AJP - Endocrinology and Metabolism, Vol 252, Issue 5 E667-E672, Copyright © 1987 by American Physiological Society
Halothane anesthesia does not suppress sympathetic activation produced by neuroglucopenia
P. J. Havel, D. E. Flatness, J. B. Halter, J. D. Best, R. C. Veith and G. J. Taborsky Jr
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; delta = 269 +/- 86 pg/ml, P less than 0.025) and
norepinephrine (NE; delta = 157 +/- 55 pg/ml, P less than 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 (delta = 12 +/- 3 mg/dl, P less than 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 (delta of
plasma glucose = 30 +/- 8 mg/dl, P less than 0.005; P less than 0.0025 vs.
pentobarbital).(ABSTRACT TRUNCATED AT 250 WORDS)
