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Vol. 83, Issue 5, 1566-1574, 1997
1 Laboratoire de Recherche,
Received 2 September 1996; accepted in final form 3 July 1997.
Losser, Marie-Reine, Catherine Bernard, Jean-Louis Beaudeux,
Christophe Pison, and Didier Payen. Glucose modulates hemodynamic,
metabolic, and inflammatory responses to lipopolysaccharide in rabbits.
J. Appl. Physiol. 83(5):
1566-1574, 1997.
liver blood flow; tumor necrosis factor; metabolism
Glucose is important for vascular and
immunocompetent cell functions. We hypothesized that modifications in
glucose metabolism (normal feeding, 24-h fasting, glucose loading) may
influence the hemodynamic, metabolic, and inflammatory responses to
lipopolysaccharide administration (LPS; 600 µg/kg iv) in rabbits.
Aortic (ABFV), hepatic artery (HABFV), and portal vein blood flow
velocities (PVBFV) (pulsed Doppler), plasma tumor necrosis factor (TNF)
and nitrites were measured. Fasting depleted hepatic glycogen content,
and intraportal glucose load (2 g/kg) partially restored it. LPS
induced a similar hypotension (
20%,
P < 0.05) in three groups of
animals. In fed animals, systemic vasoconstriction occured with low
ABFV and PVBFV (
40%, P < 0.05), together with lactacidemia and hyperglycemia. In fasted animals,
ABFV and PVBFV were maintained, without metabolic acidosis or
hyperglycemia. Glucose loading induced hemodynamic and metabolic
patterns comparable to those observed in fed animals, although
significantly more severe. TNF release was amplified fourfold by
glucose loading, with no impact on nitrite levels. In conclusion,
glucose metabolism interferes with hemodynamic, metabolic, and
inflammatory responses to LPS.
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society
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