title: Halothane and sevoflurane decrease norepinephrine-stimulated glucose transport in neonatal cardiomyocyte.
abstract: Catecholamine regulates myocardial glucose use. However, the effect of inhaled anesthetics on myocardial glucose transport stimulated by catecholamine is unclear. We studied the effect of halothane and sevoflurane on uptake of 2-deoxyglucose stimulated by norepinephrine in neonatal cardiomyocytes and the mechanism that modulates glucose transport. We studied the effects of halothane and sevoflurane on norepinephrine (NE)-stimulated glucose uptake and the effects of halothane and sevoflurane on glucose uptake stimulated by W7 (a calcium releasing agent), phorbol 12 myristate-13-acetate (a protein kinase C agonist), and LiCl. Sevoflurane decreased NE-stimulated glucose uptake from 63.7 +/- 7.0 to 41.2 +/- 3.7 pmol h(-1) mg protein(-1), and halothane also attenuated NE-stimulated glucose uptake to 37.8 +/- 5.7 pmol h(-1) mg protein(-1). W7 at 10 micromol/L increased glucose uptake from 16.4 +/- 1.4 to 41.2 +/- 3. 4 pmol h(-1) mg protein(-1). The stimulation was inhibited in the presence of 0.8 mmol/L sevoflurane and 0.58 mmol/L halothane to 23.9 +/- 3.7 and 25.6 +/- 3.6 pmol h(-1) mg protein(-1), respectively. Halothane and sevoflurane did not significantly affect the glucose uptake stimulated by 1 nmol/L insulin, 10 micromol/L PMA, or 10 mmol/L LiCl. We conclude that halothane and sevoflurane decrease NE-stimulated glucose uptake through decrease in intracellular calcium in cardiomyocytes.
  
  
  CONCLUSIONS
  The effect of inhaled anesthetics on myocardial glucose uptake during administration of catecholamine is unclear. The myocardial glucose uptake is stimulated not only by catecholamine, but also by insulin, protein kinase C, and increase of intracellular calcium. We examined the effects of halothane and sevoflurane on glucose uptake.
authors.affiliation: Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Kudoh
authors.forename: A
authors.initials: A
authors.lastname: Matsuki
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism; D003847:Deoxyglucose / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D006221:Halothane / Q000494:pharmacology*; D066298:In Vitro Techniques; D018021:Lithium Chloride / Q000494:pharmacology; D008738:Methyl Ethers / Q000494:pharmacology*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology*; D011493:Protein Kinase C / Q000378:metabolism; D051381:Rats; D000077149:Sevoflurane; D013449:Sulfonamides / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D018685:Anesthetics, Inhalation; D004791:Enzyme Inhibitors; D008738:Methyl Ethers; D013449:Sulfonamides; D000077149:Sevoflurane; C017967:W 7; D003847:Deoxyglucose; D011493:Protein Kinase C; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D018021:Lithium Chloride; D005947:Glucose; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium; D006221:Halothane; D009638:Norepinephrine