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      Chronic but Not Acute Hydrocortisone Treatment Shifts the Response to an Orthostatic Challenge towards Parasympathetic Activity

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          Adrenocortical steroid hormones play a major role in the regulation of both action and metabolism of catecholamines. However, there is limited information on the effect of prolonged increase in plasma steroid hormone concentration on the sympathetic nervous system, which is the main source of norepinephrine. Using a double-blind, placebo-controlled cross-over design, we examined 20 male healthy volunteers after acute administration of 40 mg hydrocortisone or matching placebo as well as after a 1-week treatment with this steroid (daily dose, 40 mg) or placebo. Sympathetic nervous system activity was assessed by determination of overnight urinary norepinephrine and epinephrine secretion and by analysis of short-time heart rate variability (HRV) measures in the frequency domain. The low-frequency (LF) component of the HRV spectrum was considered to reflect both sympathetic and parasympathetic modulation and the high-frequency (HF) band vagal activity. HRV testing included the response to a mild cardiovascular challenge, orthostasis. After 1 subject had been excluded because of incompliance with the study medication, the data of 19 subjects were used for further analyses. Prolonged hydrocortisone treatment was associated with a significant shift of relative power from the LF to the HF band in the upright position, resulting in a significant decrease in the LF/HF ratio (placebo 6.77 ± 3.35 and hydrocortisone 4.72 ± 3.27; p < 0.05). No differences between groups were observed after acute steroid administration or after prolonged treatment in the supine position. Neither acute nor chronic hydrocortisone treatment resulted in significant changes in the overnight urinary catecholamine secretion. Our data suggest that prolonged but not acute hydrocortisone administration shifts the autonomic response to an orthostatic challenge towards parasympathetic activity.

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              Heart rate variability as an index of sympathovagal interaction after acute myocardial infarction.

              By analysis of spectral components of heart rate variability, sympathovagal interaction was assessed in patients after acute myocardial infarction (AMI). At 2 weeks after AMI (n = 70), the low-frequency component was significantly greater (69 +/- 2 vs 53 +/- 3 normalized units [NU], p less than 0.05) and the high-frequency component was significantly smaller (17 +/- 1 vs 35 +/- 3 NU) than in 26 age-matched control subjects. This difference was likely to reflect an alteration of sympathovagal regulatory outflows with a predominance of sympathetic activity. At 6 (n = 33) and 12 (n = 29) months after AMI, a progressive decrease in the low- (62 +/- 2 and 54 +/- 3 NU) and an increase in the high-frequency (23 +/- 2 and 30 +/- 2 NU) spectral components was observed, which suggested a normalization of sympathovagal interaction. An increase in sympathetic efferent activity induced by tilt did not further modify the low-frequency spectral component (78 +/- 3 vs 74 +/- 3 NU) in a subgroup of 24 patients at 2 weeks after AMI. Instead, 1 year after AMI, this maneuver was accompanied by an increase in the low-frequency component (77 +/- 3 vs 53 +/- 3 NU, p less than 0.05) of a magnitude similar to the one observed in control subjects (78 +/- 3 vs 53 +/- 3 NU). These data indicate that the sympathetic predominance that is detectable 2 weeks after AMI is followed by recovery of vagal tone and a normalization of sympathovagal interaction, not only during resting conditions, but also in response to a sympathetic stimulus.

                Author and article information

                S. Karger AG
                May 2005
                26 May 2005
                : 81
                : 1
                : 63-68
                Central Institute of Mental Health, Mannheim, Germany
                84894 Neuroendocrinology 2005;81:63–68
                © 2005 S. Karger AG, Basel

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                Tables: 3, References: 36, Pages: 6
                Original Paper


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