Plasma catecholamines—analytical challenges and physiological limitations

Hjemdahl, Paul

doi:10.1016/s0950-351x(05)80179-x

Cited by 127 publications

(102 citation statements)

References 126 publications

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“…Hjemdahl has noted that urinary norepinephrine(NE) reflects arterial NE levels, and that changes in urinary epinephrine appear to reflect its secretion during stress, as well 16) . The relevant measures are the amounts of excreted adrenaline and NA into the urine per time unit.…”

Section: Discussionmentioning

confidence: 99%

Regular Overtime and Cardiovascular Functions.

Park¹,

Kim

Cho³

et al. 2001

INDUSTRIAL HEALTH

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It was concluded that there was sufficient evidence about a possible link between long working hours particularly exceeding 50 a week and the risk of significant health outcomes, including cardiovascular disease from literature review by Spurgeon et al.. This study was conducted to find out the single effect of regular overtime work on the cardiovascular functions through objective biological indices such as blood pressure or heart rate variability. We conducted a field survey of 238 male engineers who were working at the department of research & development of three electronics manufacturing companies in S. Korea. The field survey consisted of (1) self-report questionnaire (working hours and health conditions, and fatigue) and (2) measurements of blood pressure and heart rate variability. By multivariate analyses we could show the relationship between overtime work and some cardiovascular functions after controlling the effects of major confounders such as age and sleeping hours, which were pointed out by Iwasaki et al. (1998) and Sasaki et al. (1999). Especially, low frequency component (power in the low frequency range, 0.04-0.15 Hz) of the heart rate variability during work might be used as early objective biological indices for chronic effect of regular overtime work on cardiovascular functions. However, we should confirm those effect through the well-designed prospective study.

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Section: Discussionmentioning

confidence: 99%

Regular Overtime and Cardiovascular Functions.

Park¹,

Kim

Cho³

et al. 2001

INDUSTRIAL HEALTH

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“…This effect of Epi infusion was not solely due to Epi in the blood sample, as the plasma concentration during highdose infusion was =3 nmol/L and the sample was diluted by more than 1/10 in the flow-cytometric assay. Approximately 40% to 50% of the Epi in arterial plasma is extracted during one passage through the forearm, 28 indicating that the arterial concentration of Epi to which platelets have been exposed in vivo is ~5 to 6 nmol/L. It is interesting to note that such concentrations of Epi in vivo had platelet-sensitizing effects almost identical to 10 nmol/L Epi in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…40 - 41 Furthermore, local NE levels in plasma from a target organ such as the heart may increase more than in the systemic circulation during stress because of the differentiated pattern with which sympathetic activation occurs. 28 The a-agonist NE may thus contribute significantly to the plateletactivating properties of sympathoadrenal activation in vivo. The present and previous in vivo-related data are in good agreement and clearly support the idea that sympathoadrenal activation may have a role in thrombosis via direct catecholamine-mediated sensitization of circulating platelets.…”

Section: Discussionmentioning

confidence: 99%

Epinephrine sensitizes human platelets in vivo and in vitro as studied by fibrinogen binding and P-selectin expression.

Hjemdahl

Chronos

Wilson

et al. 1994

Arterioscler Thromb

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Epinephrine (Epi) infusion influences platelet activation markers in vivo, but in vitro studies have mainly examined supraphysiologica] Epi concentrations and have yielded conflicting results. In this study whole-blood flowcytometric measurements of platelet fibrinogen binding and P-selectin expression were used to compare enhancement of ADP (0.1 to 10 /irnol/L)-induced platelet activation by Epi infusion in vivo (0.1 and 0.4 nmol • kg" 1 • min" 1 ) and by Epi in vitro (10 and 50 nmol/L) in nine healthy volunteers. ADP caused concentration-dependent increases in the percentage of platelets that bound fibrinogen (from 4.4 ±0.9% to 69.9±4.2%) and that expressed P-selectin (from 4.5±0.5% to 44.2±3.8%). Fibrinogen and P-selectin binding indices (FgBI and PSBI; calculated from mean fluorescence intensity and percentage of positive cells) also increased from 0.18 ±0.03 to 11.70±1.99 for FgBI and from 0.22±0.03 to 2.34±0.29 for PSBI. Epi concentration-dependently enhanced fibrinogen binding and P-selectin expression in vitro (by »»30% at the midportion of the ADP curve at 10 nmol/L Epi; P<.001 for both by ANOVAs). High-dose Epi infusion enhanced FgBI similarly and increased maximal P-selectin expression by 38%. Epi (50 nmol/L in vitro) enhanced platelet activation further, whether samples were taken with or without prior Epi infusion. Total expression of gfycoprotein Ilb/IIIa was unaffected by Epi infusion, but glycoprotein Ib expression per platelet was reduced (/*<.05). These in vivo and in vitro effects of Epi on platelet responses to agonist stimulation indicate a prothrombotic potential for sympathoadrenal activation in humans.

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“…Catecholamines, especially norepinephrine should not be measured in plasma taken from a peripheral vein due to peripheral production [44]. However metanephrine has a longer half life time and is more evenly distributed in the vascular system.…”

Section: Limitationsmentioning

confidence: 99%