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AJP - Endocrinology and Metabolism, Vol 256, Issue 6 E714-E720, Copyright © 1989 by American Physiological Society
ARTICLES |
J. Fagius and C. Berne
Department of Neurology, University Hospital, Uppsala, Sweden.
Microelectrode recording of sympathetic signals in the peroneal nerve was performed in 14 healthy volunteers following infusion of 2-deoxy-D-glucose (50 ml/kg body wt). Heart rate, blood pressure, body temperature, hematocrit, and blood levels of glucose, insulin, and catecholamines were monitored. Muscle nerve sympathetic activity (MSA), which is involved in cardiovascular homeostasis, increased significantly from a base-line level of 19.9 +/- 4.5 (mean +/- SE) bursts/min to a peak 30 min after the start of the infusion of 33.1 +/- 5.1 bursts/min. Skin nerve sympathetic activity (SSA), which is a mixture of sudomotor and vasoconstrictor signals, also increased to a peak at 30 min. The impulse pattern of SSA suggested that the increase involved mainly sudomotor activity, with simultaneous inhibition of vasoconstrictor signals. The time courses of MSA and the circulatory responses suggested that the increase in MSA was not a baroreceptor-induced counteraction of the cardiovascular changes during glucopenia. The responses of MSA and SSA were remarkably similar to those observed previously during insulin-induced hypoglycemia. The relationship between changes of sympathetic outflow, glucose levels, and insulin levels in the present study indicates that the effects observed are consequences of central nervous system glucopenia, with insulin playing a minor role. It is concluded that the sympathoadrenal system responds in a markedly differentiated way to glucopenia.
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