Vol. 91, Issue 1, 130-136, July 2001
Role of nitric oxide in the regulation of glucose kinetics in
response to endotoxin in dogs
H. S.
Moeniralam1,
F.
Sprangers1,
E.
Endert1,
M. T.
Ackermans1,
J. J. B.
Van
Lanschot2,
H. P.
Sauerwein1, and
J. A.
Romijn3
1 Department of Endocrinology and Metabolism and
2 Department of Surgery, Acade-mic Medical Center, University of
Amsterdam, 1100 DD Amsterdam; and 3 Department of
Endocrinology, Leiden University Medical Center, 2300 RC Leiden,
The Netherlands
The purpose of the present in vivo study
was to determine the role of nitric oxide (NO) in the regulation of
glucose metabolism in response to endotoxin by blocking NO synthesis
with NG-monomethyl-L-arginine
(L-NMMA). In five dogs, the appearance and disappearance
rates of glucose (by infusion of
[6,6-2H2]glucose), plasma glucose
concentration, and plasma hormone concentrations were measured on five
different occasions: saline infusion, endotoxin alone (E
coli, 1.0 µg/kg iv), and endotoxin administration plus three
different doses of primed, continuous infusion of L-NMMA.
Endotoxin increased rate of appearance of glucose from 13.7 ± 1.6 to 23.6 ± 3.3 µmol · kg
1 · min1
(P < 0.05), rate of disappearance of glucose from
13.9 ± 1.1 to 24.8 ± 3.1 µmol · kg1 · min1
(P < 0.001), plasma lactate from 0.5 ± 0.1 to
1.7 ± 0.1 mmol/l (P < 0.01), and
counterregulatory hormone concentrations. L-NMMA did not
affect the rise in rate of appearance and disappearance of glucose,
plasma lactate, or the counterregulatory hormone response to endoxin.
Plasma glucose levels were not affected by endotoxin with or without
L-NMMA. In conclusion, in vivo inhibition of NO synthesis
by high doses of L-NMMA does not affect glucose metabolism in response to endotoxin, indicating that NO is not a major mediator of
glucose metabolism during endotoxemia in dogs.
NG-monomethyl-L-arginine; glucose production; hypoglycemia
