SUMMARY1. Recordings of multi-unit sympathetic activity were made from median or peroneal muscle nerve fascicles in thirty-three healthy subjects, resting in recumbent position. Simultaneous recordings of intra-arterial blood pressure were made in seventeen subjects. The neural activity, quantified by counting the number of pulse synchronous sympathetic bursts in the mean voltage neurogram (burst incidence), was plotted against the arterial blood pressure level and the age of the subjects. The effects of spontaneous temporary blood pressure fluctuations were studied by correlating different pressure parameters of individual heart beats to the probability of occurrence of a sympathetic burst and to the amplitude of the occurring burst.2. Between different subjects there were marked differences in burst incidence, from less than 10 to more than 90 bursts/100 heart beats. No correlation was found to interindividual differences in the arterial blood pressure level but there was a slight tendency for increasing burst incidence with increasing age.3. Irrespective of the magnitude of the burst incidence, the bursts always occurred more frequently during spontaneous transient blood pressure reductions than during transient increases in blood pressure. When, for each heart cycle, the occurrence of a sympathetic burst was correlated with different blood pressure parameters there was regularly a close negative correlation to diastolic pressure, a low correlation to systolic and an intermediary negative correlation to mean blood pressure. There was a positive correlation to pulse pressure and to pulse interval.4. When measured for individual heart beats, not only the occurrence but also the mean voltage amplitude of the sympathetic bursts tended to increase with decreasing diastolic pressure.5. In a given subject when comparing heart beats with the same diastolic pressure, the occurrence as well as the amplitude of the sympathetic bursts was higher for heart beats occurring during falling than for heart beats occurring during rising blood pressure. For a given change in diastolic blood pressure, sympathetic activity changed more if pressure was falling than if it was rising.6. The findings suggest that the sympathetic outflow is modulated by arterial baroreflex mechanisms and that transient variations in the strength of the activity are, to a large extent, determined by diastolic blood pressure fluctuations. The intimate correlation with 'dynamic' variations in blood pressure and the absence of correlation to the 'static' blood pressure level suggests that the sympathetic outflow 6. SUNDLJF AND B. G. WALLIN to skeletal muscles is of importance for buffering acute blood pressure changes but has little influence on the long term blood pressure level. The difference in reflex sensitivity between falling and rising pressure indicates that acute blood pressure decreases may be buffered more efficiently than acute blood pressure increases.7. In twenty-seven subjects baroreflex latency was calculated from the QRScomplexes in the e...
Patients with heart failure have increased vascular resistance and evidence for increased neurohumoral drive. High levels of circulating norepinephrine are found in patients with heart failure, but it is not known whether they reflect increased sympathetic neural activity or result from altered synthesis, release, or metabolism of norepinephrine. We used microneurography (peroneal nerve) to directly record sympathetic nerve activity to muscle (mSNA) and also measured plasma norepinephrine levels in patients with heart failure and in normal control subjects. Our goal was to determine whether sympathetic nerve activity is increased in patients with heart failure and whether plasma norepinephrine levels correlate with levels of mSNA in heart failure. Resting muscle sympathetic nerve activity in 16 patients with moderate to severe heart failure (54 + 5 bursts/min, mean + SE) was significantly higher (p < .01) than the levels of activity in either nine age-matched normal control subjects (25 ± 4 bursts/min) or 19 "young" normal control subjects (24 + 2 bursts/min). We found a significant correlation between plasma norepinephrine levels and mSNA (r = .73, p < .05). Neither mSNA nor plasma norepinephrine levels correlated with total systemic vascular resistance, cardiac index, left ventricular ejection fraction, or heart rate. However, both mSNA and plasma norepinephrine levels showed significant positive correlations (p < .05) with left ventricular filling pressures (r = .80, mSNA vs filling pressures; r = .82, norepinephrine levels vs filling pressures) and mean right atrial pressure. The results of the study provide the first direct evidence of increased central sympathetic nerve outflow in patients with heart failure and the first direct evidence that plasma norepinephrine levels show a reasonable correlation with sympathetic nerve activity to muscle in these patients. Furthermore, the data suggest that preload is an important determinant of SNA in these patients. Circulation 73, No. 5, 913-919, 1986. A HALLMARK of advanced heart failure is high peripheral vascular resistance.' Several neurohumoral factors may contribute to the increased vascular resistance, including increased activity of the renin-angiotensin system,24 elevated levels of arginine vasopressin,5 and increased activity of the sympathetic nervous
SUMMARY1. Pulse synchronous bursts of multi-unit sympathetic activity was recorded from median or peroneal muscle nerve fascicles in fourteen subjects resting in the recumbent position. The neural activity was quantitated in terms of burst incidence, i.e. the number of bursts in the mean voltage neurogram/100 heart beats, during successive rest periods of 2-4 min.2. For each individual the burst incidence was fairly constant between different rest periods but the mean burst incidence varied widely between individuals, the range being from less than 10 to more than 90 bursts/100 heart beats.3. Simultaneous double nerve recordings were made on one subject from median and peroneal nerves and on eight subjects from the two peroneal nerves. There was always close similarity between the two records in such experiments regardless of which muscles the nerve fascicles innervated. When analysed separately the difference in burst incidence between the two sides ranged from 0-7 to 5-1 bursts/100 heart beats. The findings suggest that sympathetic neurones destined to skeletal muscles are subjected to a homogenous central drive and that contributions to the activity from ganglionic or segmental sources are of lesser importance.4. On seven subjects repeated recordings at rest were made with intervals of 3 weeks-21 months between recordings. In each subject mean burst incidences were similar in all recordings (range of differences 0-5-11-2
Micro-electrode multi-unit recordings of muscle nerve sympathetic activity (MSA) involved in cardiovascular homeostasis or skin nerve sympathetic activity (SSA) involved in thermoregulation were made in the right peroneal nerve of 48 healthy volunteers during performance of the cold pressor test, i.e. immersion of one hand in ice water (2 +/- 0.5 degrees C) for 1 min. Eleven subjects underwent the same procedure on a second MSA recording occasion. As a rule, immersion evoked an increase in MSA, with a gradual decrease on emersion. The response showed a wide range of variation between and within subjects; the intra-individual difference between first and second immersion on the same recording occasion was up to sevenfold, and from first to second recording up to fivefold. The increase in MSA correlated with the degree of discomfort from the ice water. In nine subjects with a large increase in MSA on ice water immersion, intracutaneous painful electrical stimulation to a level equalling the discomfort from the ice water was added, but it was not accompanied by any change in MSA. The increase in MSA was accompanied by and correlated quite well with an increase in blood pressure. Intra-arterial blood pressure recordings showed that MSA occurred at pressure levels normally associated with total inhibition of MSA, and that an inverse linear relationship between diastolic blood pressure and MSA at rest was abolished during the ice water immersion. SSA showed no consistent change with ice water immersion. It is concluded that the cold pressor test is a powerful activator of MSA, i.e. baroreceptor-governed vasoconstrictor outflow; that MSA contributes to the blood pressure elevation with this manoeuvre; that MSA operates at another blood pressure level during the manoeuvre and that the baroreflex inhibitory level consequently is changed; and that the response is not a reaction to pain only.
1. Recordings of multi‐unit sympathetic activity were made from muscle branches of the median nerve in five healthy subjects during application of lower body negative pressure (l.b.n.p.). Simultaneous recordings of arterial blood pressure were made in four subjects. The strength of the neural activity was quantitated by counting the number of pulse synchronous sympathetic bursts and their amplitudes in the mean voltage neurogram. 2. The general appearance of the sympathetic activity in pulse synchronous bursts was similar during control periods and during l.b.n.p., but during l.b.n.p. there was always an increase in the number of sympathetic bursts and usually also in the mean voltage amplitude of the bursts. 3. The probability of occurrence of a burst was correlated to different blood pressure parameters of individual heart beats and both during control periods and during l.b.n.p. there was regularly a close negative correlation to diastolic, a low correlation to systolic, an intermediate negative correlation to mean and a positive correlation to pulse pressures. 4. The changes in arterial blood pressure during l.b.n.p. were small and in most cases statistically insignificant. The observed increases in the number of sympathetic bursts during l.b.n.p. were significantly greater than what could be expected on the basis of the blood pressure changes. 5. The findings suggest that the reflex control from the arterial baroreceptors is maintained during l.b.n.p. but, since the increase of sympathetic activity during l.b.n.p. could not be explained by a change in stimulation of the arterial baroreceptors, influence from other receptor groups (presumably intrathoracic volume receptors) must also have occurred.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.