Relative burst amplitude in human muscle sympathetic nerve activity: a sensitive indicator of altered sympathetic traffic
Tóm tắt
Microneurographically recorded sympathetic outflow to the human muscle vascular bed is traditionally quantified by identifying pulse-synchronous bursts of impulses in a mean voltage neurogram and expressing them in terms of bursts per minute (burst frequency) or bursts per 100 heart beats (burst incidence). As both these measures show large inter-individual differences in resting healthy subjects, a problem arises when comparing sympathetic traffic in cross-sectional studies, making moderate differences in muscle sympathetic nerve activity (MSA) between groups difficult to identify. Absolute measures of the strength of the sympathetic discharges (burst amplitude or area) can also be evaluated. However, as they critically depend on the proximity of the microelectrode to the recorded fibres, such measures cannot be used for inter-individual comparisons. The aim of the present study was to evaluate the use of relative burst amplitude spectra for quantification of MSA, describing the proportion of small vs large bursts in a neurogram. We recorded MSA in 18 patients with mild to moderate congestive heart failure (CHF) (New York Heat Association functional classes I–IIIA) and 18 matched healthy controls. Sympathetic activity was expressed as burst frequency, burst incidence and burst amplitude spectra. When comparing the traditional burst counts between the groups (presented as the median and 25th–75th percentiles) there was a tendency towards higher MSA in CHF patients, but the difference was not significant (42 (34–52) vs 53 (41–63) bursts/min, 62 (51–78) vs 69 (52–84) bursts/100 heart beats, both ns). Relative burst amplitude spectra, on the other hand, were clearly shifted to the right in the CHF group compared to the control group (median burst amplitudes 42 (34–45) vs 30 (28–35),P=0.0002). Relative burst amplitude spectra thus appear to provide a more sensitive indicator of altered MSA than traditional burst counts. The right-ward shift of these spectra may suggest that sympatho-excitation occurs early in the development of CHF.
Tài liệu tham khảo
Hagbarth KE, Vallbo ÅB. Mechanoreceptor activity recorded percutaneously with semi-microelectrodes in human peripheral nerves.Acta Physiol Scand 1968;69:121–122.
Vallbo ÅB, Hagbarth KE, Torebjörk HE, Wallin BG. Somatosensory, proprioceptive, and sympathetic activity in human peripheral nerves.Physiol Rev 1979;59:919–957.
Sundlöf G, Wallin BG. The variability of muscle sympathetic activity in resting recumbent man.J Physiol (Lond) 1977;272:383–397.
Sundlöf G, Wallin BG. Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age.J Physiol (Lond) 1978;274:621–637.
Fagius J, Wallin BG. Long-term variability and reproducibility of resting human muscle nerve sympathetic activity at rest, as reassessed after a decade.Clin Auton Res 1993;3:201–205.
Wallin BG, Kunimoto MM, Sellgren J. Possible genetic influence in the strength of human muscle nerve sympathetic activity at rest.Hypertension 1993;22:282–284.
Ng AV, Callister R, Johnson DG Seals DR. Age and gender influence muscle sympathetic nerve activity at rest in healthy humans.Hypertension 1993;21:498–503.
Spraul M, Ravussin E, Fontvielle AM, Russel R, Larson ED, Anderson EA. Reduced sympathetic nervous activity. A potential mechanism predisposing to body weight gain.J Clin Invest 1993;92:1730–1735.
Scherrer U, Randin D, Tappy L, Vollenweider P, Jéquier E, Nicod P. Body fat and sympathetic nerve activity in healthy subjects.Circulation 1994;89:2634–2640.
Lundin S, Ricksten S-E, Thorén P. Renal sympathetic activity in spontaneously hypertensive rats and normotensive controls as studied by three different methods.Acta Physiol Scand 1984;120:265–272.
Carlsson C, Skarphedinsson JO, Jenniche E, Delle M, Thorén P. Neurophysiological evidence for and characterization of the postganglionic innervation of the adrenal gland in the rat.Acta Physiol Scand 1990;140:491–499.
Wallin BG, Victor RG, Mark AL. Sympathetic outflow to resting muscles during static handgrip and postcontraction muscle ischemia.Am J Physiol 1989;256:H105-H110.
Leimbach WN, Wallin BG, Victor RG, Aylward PE, Sundlöf G, Mark AL. Direct evidence from intraneural recordings for increased central sympathetic outflow in patients with heart failure.Circulation 1986;73:913–919.
Porter TR, Eckberg DL, Fritsch JM et al. Autonomic pathophysiology in heart failure patients. sympathetic-cholinergic interrelations.J Clin Invest 1990;85:1362–1371.
Ferguson DW, Berg WJ, Roach PJ, Oren RM, Mark AL, Kempf JS. Effects of heart failure on baroreflex control of sympathetic neural activity.Am J Cardiol 1992;69:523–531.
Elam M, Casale R, La Rovere MT, Mortara A, Tavazzi L. Is sympathetic neural hyperactivity in chronic heart failure affected by heart transplantation.Eur Heart J 1993;14:521–525.
Rundqvist B, Elam M, Sverrisdottir YB, Elsenhoter G, Friberg P. Increased cardiac adrenergic drive precedes generalized sympathetic activation in early heart failure.Circulation 1997;95:169–175.
van de Borne P, Montano N, Pagani M, Oren R, Somers VK. Absence of low-frequency variability of sympathetic nerve activity in severe heart failure.Circulation 1997;95:1449–1454.
Karlsson A-K, Elam M, Lönnroth P, Sullivan L, Friberg P. Differentiated norepinephrine spillover in human skeletal muscle.Am J Physiol 1998; in press.
Eckberg DL, Rea RF, Andersson OK et al. Baroreflex modulation of sympathetic activity and sympathetic neurotransmitters in humans.Acta Physiol. Scand 1988;133:221–231.
Esler M Jennings G, Korner P Blombery P, Sacharias N, Leonard P. Measurement of total and organ-specific norepinephrine kinetics in humans.Am J Physiol 1984;247:E21-E28.