Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits

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.Glucose is important for vascular andimmunocompetent cell functions. We hypothesized that modifications inglucose metabolism (normal feeding, 24-h fasting, glucose loading) mayinfluence the hemodynamic, metabolic, and inflammatory responses tolipopolysaccharide administration (LPS; 600 µg/kg iv) in rabbits.Aortic (ABFV), hepatic artery (HABFV), and portal vein blood flowvelocities (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. LPSinduced a similar hypotension (20%,P < 0.05) in three groups ofanimals. In fed animals, systemic vasoconstriction occured with lowABFV and PVBFV (40%, P < 0.05), together with lactacidemia and hyperglycemia. In fasted animals,ABFV and PVBFV were maintained, without metabolic acidosis orhyperglycemia. Glucose loading induced hemodynamic and metabolicpatterns comparable to those observed in fed animals, althoughsignificantly more severe. TNF release was amplified fourfold byglucose loading, with no impact on nitrite levels. In conclusion,glucose metabolism interferes with hemodynamic, metabolic, andinflammatory responses to LPS.