title: Hemodynamic, metabolic and hormonal responses to oral glibenclamide in patients with cirrhosis receiving glucose.
abstract: BACKGROUND
  In patients with cirrhosis, glucose may induce splanchnic and renal vasodilation. Since the antidiabetic sulfonylurea glibenclamide is known to induce splanchnic and renal vasoconstriction in portal hypertensive animals, this drug may inhibit glucose-induced hemodynamic responses in patients with cirrhosis. The aim of the present study was to investigate, in patients with cirrhosis, the short-term effects of glibenclamide on hemodynamic and humoral responses to glucose.
  
  
  METHODS
  Patients were randomly assigned to receive either glibenclamide (5-mg tablet) or a placebo. All patients received an infusion of 10% glucose (62.5 ml/h for 12 h) that was started at the same time as glibenclamide or placebo administration. Studies were performed prior to and 90 min after glibenclamide or placebo.
  
  
  RESULTS
  Glibenclamide (i.e. glibenclamide plus glucose) significantly increased plasma insulin concentrations and glycemia while placebo (i.e. glucose alone) significantly increased glycemia but did not change plasma insulin levels. Glibenclamide did not significantly change the hepatic venous pressure gradient while this value was significantly increased following glucose alone. Glibenclamide did not significantly change renal blood flow and glomerular filtration rate while glucose alone significantly increased renal blood flow without affecting the glomerular filtration rate. Glibenclamide significantly decreased cardiac index while glucose alone did not change this value.
  
  
  CONCLUSIONS
  In patients with cirrhosis receiving glucose, glibenclamide blunted glucose-induced splanchnic and renal vasodilation. In addition, glibenclamide per se induced a decrease in cardiac index. These findings should be taken into account when glibenclamide is administered to patients with cirrhosis and type 2 diabetes.
authors: Laboratoire d'Hémodynamique Splanchnique et de Biologie Vasculaire, INSERM U-481 and Hopital Beaujon, Clichy, France.
authors: R
authors: R
authors: Moreau
authors: C
authors: C
authors: Chagneau
authors: J
authors: J
authors: Heller
authors: D
authors: D
authors: Chevenne
authors: P
authors: P
authors: Langlet
authors: P
authors: P
authors: Deltenre
authors: S
authors: S
authors: Hillaire
authors: P
authors: P
authors: Lefilliatre
authors: D
authors: D
authors: Pateron
authors: P
authors: P
authors: Sogni
authors: D
authors: D
authors: Valla
authors: D
authors: D
authors: Lebrec
mesh_terms: D000284:Administration, Oral; D005260:Female; D005947:Glucose / Q000008:administration & dosage*; D005905:Glyburide / Q000008:administration & dosage*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007262:Infusions, Intravenous; D007328:Insulin / Q000378:metabolism*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008103:Liver Cirrhosis / Q000503:physiopathology*; D008111:Liver Function Tests; D008297:Male; D008875:Middle Aged; D011336:Probability; D012016:Reference Values; D012129:Respiratory Function Tests; D016896:Treatment Outcome
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D005947:Glucose; D005905:Glyburide