Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

Wallin, B. G.; Eckberg, D. L.

doi:10.1152/ajpheart.1982.242.2.h185

Cited by 92 publications

(95 citation statements)

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“…To obtain a relative burst amplitude distribution, the amplitude of the largest burst that occurred during the analyzed period was set to 100%, and other burst amplitudes were expressed as a percentage of the maximal burst. 6,17,19,20 From the burst amplitude distribution, a median burst amplitude (the value at which 50% of the burst amplitudes were larger and 50% were smaller) was extracted and used for statistical analysis.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic Neural Burst Amplitude Distribution

et al. 2000

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Background —Human muscle sympathetic nerve activity (MSNA) is usually measured as the number of pulse-synchronous bursts in multiunit mean voltage recordings. We recently suggested burst amplitude distribution as a more sensitive indicator of altered MSNA in congestive heart failure (CHF). Here, we test whether this distribution can discriminate between different conditions with increased MSNA burst frequency and whether it reflects single vasoconstrictor fiber firing intensity. Methods and Results —We analyzed resting multiunit MSNA in 36 CHF patients (24 with mild to moderate CHF, 12 with severe CHF investigated before and after heart transplantation), 14 patients with pituitary deficiency, 25 matched healthy control subjects, and an additional 56 healthy men with a wider age range (21 to 71 years). Pituitary deficiency was associated with increased MSNA burst frequency (60 versus 37 bursts/min in control subjects), equivalent to that in mild to moderate CHF (61 bursts/min). However, burst amplitude distribution in hypopituitary patients (median burst amplitude, 37%) did not deviate from matched control subjects (36%), whereas amplitudes increased with disease severity in CHF (43% in mild to moderate, 52% in severe) and normalized after transplantation (36%). In the larger healthy group, MSNA burst frequency increased with age, and burst amplitude distribution remained unaffected. In 8 CHF patients, single-unit firing frequency showed a close positive relationship to multiunit burst amplitude distribution ( r =0.82, P <0.01) but none to burst frequency ( r =0.39, P =0.3). Conclusions —Muscle vasoconstrictor fiber activity is better reflected by multiunit MSNA burst amplitude distribution than by burst frequency, at least in CHF. This distribution can discriminate between conditions with increased burst frequency.

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Section: Discussionmentioning

confidence: 99%

Sympathetic Neural Burst Amplitude Distribution

et al. 2000

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“…6 Briefly, a sterile microelectrode was inserted into a fascicle of the peroneal nerve near the fibular head. The nerve signals were amplified, filtered (70 to 2000 Hz), rectified, and discriminated.…”

Section: Measurementsmentioning

confidence: 99%

Baroreflex Gain Predicts Blood Pressure Recovery During Simulated Ventricular Tachycardia in Humans

et al. 1999

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Background-Despite similar degrees of left ventricular dysfunction and similar tachycardia or pacing rate, blood pressure (BP) response and symptoms vary greatly among patients. Sympathetic nerve activity (SNA) increases during sustained ventricular tachycardia (VT), and the magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome. We hypothesize that the magnitude of sympathoexcitation and thus arterial baroreflex gain is an important determinant of the hemodynamic outcome of VT. Methods and Results-We evaluated the relation between arterial baroreflex sympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electrophysiological study. Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside infusion and during VP at 150 (nϭ12) or 120 (nϭ2) bpm. Arterial baroreflex gain was defined as the slope of the relationship of change in SNA to change in diastolic BP during nitroprusside infusion. Recovery of mean arterial pressure (MAP) during VP was measured as the increase in MAP from the nadir at the onset of pacing to the steady-state value during sustained VP. Arterial baroreflex gain correlated positively with recovery of MAP (rϭ0.57, Pϭ0.034). No significant correlation between ejection fraction and baroreflex gain (rϭ0.48, Pϭ0.08) or BP recovery (rϭ0.41, Pϭ0.15) was found. When patients were separated into high versus low baroreflex gain, the recovery of MAP during simulated VT was significantly greater in patients with high gain. Conclusions-These data strongly suggest that arterial baroreflex gain contributes significantly to hemodynamic stability during simulated VT. Knowledge of baroreflex gain in individual patients may help the clinician tailor therapy directed toward sustained VT. (Circulation. 1999;100:381-386.)

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“…Theoretically, however, systemic chemoreceptors could be responsible for the correlation between resting MSA and cardiac noradrenaline spillover since stimulation of such receptors have been found to increase sympathetic outflow to the heart in cats (Kollai, Koizumi & Brooks, 1978 a) and to muscle in humans (Saito, Mano, Iwase, Koga, Abe & Yamazaki, 1988;Somers, Mark, Zavala & Abboud, 1989). Although unloading of arterial baroreceptors increases sympathetic nerve traffic to the heart in cats (Green & Heffron, 1968;Kollai & Koizumi, 1979) and to muscles in humans (Wallin & Eckberg, 1982;Sanders, Mark & Ferguson, 1988) they are unlikely candidates since arterial baroreceptors are known to adapt to the prevailing blood pressure (Korner, 1989). Similarly, reflex effects from cardiopulmonary receptors are unlikely to be important since atrial distension (i.e.…”

Section: Sympathetic Activity At Restmentioning

confidence: 99%

Simultaneous measurements of cardiac noradrenaline spillover and sympathetic outflow to skeletal muscle in humans.

Wallin

Esler

Dorward

et al. 1992

The Journal of Physiology

273

193

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SUMMARY1. Muscle sympathetic nerve activity (MSA) was recorded in the peroneal nerve at the knee by microneurography in ten healthy subjects and determinations were made simultaneously of intra-arterial blood pressure, and whole-body and cardiac noradrenaline spillover to plasma. Measurements were made at rest, during isometric handgrip at 30% of maximum power and during stress induced by forced mental arithmetic.2. At rest there were significant positive correlations between spontaneous MSA (expressed as number of sympathetic bursts min-) and both spillover of noradrenaline from the heart and concentration of noradrenaline in coronary sinus venous plasma.3. Both isometric handgrip and mental arithmetic led to sustained increases of blood pressure, heart rate and MSA. Plasma concentrations of noradrenaline and spillover of noradrenaline (total body and cardiac) increased. In general the effects were more pronounced during handgrip than during stress. 4. When comparing effects during handgrip and stress the ratio between the fractional increases of MSA and cardiac noradrenaline spillover were significantly greater during handgrip.5. The data suggest (a) that there are proportional interindividual differences in the strength of resting sympathetic activity to heart and skeletal muscle which are determined by a common mechanism and (b) that handgrip and mental stress are associated with differences in balance between sympathetic outflows to heart and skeletal muscle.

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Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

Cited by 92 publications

References 0 publications

Sympathetic Neural Burst Amplitude Distribution

Sympathetic Neural Burst Amplitude Distribution

Baroreflex Gain Predicts Blood Pressure Recovery During Simulated Ventricular Tachycardia in Humans

Simultaneous measurements of cardiac noradrenaline spillover and sympathetic outflow to skeletal muscle in humans.

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