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Halothane and sevoflurane decrease norepinephrine-stimulated glucose transport in neonatal cardiomyocyte.

A Kudoh1, A Matsuki

  • 1Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan.

Anesthesia and Analgesia
|October 26, 2000
PubMed
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Inhaled anesthetics like halothane and sevoflurane reduce norepinephrine-stimulated myocardial glucose uptake. This occurs by decreasing intracellular calcium levels in cardiomyocytes, impacting glucose transport.

Area of Science:

  • Cardiology
  • Anesthesiology
  • Cell Physiology

Background:

  • Catecholamines regulate myocardial glucose utilization.
  • The impact of inhaled anesthetics on catecholamine-stimulated glucose transport in the heart remains unclear.

Purpose of the Study:

  • To investigate the effects of halothane and sevoflurane on norepinephrine-stimulated glucose uptake in neonatal cardiomyocytes.
  • To elucidate the underlying mechanisms, including the role of intracellular calcium.

Main Methods:

  • Neonatal cardiomyocytes were used to assess 2-deoxyglucose uptake.
  • Cells were stimulated with norepinephrine (NE), W7 (calcium agent), PMA (PKC agonist), or LiCl.
  • The influence of halothane and sevoflurane on stimulated glucose uptake was measured.

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Main Results:

  • Both halothane and sevoflurane significantly decreased NE-stimulated glucose uptake.
  • Sevoflurane reduced uptake to 41.2 pmol/h/mg protein, and halothane to 37.8 pmol/h/mg protein.
  • Anesthetics inhibited W7-stimulated glucose uptake, suggesting a role for intracellular calcium.
  • Halothane and sevoflurane did not affect glucose uptake stimulated by insulin, PMA, or LiCl.

Conclusions:

  • Halothane and sevoflurane impair norepinephrine-stimulated myocardial glucose uptake.
  • The mechanism involves a reduction in intracellular calcium concentration within cardiomyocytes.
  • These findings highlight anesthetic effects on cardiac metabolic regulation.