Analysis of sympathetic neural discharge in rats and humans

Montano, Nicola; Furlan, Raffaello; Guzzetti, Stefano; McAllen, Robin M.; Julien, Claude

doi:10.1098/rsta.2008.0285

Cited by 26 publications

(25 citation statements)

References 88 publications

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“…We documented, therefore, that toxin infusion is responsible for a quick and drastic impairment of the baroreflex function, independent from the level of BP and large enough to alter cardiovascular homeostasis. Reported similarities between rats and humans in integrative mechanisms of BP control (34,35) suggest that our model describes pathophysiological mechanisms that may be present also in humans. The presence of baroreflex impairment therefore could help the early recognition of endotoxemia.…”

Section: Discussionmentioning

confidence: 89%

Infusion of Escherichia coli Lipopolysaccharide Toxin in Rats Produces an Early and Severe Impairment of Baroreflex Function in Absence of Blood Pressure Changes

Radaelli

Castiglioni

Cerrito

et al. 2013

Shock

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The assessment of baroreflex function since the first appearance of endotoxemia is important because the arterial baroreflex should exert a protective role during sepsis. Nevertheless, contrasting results were previously reported. This could be due to the hemodynamic instability characterizing this condition that may per se interfere with reflex cardiovascular adjustments. The aim of our study was therefore to study the baroreflex function (a) since the very beginning of infusion of Escherichia coli lipopolysaccharide (LPS) toxin and (b) in absence of the unloading effect produced by a decrease in blood pressure. Lipopolysaccharide was infused in 10 rats for 20 min at the infusion rate of 0.05 mg · kg · min. Blood pressure was continuously measured before, during, and after infusion, and the baroreflex function was evaluated analyzing spontaneous fluctuations of systolic blood pressure and pulse interval by the sequence and transfer-function techniques. Plasma concentrations of inflammatory (interleukin 6, tumor necrosis factor α) and anti-inflammatory (interleukin 10) cytokines were measured in other eight rats, similarly instrumented, four of which receiving the same LPS infusion. We found that blood pressure levels did not change with the infusion of LPS, whereas inflammatory cytokines increased significantly. The baroreflex sensitivity was significantly reduced 10 min after the beginning of LPS infusion, reached values about half those at baseline within 15 min after the start of infusion, and remained significantly low after the end of infusion. In conclusion, we documented that septic shock inducing LPS infusion is responsible for a very rapid impairment of the baroreflex function, independent from the level of blood pressure.

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Section: Discussionmentioning

confidence: 89%

Infusion of Escherichia coli Lipopolysaccharide Toxin in Rats Produces an Early and Severe Impairment of Baroreflex Function in Absence of Blood Pressure Changes

Radaelli

Castiglioni

Cerrito

et al. 2013

Shock

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“…As mentioned earlier, the information emanating from the central integration of many reflex mechanisms is transmitted by the autonomic fibers using intensity and rhythm of firing as codes. Importantly, certain clinical conditions can lead to the collapse of the autonomic nervous system and to the loss of rhythmicity of cardiovascular variability (Montano et al, 2009). Due to random distribution of spikes during time, the sympathetic afferent can be expressed in terms of phasic and tonic activities, thus reflecting the dynamic integration of the reflex mechanisms controlling cardiovascular functions.…”

Section: Questions To Ponder For Future Studiesmentioning

confidence: 99%

Contribution of Autonomic Reflexes to the Hyperadrenergic State in Heart Failure

et al. 2017

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Heart failure (HF) is a complex syndrome representing the clinical endpoint of many cardiovascular diseases of different etiology. Given its prevalence, incidence and social impact, a better understanding of HF pathophysiology is paramount to implement more effective anti-HF therapies. Based on left ventricle (LV) performance, HF is currently classified as follows: (1) with reduced ejection fraction (HFrEF); (2) with mid-range EF (HFmrEF); and (3) with preserved EF (HFpEF). A central tenet of HFrEF pathophysiology is adrenergic hyperactivity, featuring increased sympathetic nerve discharge and a progressive loss of rhythmical sympathetic oscillations. The role of reflex mechanisms in sustaining adrenergic abnormalities during HFrEF is increasingly well appreciated and delineated. However, the same cannot be said for patients affected by HFpEF or HFmrEF, whom also present with autonomic dysfunction. Neural mechanisms of cardiovascular regulation act as “controller units,” detecting and adjusting for changes in arterial blood pressure, blood volume, and arterial concentrations of oxygen, carbon dioxide and pH, as well as for humoral factors eventually released after myocardial (or other tissue) ischemia. They do so on a beat-to-beat basis. The central dynamic integration of all these afferent signals ensures homeostasis, at rest and during states of physiological or pathophysiological stress. Thus, the net result of information gathered by each controller unit is transmitted by the autonomic branch using two different codes: intensity and rhythm of sympathetic discharges. The main scope of the present article is to (i) review the key neural mechanisms involved in cardiovascular regulation; (ii) discuss how their dysfunction accounts for the hyperadrenergic state present in certain forms of HF; and (iii) summarize how sympathetic efferent traffic reveal central integration among autonomic mechanisms under physiological and pathological conditions, with a special emphasis on pathophysiological characteristics of HF.

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“…The breathing frequency was guided throughout the interventions because of its considerable variations during spontaneous breathing (Kiviniemi et al 2010b). Although the breathing frequency was well maintained, it is an intervention on the cardiovascular system (Morris et al 2010), which may alter the oscillatory patterns studied here (Montano et al 2009). …”

Section: Study Limitationsmentioning

confidence: 99%

α-Adrenergic effects on low-frequency oscillations in blood pressure and R-R intervals during sympathetic activation

Kiviniemi

Frances²,

Tiinanen

et al. 2011

Experimental Physiology

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The present study was designed to address the contribution of α-adrenergic modulation to the genesis of low-frequency (LF; 0.04-0.15 Hz) oscillations in R-R interval (RRi), blood pressure (BP) and muscle sympathetic nerve activity (MSNA) during different sympathetic stimuli. Blood pressure and RRi were measured continuously in 12 healthy subjects during 5 min periods each of lower body negative pressure (LBNP; −40 mmHg), static handgrip exercise (HG; 20% of maximal force) and postexercise forearm circulatory occlusion (PECO) with and without α-adrenergic blockade by phentolamine. Muscle sympathetic nerve activity was recorded in five subjects during LBNP and in six subjects during HG and PECO. Low-frequency powers and median frequencies of BP, RRi and MSNA were calculated from power spectra. Low-frequency power during LBNP was lower with phentolamine versus without for both BP and RRi oscillations (1.6 ± 0.6 versus 1.2 ± 0.7 ln mmHg 2 , P = 0.049; and 6.9 ± 0.8 versus 5.4 ± 0.9 ln ms 2 , P = 0.001, respectively). In contrast, the LBNP with phentolamine increased the power of high-frequency oscillations (0.15-0.4 Hz) in BP and MSNA (P < 0.01 for both), which was not observed during saline infusion. Phentolamine also blunted the increases in the LBNP-induced increase in frequency of LF oscillations in BP and RRi. Phentolamine decreased the LF power of RRi during HG (P = 0.015) but induced no other changes in LF powers or frequencies during HG. Phentolamine resulted in decreased frequency of LF oscillations in RRi (P = 0.004) during PECO, and a similar tendency was observed in BP and MSNA. The power of LF oscillation in MSNA did not change during any intervention. We conclude that α-adrenergic modulation contributes to LF oscillations in BP and RRi during baroreceptor unloading (LBNP) but not during static exercise. Also, α-adrenergic modulation partly explains the shift to a higher frequency of LF oscillations during baroreceptor unloading and muscle metaboreflex activation.

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Analysis of sympathetic neural discharge in rats and humans

Cited by 26 publications

References 88 publications

Infusion of Escherichia coli Lipopolysaccharide Toxin in Rats Produces an Early and Severe Impairment of Baroreflex Function in Absence of Blood Pressure Changes

Infusion of Escherichia coli Lipopolysaccharide Toxin in Rats Produces an Early and Severe Impairment of Baroreflex Function in Absence of Blood Pressure Changes

Contribution of Autonomic Reflexes to the Hyperadrenergic State in Heart Failure

α-Adrenergic effects on low-frequency oscillations in blood pressure and R-R intervals during sympathetic activation

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