NDLI: Hyperglycemia impairs isoflurane-induced adenosine triphosphate-sensitive potassium channel activation in vascular smooth muscle cells.

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Hyperglycemia impairs isoflurane-induced adenosine triphosphate-sensitive potassium channel activation in vascular smooth muscle cells.

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Hyperglycemia impairs isoflurane-induced adenosine triphosphate-sensitive potassium channel activation in vascular smooth muscle cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kawano, Takashi Tanaka, Katsuya Mawatari, Kazuaki Oshita, Shuzo Takahashi, Akira Nakaya, Yutaka
Description	Country affiliation: Japan Author Affiliation: Kawano T ( Department of Anesthesiology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. bass@clin.med.tokushima-u.ac.jp)
Abstract	BACKGROUND: Isoflurane activates vascular adenosine triphosphate sensitive potassium (K(ATP)) channels, and may induce vasodilation. In the present study, we investigated whether hyperglycemia modifies isoflurane activation of vascular K(ATP) channel. METHODS: We used a cell-attached patch-clamp configuration to test the effects of isoflurane on K(ATP) channel activity in vascular smooth muscle cells (VSMCs) after incubation for 24 h in medium containing normal glucose (NG, 5.5 mM D-glucose), L-glucose (LG, 5.5 mM D-glucose plus 17.5 mM L-glucose), or high glucose (HG, 23 mM D-glucose). Superoxide levels in aortas were measured by the lucigenin-enhanced chemiluminescence technique. RESULTS: Isoflurane-induced open probabilities were significantly reduced in VSMCs from arteries incubated in HG (0.06 +/- 0.01) compared with NG (0.17 +/- 0.02; P < 0.05) and LG (0.15 +/- 0.02; P < 0.05). Pretreatment of VSMCs with protein kinase C (PKC) inhibitors, calphostin C and PKC inhibitor 20-28, greatly reduced HG inhibition of isoflurane-induced K(ATP) channel activity. In addition, a PKC activator, PMA, mimicked the effects of HG. Superoxide release was significantly increased in arteries incubated in HG (18.3 +/- 11.5 relative light units (RLU) x s(-1) x mg(-1); P < 0.05 versus NG). Coincubated with polyethylene glycol-superoxide dismutase (250 U/mL), a cell-permeable superoxide scavenger, greatly reduced the HG-induced increase of superoxide, but failed to reduce HG inhibition of isoflurane-induced K(ATP) channel activity. CONCLUSIONS: Our results suggest that the metabolic stress of hyperglycemia can impair isoflurane-induced vascular K(ATP) channel activity mediated by excessive activation of PKC. This could impede the coronary vasodilation response to isoflurane, causing ischemia or hypoxia in patients with perioperative hyperglycemia.
File Format	HTM / HTML
ISSN	00032999
Issue Number	3
Volume Number	106
e-ISSN	15267598
Journal	Anesthesia & Analgesia
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2008-03-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Anesthesiology Anesthetics, Inhalation Pharmacology Glucose Metabolism Hyperglycemia Isoflurane Katp Channels Agonists Muscle, Smooth, Vascular Drug Effects Myocytes, Smooth Muscle Animals Cells, Cultured Enzyme Activators Free Radical Scavengers Physiopathology Male Membrane Potentials Enzymology Naphthalenes Polyethylene Glycols Protein Kinase C Protein Kinase Inhibitors Rats Rats, Wistar Signal Transduction Superoxide Dismutase Superoxides Tetradecanoylphorbol Acetate Time Factors Vasodilation Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine

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