title: Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits.
abstract: 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.
authors.affiliation: Département d'Anesthésie-Réanimation, Hôpital Lariboisière, Paris, France.
authors.forename: M R
authors.initials: MR
authors.lastname: Losser
authors.forename: C
authors.initials: C
authors.lastname: Bernard
authors.forename: J L
authors.initials: JL
authors.lastname: Beaudeux
authors.forename: C
authors.initials: C
authors.lastname: Pison
authors.forename: D
authors.initials: D
authors.lastname: Payen
mesh_terms: D000818:Animals; D001427:Bacterial Toxins / Q000633:toxicity; D001786:Blood Glucose / Q000378:metabolism; D004032:Diet; D004731:Endotoxins / Q000633:toxicity; D005947:Glucose / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D019344:Lactic Acid / Q000097:blood; D008070:Lipopolysaccharides / Q000633:toxicity*; D008112:Liver Glycogen / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001427:Bacterial Toxins; D001786:Blood Glucose; D004731:Endotoxins; D008070:Lipopolysaccharides; D008112:Liver Glycogen; D014409:Tumor Necrosis Factor-alpha; C027952:salmonella toxin; D009569:Nitric Oxide; D019344:Lactic Acid; C044101:endotoxin, Escherichia coli; D005947:Glucose