title: Relationship between overnight neuroendocrine activity and morning haemostasis in working men.
abstract: Sustained effects of SNS (sympathetic nervous system) and HPAA (hypothalamic-pituitary-adrenal axis) hyperactivity on haemostasis have not been investigated. In the present study, we tested for an association of overnight urinary catecholamine and cortisol excretion with morning plasma levels of fibrinogen, PAI-1 (plasminogen activator inhibitor-1) and D-dimer. Participants (639 male industrial employees) with a complete dataset were studied (age, 41+/-11 years; mean+/-S.D.). Subjects collected overnight urinary samples and had a fasting morning blood sample drawn. Measurement of urinary adrenaline (epinephrine), noradrenaline (norepinephrine) and cortisol were dichotomized to perform multivariate analyses of (co)variance. Haemostatic parameters were measured by ELISA. Fibrinogen was higher in men with high adrenaline (F(7,631)=5.68, P=0.018; where the subscripted value represents the degrees of freedom) and high noradrenaline (F(7,631)=4.19, P=0.041) compared with men with low excretion of the respective hormones. PAI-1 was higher in men with high cortisol than in men with low cortisol (F(7,631)=4.77, P=0.029). Interaction revealed that subjects with high cortisol/low noradrenaline had higher PAI-1 than subjects with low cortisol/high noradrenaline (P=0.038). Subjects with high adrenaline/high noradrenaline had higher D-dimer than subjects with high adrenaline/low noradrenaline (P=0.029), low adrenaline/high noradrenaline (P=0.022) and low adrenaline/low noradrenaline (not significant). When covariance for several confounders of haemostatic function was determined, the main effect of adrenaline on fibrinogen and the interaction between adrenaline and noradrenaline for D-dimer maintained significance. Although overnight SNS hyperactivity was associated independently with morning hypercoagulability, the relationship between the activity of HPAA and haemostasis was mediated by traditional cardiovascular risk factors.
authors.affiliation: Institute for Behavioral Sciences, Federal Institute of Technology, Zürich, Switzerland. roland.vonkaenel@insel.ch
authors.forename: Roland
authors.initials: R
authors.lastname: von Känel
authors.forename: Brigitte M
authors.initials: BM
authors.lastname: Kudielka
authors.forename: Adham
authors.initials: A
authors.lastname: Abd-el-Razik
authors.forename: Marie-Louise
authors.initials: ML
authors.lastname: Gander
authors.forename: Karl
authors.initials: K
authors.lastname: Frey
authors.forename: Joachim E
authors.initials: JE
authors.lastname: Fischer
mesh_terms: D000328:Adult; D002940:Circadian Rhythm / Q000502:physiology*; D004837:Epinephrine / Q000652:urine; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000652:urine; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D016014:Linear Models; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000652:urine; D010913:Pituitary-Adrenal System / Q000502:physiology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D013564:Sympathetic Nervous System / Q000502:physiology
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D005340:Fibrinogen; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine