Autonomic Nervous System-Controlled Cardiac Pacing: A Comparison Between Intracardiac Impedance Signal and Muscle Sympathetic Nerve Activity

Baroreceptor-heart rate reflex sensitivity is decreased in congestive heart failure. The reflex control of heart rate and sympathetic nerve activity in rats with chronic volume overload, an established model for moderate heart failure, is still unknown. Therefore, we investigated the regulation of humoral and neuronal sympathetic activity and the baroreflex control of heart rate and sympathetic nerve activity in conscious, unrestrained rats with aortocaval shunt. Rats with aortocaval shunts had larger hearts (388 ± 11 vs. 277 ± 4 mg/100 g body wt), elevated central venous pressures (14 ± 4 vs. 4 ± 3 mmHg), and higher atrial natriuretic peptide plasma levels (87 ± 16 vs. 25 ± 3 pmol/l) than controls but had similar systemic blood pressure and heart rate values. Plasma epinephrine (0.63 ± 0.16 vs. 0.21 ± 0.08 pmol/l, P < 0.05) and norepinephrine concentrations (0.27 ± 0.03 vs. 0.16 ± 0.02 pmol/l, P < 0.05) were elevated in shunted rats compared with controls. Nitroprusside-induced hypotension led to a significantly greater increase in efferent splanchnic sympathetic nerve activity in shunted rats than in controls (0.9 ± 0.1 vs. 2.6 ± 0.6 μV, P < 0.05), whereas the heart rate responses were not different between the groups. These results indicate that the regulation of the autonomic nervous system is altered in chronically volume-overloaded rats. The arterial baroreflex control of efferent splanchnic sympathetic nerve activity was dissociated from the control of heart rate. Therefore, analysis of the activation of sympathetic nervous system assessed by direct measurements of efferent sympathetic nerve activity appears to be more sensitive for the detection of altered autonomic nervous system function than the analysis of baroreflex control of heart rate.

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Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans

Journal of the American Heart Association ◽

10.1161/jaha.120.018448 ◽

2021 ◽

Author(s):

Gregory D. Rankin ◽

Mikael Kabéle ◽

Rachael Brown ◽

Vaughan G. Macefield ◽

Thomas Sandström ◽

...

Keyword(s):

Heart Rate ◽

Heart Rate Variability ◽

Nervous System ◽

Particulate Matter ◽

Autonomic Nervous System ◽

Diesel Exhaust ◽

Cardiovascular Events ◽

Sympathetic Nerve Activity ◽

Muscle Sympathetic Nerve Activity ◽

Nerve Activity

Background Diesel exhaust (DE) emissions are a major contributor to ambient air pollution and are strongly associated with cardiovascular morbidity and mortality. Exposure to traffic‐related particulate matter is linked with acute adverse cardiovascular events; however, the mechanisms are not fully understood. We examined the role of the autonomic nervous system during exposure to DE that has previously only been indirectly investigated. Methods and Results Using microneurography, we measured muscle sympathetic nerve activity (MSNA) directly in the peroneal nerve of 16 healthy individuals. MSNA, heart rate, and respiration were recorded while subjects rested breathing filtered air, filtered air with an exposure mask, and standardized diluted DE (300 µg/m 3 ) through the exposure mask. Heart rate variability was assessed from an ECG. DE inhalation rapidly causes an increase in number of MSNA bursts as well as the size of bursts within 10 minutes, peaking by 30 minutes ( P <0.001), compared with baseline filtered air with an exposure mask. No significant changes occurred in heart rate variability indices during DE exposure; however, MSNA frequency correlated negatively with total power ( r 2 =0.294, P =0.03) and low frequency ( r 2 =0.258, P =0.045). Heart rate correlated positively with MSNA frequency ( r 2 =0.268, P =0.04) and the change in percentage of larger bursts (burst amplitude, height >50% of the maximum burst) from filtered air with an exposure mask ( r 2 =0.368, P =0.013). Conclusions Our study provides direct evidence for the rapid modulation of the autonomic nervous system after exposure to DE, with an increase in MSNA. The quick increase in sympathetic outflow may explain the strong epidemiological data associating traffic‐related particulate matter to acute adverse cardiovascular events such as myocardial infarction. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02892279.

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