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

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 micrograms/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 occurred 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.