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Division of Gerontology and Geriatric Medicine and the Division of Metabolism and Endocrinology, University of Washington School of Medicine Seattle, Washington 98108
The Geriatric Research, Education, and Clinical Center of the Veterans Administration Medical Center Seattle, Washington 98108
Address all correspondence and requests for reprints to: Jeffrey B. Halter, M.D., Turner Clinic Building, 1010 Wall Street, Ann Arbor, Michigan 48109.
Abstract
To assess the effect of barbiturate anesthesia on sympathetic nervous system activity, plasma norepinephrine (NE) kinetics were measured in trained dogs with an indwelling right atrial catheter before and during iv administration of pentobarbital sodium (30 mg/kg, iv, plus continuous infusion at 0.1–0.2 mg/kg · min). Plasma NE levels fell by 64 ± 6% from 103 ± 22 to 42 ± 18 pg/ml (mean ± SEM; n = 6; P < 0.001) during pentobarbital anesthesia. As measured with the isotope dilution method using steady state kinetics, basal NE spillover rate into plasma was 203 ± 92 ng/min; this level fell by 91 ± 2% (P < 0.001) to 24 ± 13 ng/min during anesthesia. Clearance of NE from plasma was also impaired by the anesthesia. Before pen-tobarbital administration, the NE clearance rate from plasma was 1.7 ± 0.4 liters/min; this rate fell during anesthesia by 71 ± 6% (P < 0.001) to 0.5 ± 0.2 liters/min. During control studies in which no barbiturate was administered, there was no change i n plasma NE levels (111 ± 11 vs. 116 ± 19 pg/ml; n = 3), NE spillover rate into plasma (209 ± 56 vs. 204 ± 61 ng/min), or clearance of NE from plasma (1.8 ± 0.4 vs. 1.7 ± 0.2 liters/min). The marked suppression of the NE spillover rate into plasma during pentobarbital administration suggests that this type of anesthesia causes a profound suppression of baseline sympathetic nervous system activity in trained dogs. The observed fall of plasma NE levels underestimated the degree of suppression of sympathetic nervous activity by the anesthesia, since there was a concurrent fall in NE clearance from plasma. (Endocrinology 115: 853–857, 1984)
Footnotes
* This work was supported by NIH Grant AG-01926 and the Medical Research Service of the V.A.
Current address: Department of Endocrinology, St. Vincents Hospital, Victoria Parade, Fitzroy, Victoria, Australia 3065. Fellow of the Juvenile Diabetes Foundation.
Received September 12, 1983.
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