Effect of oral glucocorticoid intake on autonomic cardiovascular control

Cottin, François; Malcurat, V.; Zorgati, H.; Prieur, Fabrice; Labsy, Z.; Do, M. C.; Gagey, Olivier; Collomp, K.

doi:10.1186/s40064-015-1378-8

Cited by 7 publications

(12 citation statements)

References 31 publications

(47 reference statements)

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“…) and no differences (Cottin et al . ) being reported. The contrast with the present study findings maybe attributable to our selection of an acute iv dose (200 mg hydrocortisone), rather than a 1‐week oral dose (200 mg day −1 hydrocortisone (Tam et al .…”

Section: Discussionmentioning

confidence: 99%

“…) or 60 mg day −1 prednisone (Cottin et al . ), which obviates potential longer‐term peripheral effects (e.g. change in total body water, sodium content) with potential hemodynamic and neural autonomic control implications.…”

Section: Discussionmentioning

confidence: 99%

“…Time ( administered glucocorticoids on BRS, with both increases (Tam et al 1997) and no differences (Cottin et al 2015) being reported. The contrast with the present study findings maybe attributable to our selection of an acute IV dose (200 mg hydrocortisone), rather than a 1-week oral dose (200 mg day −1 hydrocortisone (Tam et al 1997) or 60 mg day −1 prednisone (Cottin et al 2015), which obviates potential longer-term peripheral effects (e.g. change in total body water, sodium content) with potential hemodynamic and neural autonomic control implications.…”

Section: Restmentioning

confidence: 95%

“…), no alteration in BRS was observed following 7 days of the synthetic glucocorticoid prednisone (60 mg day −1 ) (Cottin et al . ). Examination of the acute effects of glucocorticoids on BRS circumvents the potential confounding influence of longer‐term peripheral effects (e.g.…”

Section: Introductionmentioning

confidence: 97%

“…The effect of longer-term oral glucocorticoid therapy on BRS in humans has been examined with equivocal results that are at odds with the animal studies noted above (Rong et al 1999;Ouyang & Wang, 2000;Bechtold & Scheuer, 2006;Scheuer, 2010). Although 7 days of administration of hydrocortisone (200 mg day −1 ) increased BRS (Tam et al 1997), no alteration in BRS was observed following 7 days of the synthetic glucocorticoid prednisone (60 mg day −1 ) (Cottin et al 2015). Examination of the acute effects of glucocorticoids on BRS circumvents the potential confounding influence of longer-term peripheral effects (e.g.…”

Section: Introductionmentioning

confidence: 99%

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Acute hydrocortisone administration reduces cardiovagal baroreflex sensitivity and heart rate variability in young men

Adlan

Zanten

Lip

et al. 2018

The Journal of Physiology

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Key points A surge in cortisol during acute physiological and pathophysiological stress may precipitate ventricular arrhythmia and myocardial infarction.Reduced cardiovagal baroreflex sensitivity and heart rate variability are observed during acute stress and are associated with an increased risk of acute cardiac events.In the present study, healthy young men received either a single iv bolus of saline (placebo) or hydrocortisone, 1 week apart, in accordance with a randomized, placebo‐controlled, cross‐over study design.Hydrocortisone acutely increased heart rate and blood pressure and reduced cardiovagal baroreflex sensitivity and heart rate variability in young men.These findings suggest that, by reducing cardiovagal baroreflex sensitivity and heart rate variability, acute surges in cortisol facilitate a pro‐arrhythmic milieu and provide an important mechanistic link between stress and acute cardiac events AbstractSurges in cortisol concentration during acute stress may increase cardiovascular risk. To better understand the interactions between cortisol and the autonomic nervous system, we determined the acute effects of hydrocortisone administration on cardiovagal baroreflex sensitivity (BRS), heart rate variability (HRV) and cardiovascular reactivity. In a randomized, placebo‐controlled, single‐blinded cross‐over study, 10 healthy males received either a single iv bolus of saline (placebo) or 200 mg of hydrocortisone, 1 week apart. Heart rate (HR), blood pressure (BP) and limb blood flow were monitored 3 h later, at rest and during the sequential infusion of sodium nitroprusside and phenylephrine (modified Oxford Technique), a cold pressor test and a mental arithmetic stress task. HRV was assessed using the square root of the mean of the sum of the squares of differences between successive R‐R intervals (rMSSD). Hydrocortisone markedly increased serum cortisol 3 h following infusion and also compared to placebo. In addition, hydrocortisone elevated resting HR (+7 ± 4 beats min−1; P < 0.001) and systolic BP (+5 ± 5 mmHg; P = 0.008); lowered cardiovagal BRS [geometric mean (95% confidence interval) 15.6 (11.1–22.1) ms/mmHg vs. 26.2 (17.4––39.5) ms/mmHg, P = 0.011] and HRV (rMSSD 59 ± 29 ms vs. 84 ± 38 ms, P = 0.004) and increased leg vasoconstrictor responses to cold pressor test (Δ leg vascular conductance −45 ± 20% vs. −23 ± 26%; P = 0.023). In young men, an acute cortisol surge is accompanied by increases in HR and BP, as well as reductions in cardiovagal BRS and HRV, potentially providing a pro‐arrhythmic milieu that may precipitate ventricular arrhythmia or myocardial infarction and increase cardiovascular risk.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Restmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Acute hydrocortisone administration reduces cardiovagal baroreflex sensitivity and heart rate variability in young men

Adlan

Zanten

Lip

et al. 2018

The Journal of Physiology

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Early Signs of Sinoatrial Reinnervation in the Transplanted Heart

et al. 2021

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Background. Heart transplantation (HTx) surgically transects all connections to the heart, including the autonomic nerves. We prospectively examined signs, timing and consequences of early sympathetic and parasympathetic sinoatrial reinnervation, as well as explored indirect evidence of afferent cardiopulmonary reinnervation. Methods. Fifty HTx recipients were assessed at 2.5, 6, and 12 mo after HTx. For comparison, 50 healthy controls were examined once. Continuous, noninvasive recordings of hemodynamic variables and heart rate variability indices were performed at supine rest, 0.2 Hz controlled breathing, 60° head-up-tilt, during the Valsalva maneuver and during handgrip isometric exercise. Results. In HTx recipients, supine low-frequency heart rate variability gradually increased; supine high-frequency variability did not change; heart rate variability indices during controlled breathing remained unaltered; heart rate responses during tilt and isometric exercise gradually increased; the tachycardia response during Valsalva maneuver increased, while the bradycardia response remained unchanged; and indices of baroreflex sensitivity improved. Responses remained low compared to healthy controls. A negative correlation between indices of preload and heart rate response during head-up tilt emerged at 12 mo. Conclusions. Results suggest that sympathetic reinnervation of the sinoatrial node starts within 6 mo after HTx and strengthens during the first year. No evidence of early parasympathetic reinnervation was found. Indirect signs of afferent reinnervation of cardiopulmonary low-pressure baroreceptors emerged at 12 mo. Better sympathetic sinoatrial control improved heart rate responsiveness to orthostatic challenge and isometric exercise, as well as heart rate buffering of blood pressure fluctuations.

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