Halothane anesthesia does not suppress sympathetic activation produced by neuroglucopenia

Peter J Havel, D. E. Flatness, J. B. Halter, J. D. Best, R. C. Veith, G. J. Taborsky

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

To determine the suitability of halothane anesthesia for studies of sympathetic control of the endocrine pancreas in dogs, we assessed the effect of halothane anesthesia (0.8% inspired concentration) on the sympathetic response to central neuroglucopenia. In dogs anesthetized with halothane, intravenous administration of the neuroglucopenic agent, 2-deoxy-d-glucose (2-DG; 100 mg/kg), produced increases of both systemic plasma epinephrine (EPI; Δ = 269 ± 86 pg/ml, P < 0.025) and norepinephrine (NE; Δ = 157 ± 55 pg/ml, P < 0.025) equivalent to those previously observed in conscious dogs. Measurement of plasma NE kinetics revealed that the plasma NE response to 2-DG during halothane was due to an increase in the rate of NE appearance that was identical to that of conscious dogs, rather than to an impairment of NE clearance. In contrast, 2-DG at this dose did not increase plasma EPI or NE levels in dogs anesthetized with pentobarbital sodium (30 mg/kg). Plasma glucose increased modestly after 2-DG (100 mg/kg) in both conscious and halothane-anesthetized dogs but not in the pentobarbital-anesthetized dogs. Although 2-DG at a threefold higher dose (300 mg/kg) caused plasma EPI, NE, and glucose (Δ = 12 ± 3 mg/dl, P < 0.001) to increase in pentobarbital-anesthetized dogs, the responses to this higher dose of 2-DG were all significantly larger in halothane-anesthetized dogs (Δ of plasma glucose = 30 ± 8 mg/dl, P < 0.005; P < 0.0025 vs. pentobarbital). The catecholamine data demonstrate that halothane is a more suitable anesthetic than pentobarbital for use in experiments studying reflex neuroglucopenic activation of the sympathetic nervous system. The glucose data suggest that certain metabolic responses secondary to sympathetic activation are also preserved in halothane-anesthetized animals.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume252
Issue number5
StatePublished - 1987
Externally publishedYes

Fingerprint

Halothane
Anesthesia
Chemical activation
Dogs
Pentobarbital
Plasmas
Glucose
Neurology
Sympathetic Nervous System
Epinephrine
Catecholamines
Islets of Langerhans
Anesthetics
Intravenous Administration
Norepinephrine
Animals
Reflex
Kinetics

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Biochemistry

Cite this

Halothane anesthesia does not suppress sympathetic activation produced by neuroglucopenia. / Havel, Peter J; Flatness, D. E.; Halter, J. B.; Best, J. D.; Veith, R. C.; Taborsky, G. J.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 252, No. 5, 1987.

Research output: Contribution to journalArticle

Havel, Peter J ; Flatness, D. E. ; Halter, J. B. ; Best, J. D. ; Veith, R. C. ; Taborsky, G. J. / Halothane anesthesia does not suppress sympathetic activation produced by neuroglucopenia. In: American Journal of Physiology - Endocrinology and Metabolism. 1987 ; Vol. 252, No. 5.
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