituation of free cortisol responses to repeated stress exposure. The study comprised 25 healthy male subjects (38-59 years) who were confronted three times with the Trier Social Stress Test. Mean cortisol responses showed the well-known general habituation effect.

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Exaggerated procoagulant responses to acute mental stress may contribute to coronary thrombosis, and continuing low-grade systemic coagulation activation may link negative affect with the development of coronary artery disease. We investigated whether negative and positive affect and perceived social support would moderate stress procoagulant reactivity. Psychological functioning, exhaustion, negative affectivity, depression, anxiety, worrying, vigor, and social support were assessed in 27 apparently healthy men (mean age 47 +/- 8 years) who underwent the 13-min Trier Social Stress Test combining preparation, speech, and mental arithmetic.

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Acute mental stress elicits hemoconcentration and polycytosis. We investigated whether haematological response to repeated acute mental stress would habituate and be sustained 45 min and 105 min after stress. Twenty-four men underwent a 13-min stressor three times, one week apart; hematological variables were measured at week one and three.

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Acute mental stress induces a significant increase in plasma interleukin (IL)-6 levels as a possible mechanism for how psychological stress might contribute to atherosclerosis. We investigated whether the IL-6 response would habituate in response to a repetitively applied mental stressor and whether cortisol reactivity would show a relationship with IL-6 reactivity. Study participants were 21 reasonably healthy men (mean age 46+/-7 years) who underwent the Trier Social Stress Test (combination of a 3-min preparation, 5-min speech, and 5-min mental arithmetic) three times with an interval of 1 week.

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Acute mental stress may contribute to atherosclerosis by affecting inflammation and coagulation; however, the crosstalk between inflammation and coagulation during stress has not been studied. In the present study, we investigated the association of plasma fibrinogen, plasma IL-6 (interleukin-6) and free salivary cortisol with the procoagulant marker D-dimer reflecting fibrin formation both over a 2-h period and in response to acute mental stress. Twenty-one male volunteers (mean age, 47+/-8 years) underwent the Trier Social Stress Test combining a 3-min preparation phase, a 5-min job interview and 5-min mental arithmetic test before an audience.

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Objectives: Vital exhaustion has been shown to predict the progression and manifestation of cardiovascular disease. Little is known about the relationship between vital exhaustion and overcommitment, the inability to withdraw from obligations at work. The aim of this study was to explore the relationship between vital exhaustion and overcommitment at work, as measured by the intrinsic-effort scale of the effort-reward model after consideration of other potentially salutogenetic and pathogenetic working conditions.

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Background: Acute mental stress elicits reliable changes in blood coagulation factors. We studied whether stress-related changes in coagulation measures are associated with concomitant hemoconcentration.

Methods: Twenty-two men (mean age 47+/-8 years) underwent the Trier Social Stress Test (TSST) combining 13 min of task preparation, job interview, and mental arithmetic.

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Blood coagulation activation might be one mechanism linking acute mental stress with coronary events. We investigated the natural habituation of coagulation responses and recovery to short-term mental stress. Three times with one-week intervals, 24 men (mean age 47 +/- 7 years) underwent the same 13-min stressor (preparation, job interview, mental arithmetic).

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Within the last two decades, hemostasis factors have emerged as 'new' risk factors for coronary artery disease. Historical studies on the physiology of the sympathetic nervous system (SNS) attributed accelerated blood clotting to the components of the fight-flight response. Although this has not been demonstrated, exaggerated clotting related to SNS hyperactivity might confer an increased arterial thrombotic risk.

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