Spectral analysis of sympathetic discharge, R-R interval and systolic arterial pressure in decerebrate cats

Montano, Nicola; Lombardi, Federico; Ruscone, Tomaso Gnecchi; Contini, Mauro; Finocchiaro, M. L.; Baselli, Giuseppe; Porta, Alberto; Cerutti, S.; Malliani, Alberto

doi:10.1016/0165-1838(92)90222-3

Cited by 93 publications

(54 citation statements)

References 24 publications

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“…33 Moreover, the possibility that changes in parasympathetic activity at the cessation of exercise could have contributed to some extent to the maintained increase in the LF component during ALC cannot be absolutely excluded. 18,23 However, the finding of no significant differences in HF spectral power (and in BRS as well) between ALC and recovery when, on the contrary, LF returned to control would argue against a substantial contribution of vagal mechanisms to LF spectra during ALC.…”

Section: Study Limitationsmentioning

confidence: 56%

“…Concomitantly with the decrease in HF oscillations, there was an increase in the lower-frequency oscillations of HR that, by reflecting an increased sympathetic modulation to the sinoatrial node, would indicate a significant contribution of this autonomic division to HR regulation during static exercise. The relevance of the sympathetic nervous system in regulating HR is further stressed by the fact that the increase in the LF component did occur despite the HF component that was present in sympathetic discharge variability, 23 which could have restrained LF enhancement, because vagal outflow decreases during exercise. Interestingly, the increase in the LF component was significant both in absolute values and normalized units.…”

Section: Iellamo Et Al Muscle Metaboreflex Regulation Of Heart Ratementioning

confidence: 99%

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Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise

et al. 1999

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Background-It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia. Methods and Results-Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered. Conclusions-The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation.The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation. (Circulation. 1999;100:27-32.)

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Section: Study Limitationsmentioning

confidence: 56%

Section: Iellamo Et Al Muscle Metaboreflex Regulation Of Heart Ratementioning

confidence: 99%

Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise

et al. 1999

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“…10,29 Similarly, LF and HF components are also present in vagal discharge variability, 6 but vagal excitation appears to be linked to a relative increase in the HF component of sympathetic outflow and RR variability. 10,29 These rhythms may reflect a central pattern organization in which excitation (or sympathetic activation) is associated with increased LF rhythmicity and inhibition (or vagal activation) with increased HF rhythmicity.…”

Section: Discussionmentioning

confidence: 99%

Central Vagotonic Effects of Atropine Modulate Spectral Oscillations of Sympathetic Nerve Activity

et al. 1998

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Background-Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity. Any central muscarinic effects of high-dose atropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central parasympathetic activation on sympathetic activity are not known. Methods and Results-Using power spectral analysis of RR interval, intra-arterial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of both low (2 g/kg IV) and high (15 g/kg IV) doses of atropine. After low-dose atropine, RR increased by 9Ϯ1% (PϽ0.0001), the low-frequency (LF) component (in normalized units, NU) of RR variability decreased by Ϫ32Ϯ8%, and the high-frequency (HF) NU component increased (ϩ74Ϯ19%); hence, LF/HF of RR variability fell by 52Ϯ10% (all PϽ0.01). Although overall MSNA did not change, LF NU of MSNA decreased (Ϫ15Ϯ5%), HF NU of MSNA increased (ϩ31Ϯ3%), and LF/HF of MSNA fell (Ϫ41Ϯ8%) (all PϽ0.01). After high-dose atropine, LF NU of MSNA decreased (Ϫ17Ϯ12%), HF NU of MSNA increased (ϩ22Ϯ3%), and LF/HF of MSNA fell (Ϫ51Ϯ21%) (all PϽ0.02). Conclusions-Increasing central parasympathetic activity with low-dose atropine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atropine similarly induces an increase in the HF and a decrease in the LF components of MSNA variability. Thus, central parasympathetic activation is able to modulate the oscillatory characteristics of sympathetic nerve traffic to peripheral blood vessels.

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“…4 Second, as SANS activity is clustered in low-frequency bursts, SANS-induced physiological responses are likely to exhibit low-frequency dynamics. [10][11][12][13][14] Previous studies have shown that SANS assessment based on HRV and baroreflex sensitivity is a marker of increased vulnerability to fatal cardiac arrhythmias. 15,16 However, both methods are limited by the fact that they only provide an indirect probe of the sympathetic effect on cardiac repolarisation, as they reflect influences on the sinoatrial node and blood vessels and not on the ventricular myocardium.…”

Section: Arrhythmia Mechanismsmentioning

confidence: 99%

Periodic Repolarisation Dynamics: A Natural Probe of the Ventricular Response to Sympathetic Activation

Rizas¹,

Hamm²,

Kääb³

et al. 2016

Arrhythmia &Amp; Electrophysiology Review

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Experimental and clinical studies have demonstrated that enhanced sympathetic autonomic nervous system (SANS) activity can destabilise myocardial repolarisation, 1-4 increasing vulnerability to developing fatal cardiac arrhythmias. [5][6][7][8] Accordingly, assessment of SANS activity has always been a major goal for cardiac risk stratification methods.Various non-invasive methods including assessment of heart rate variability (HRV) and baroreflex sensitivity have been employed to study the activity of the SANS under routine clinical conditions. 9 These methods are based on two principles. First, activation of the SANS evokes physiological effects on the cardiovascular system, such as acceleration of heart rate, increased vasomotor tone or systolic contractility.4 Second, as SANS activity is clustered in low-frequency bursts, SANS-induced physiological responses are likely to exhibit low-frequency dynamics. [10][11][12][13][14] Previous studies have shown that SANS assessment based on HRV and baroreflex sensitivity is a marker of increased vulnerability to fatal cardiac arrhythmias. 15,16 However, both methods are limited by the fact that they only provide an indirect probe of the sympathetic effect on cardiac repolarisation, as they reflect influences on the sinoatrial node and blood vessels and not on the ventricular myocardium. In addition, both HRV and baroreflex sensitivity are confounded by the concomitant action of other systems exhibiting periodic dynamics, such as the parasympathetic nervous system and the renin-angiotensinaldosterone system, respectively.We proposed a novel approach to SANS assessment that substantially differs from previous methods.17 So-called periodic repolarisation dynamics (PRD) evaluates sympathetic activity-associated lowfrequency periodic changes of cardiac repolarisation instability and opens new perspectives for identifying high-risk patients, who would potentially benefit from prophylactic interventions. The first section of this review briefly depicts the methodology of PRD assessments.The second section focuses on potential mechanisms of PRD. In the third section, the clinical application of PRD as risk predictor after myocardial infarction (MI) is presented. In the fourth section, we present an alternative method for PRD assessment, which provides some technical advantages over the standard method. The final sections are dedicated to ongoing and future projects aimed at developing individualised treatment strategies. Methodology of Periodic Repolarisation Dynamics AssessmentPRD is typically assessed using a high-resolution ECG recorded in or converted to the three orthogonal axes X, Y and Z ('Frank lead configuration'). As low-frequency patterns are of interest, the recording AbstractPeriodic repolarisation dynamics (PRD) refers to low-frequency (≤0.1Hz) modulations of cardiac repolarisation instability. Spontaneous PRD can be assessed non-invasively from 3D high-resolution resting ECGs. Physiological and experimental studies have indicated that PRD correlates with effere...

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Spectral analysis of sympathetic discharge, R-R interval and systolic arterial pressure in decerebrate cats

Cited by 93 publications

References 24 publications

Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise

Muscle Metaboreflex Contribution to Sinus Node Regulation During Static Exercise

Central Vagotonic Effects of Atropine Modulate Spectral Oscillations of Sympathetic Nerve Activity

Periodic Repolarisation Dynamics: A Natural Probe of the Ventricular Response to Sympathetic Activation

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