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Anesth Analg 2000;91:1151-1159
© 2000 International Anesthesia Research Society

PEDIATRIC ANESTHESIA

Halothane and Sevoflurane Decrease Norepinephrine-Stimulated Glucose Transport in Neonatal Cardiomyocyte

Akira Kudoh, MD, and Akitomo Matsuki, MD

Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan

Address correspondence and reprint requests to Akira Kudoh, MD, Department of Anesthesiology, University of Hirosaki School of Medicine, 5 Zaifucho, Hirosaki 036, Aomori, Japan.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
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 µmol/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 µmol/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.

Implications: 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.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Exogenous catecholamines are widely used as IV therapeutic agents to provide inotropic, chronotropic, and vasopressor support during critical illness and cardiac surgery in newborns and infants. For patients under such conditions, the myocardial glucose uptake plays an important role in cardiac function, including myocardial contractility. Myocardial glucose use is regulated by glucose transport across the plasma membrane and is stimulated by insulin (1), catecholamine (2), protein kinase C (PKC) (3), and an increase of intracellular calcium levels (4). Insulin plays an important role in glucose uptake. Insulin stimulates glucose uptake by initiating a well-characterized sequence once insulin binds to its receptors on the cell membrane. This promotes phosphorylation of the ß subunit, which in turn phosphorylates intracellular insulin receptor substrate 1 on tyrosine residues and activates phosphatidylinositol-3-kinase. This promotes the translocation of glucose transporter Type 4, which transports glucose into skeletal muscle cells (1). Catecholamine stimulates glucose uptake. Fischer et al. (5) showed that {alpha}-adrenergic agents, but not ß-adrenergic agents, stimulate glucose uptake in cardiac myocytes on independent of contraction. The glucose transport stimulated by catecholamine may be caused by pathways separated from insulin (5), but the mechanism is unclear. Catecholamine stimulates PKC and increases intracellular calcium. Because increased PKC activity (3) and the increase of intracellular calcium (4) can stimulate glucose transport in cardiomyocytes, the action of catecholamine on glucose transport may act through PKC and alteration of increases of intracellular calcium.

It has been reported that blood glucose in patients increases significantly during anesthesia (6). Because the insulin concentration does not increase in response to an increase in blood glucose during halothane anesthesia (7), glucose transport in cells may be decreased by inhaled anesthetics, contributing to increasing blood glucose levels. Reduction in peripheral glucose use in response to halothane has been suggested (7). Uptake of 2-deoxyglucose (2-DG) in skeletal muscle is less in halothane-anesthetized rats than in awake rats (8). However, the effect of inhaled anesthetics on myocardial glucose transport is unclear. Inhaled anesthetics depress positive inotropic effect by {alpha}-adrenergic stimulation and the concentration of intracellular calcium in the heart (9). In addition, the potency of inhaled anesthetics correlates with inhibition of PKC (10). These actions of inhaled anesthetics may hold the key to the modulation of glucose transport. The purpose of the present study, therefore, was to investigate whether halothane and sevoflurane affect catecholamine-stimulated glucose transport in neonatal cardiomyocytes and to identify the mechanism that modulates glucose transport.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Isolation of Cardiomyocytes from Neonatal Rat Heart
Research was conducted according to the Helsinki Declaration, and the official regulations of Japan were followed. Three-day-old neonatal rats were anesthetized with sevoflurane and killed by cervical dislocation. Using an aseptic technique, we isolated myocytes according to the method of Sadoshima et al. (11). Hearts were rapidly removed and placed in ice-cold Ca2+- and Mg2+-free phosphate-buffered saline (PBS) containing 40 units/mL sodium heparin, 4 mmol/L glucose, and 25 mmol/L HEPES. Hearts were washed with 4 L of PBS. The atria and ventricles were divided and stored in ice-cold minimal essential medium and PBS, respectively. The ventricles were minced with scissors into 1- to 3-mm3 fragments, which were then washed with PBS by gentle stirring in a 37°C water-jacketed Erlenmeyer flask for 10 min. The tissue was then enzymatically digested five times for 10 min each with 10 mL of PBS containing 0.1% trypsin, 0.1% collagenase (Type 5), 15 µg/mL deoxyribonuclease 1, and 1% chicken serum. Liberated cells were collected by centrifugation at 200g, and resuspended in PBS containing calf serum. Pooled and washed cells were plated in T-75 cell culture flasks in medium 199-supplemented medium (containing Earle’s balanced salts, 5% horse serum, 3 mmol/L pyruvic acid, 1 µg/mL insulin, 1 µg/mL transferrin, 10 ng/mL selenium, and 50 µg/mL gentamicin). Nonadherent cells were harvested after incubation at 37°C for 60 min in a humidified incubator with 5% CO2 in air. Cells were counted and resuspended in medium 199-supplemented medium containing 0.1 mmol/L 5-bromo-2'-deoxyuridine to inhibit cell division and thereby control nonmyocyte cell growth. The suspension was then placed on 0.1% gelatin-coated 25-cm2 flasks. The culture medium was changed after 48 h to the above medium and finally to serum-free medium 24 h before the cells were studied.

Determination of 2-DG Uptake
The cardiomyocytes were incubated for the last 12 h with 5 mM glucose. Two hours prior to the experiment, we added 10 mmol/L 2-DG to the glucose culture medium to decrease the basal uptake of [3H]2-DG during the subsequent assay. We assayed 2-DG uptake in medium containing 6 mmol/L KCl, 0.2 mmol/L Na2HPO4, 1.4 mmol/L MgSO2, 1 mmol/L CaCl2, 1 mmol/L NaH2PO4, and 10 mmol/L HEPES-NaOH to obtain a pH 7.4 and 2% bovine serum albumin. The tracer ([3H]2-DG, 2 µCi/mL) was added for 5 min, together with 0.2 µCi/mL [14C]glucose. The transport was stopped by the addition of 400 µL/well of ice-cold 600 mmol/L phloretin. Dishes were transferred to ice, and the monolayers were washed twice with 3 mL/well of ice-cold 200 mmol/L phloretin. 2-DG uptake was counted in a liquid scintillation counter 60 min after the addition of 1 mL/well of 0.2 mol/L NaOH. Each experiment was done in triplicate.

To evaluate whether halothane and sevoflurane modulate glucose uptake stimulated by catecholamine, activation of PKC, LiCl, and an increase of intracellular calcium, we designed studies using norepinephrine (NE), prazocin (an {alpha}1-adrenoreceptor antagonist), yohimbine (an {alpha}2-adrenoreceptor antagonist), propranolol (a ß-adrenoreceptor antagonist), phorbol 12 myristate-13-acetate (PMA) (a PKC agonist), W7 (a calcium releasing agent), LiCl, and verapamil (a calcium channel blocker). The antagonists and agonists, excluding PMA, were added to the cultures for 30 min before addition of halothane and sevoflurane. PMA was incubated in the cultures for 15 min. 0.4 and 0.8 mmol/L sevoflurane and 0.25 and 0.58 mmol/L halothane were added directly to 5 mL of medium containing 6 mmol/L, 0.2 mmol/L Na2HPO4, 1.4 mmol/L MgSO2, 1 mmol/L CaCl2, 1 mmol/L NaH2PO4, and 10 mmol/L HEPES-NaOH to obtain a pH 7.4. The flasks were immediately closed tightly to minimize vaporization of sevoflurane and halothane, and were incubated at 37°C for 10 min. Sevoflurane concentrations at 0.4 and 0.8 mmol/L correspond to 0.5 and 1 minimum alveolar concentration, respectively. Halothane concentrations at 0.25 and 0.58 mmol/L correspond to 1 and 2 minimum alveolar concentration, respectively. Before adding [3H] and [14C], the concentrations of sevoflurane and halothane were measured and confirmed by using gas chromatography. NE, prazocin, yohimbine, propranolol, PMA, W7, verapamil, trypsin, collagenase, cell culture medium, and supplements were purchased from Sigma Chemical Co. 2-Deoxy-D-[3H]glucose was purchased from Amersham (Braunschweig, Germany).

Protein Measurements
Protein was determined by the method of Bradford (12), with bovine serum albumin used as standard.

Statistical Analysis
Data were expressed as mean ± SEM. Statistical comparisons were made by analysis of variance for repeated measures and the Student-Newman-Keuls multiple comparison test. Differences in mean values were considered significant at P < 0.05.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
One, 10, and 100 µmol/L NE increased glucose uptake from 16.4 ± 1.4 of baseline to 34.6 ± 4.2, 49.5 ± 5.1, and 63.7 ± 7.0, respectively. The effect of NE was depressed by {alpha}1-adrenoreceptor antagonist with 1 µmol/L prazosin, but not with an {alpha}2-adrenoreceptor antagonist with 1 µmol/L yohimbine and a ß-blocker with 10 µmol/L propranolol. Prazosin, yohimbine, and propranolol had no significant effects on glucose uptake (Fig. 1).



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  		Figure 1. Effects of norepinephrine (NE) on glucose uptake in neonatal rat cardiomyocytes. Cardiomyocytes were incubated for 30 min in the presence of 1 µmol/L prazocin, yohimbine, and 10 µmol/L propranolol before 1, 10, and 100 µmol/L NE was added for another 30 min. [3H]2-Deoxyglucose uptake by cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar. *P < 0.05, vs. 100 µmol/L NE-induced glucose uptake. #P < 0.05, vs. basal.

 
As shown in Fig. 2, 0.4, and 0.8 mmol/L sevoflurane significantly decreased NE-stimulated glucose uptake from 63.7 ± 7.0 to 53.0 ± 3.9 and 41.2 ± 3.7 pmol h-1 mg protein-1, and 0.25 and 0.58 mmol/L halothane also significantly attenuated NE-stimulated glucose uptake to 49.7 ± 4.0 and 37.8 ± 5.7 pmol h-1 mg protein-1. Halothane or sevoflurane alone had no significant effect on glucose uptake.



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  		Figure 2. Effects of sevoflurane and halothane on norepinephrine (NE)-induced glucose uptake in neonatal rat cardiomyocytes. Cardiomyocytes were incubated for 10 min in the presence of 0.4 and 0.8 mmol/L sevoflurane and 0.25 and 0.58 mmol/L halothane before 100 µmol/L NE was added for another 30 min. [3H]2-Deoxyglucose uptake by cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar. *P < 0.05, vs. 100 µmol/L NE-induced glucose uptake.

 
Ten micromoles/liter of W7 (calcium releasing agent) significantly increased glucose uptake from 16.4 ± 1.4 to 41.2 ± 3.4 pmol h-1 mg protein-1. Stimulation was significantly inhibited in the presence of 0.8 mmol/L sevoflurane and 0.25 and 0.58 mmol/L halothane to 23.9 ± 3.7 and 25.6 ± 3.6 pmol h-1 mg protein-1, respectively (Fig. 3).



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  		Figure 3. Effects of sevoflurane and halothane on W7-induced glucose uptake in neonatal rat cardiomyocytes. Cardiomyocytes were incubated for 10 min in the presence of 0.4 and 0.8 mmol/L sevoflurane and 0.25 and 0.58 mmol/L halothane before 10 µmol/L W7 was added for another 30 min. [3H]2-Deoxyglucose uptake by cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar. *P < 0.05, vs. W7-induced glucose uptake.

 
The inhibition of glucose uptake by 0.8 mmol/L sevoflurane and 0.58 mmol/L halothane was enhanced by 100 µmol/L verapamil from 41.2 ± 3.7 to 29.7 ± 2.4 and 24.8 ± 3.7 pmol h-1 mg protein-1. Verapamil alone also significantly inhibited NE-induced glucose uptake (Fig. 4).



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  		Figure 4. Effects of verapamil on norepinephrine (NE)-induced glucose uptake in the presence and absence of halothane and sevoflurane in neonatal rat cardiomyocytes. Ten and 100 µmol/L verapamil were incubated for 30 min before exposure to halothane and sevoflurane. [3H]2-Deoxyglucose uptake by cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar. {dagger}P < 0.05, vs. NE-induced glucose uptake. *P < 0.05, vs. NE-induced glucose uptake in the presence of sevoflurane. #P < 0.05, vs. NE-induced glucose uptake in the presence of halothane.

 
We investigated whether sevoflurane and halothane affect insulin-induced glucose uptake in neonatal cardiomyocytes. In the presence of 1 nmol/L insulin, 0.4 and 0.8 mmol/L sevoflurane, and 0.25 and 0.58 mmol/L halothane did not significantly affect glucose uptake (Fig. 5).



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  		Figure 5. Effects of sevoflurane and halothane on insulin-induced glucose uptake in neonatal rat cardiomyocytes. Cardiomyocytes were incubated for 10 min in the presence of 0.4 and 0.8 mmol sevoflurane and 0.25 and 0.58 mmol halothane before 1 nmol/L insulin was added for another 30 min. [3H]2-Deoxyglucose uptake by cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar.

 
To determine whether sevoflurane and halothane inhibit glucose uptake stimulated by PMA and LiCl, we treated the cultures with 10 µmol/L PMA and 10 mmol/L LiCl. However, stimulation of glucose uptake with PMA and LiCl was not significantly suppressed by sevoflurane and halothane (Figs. 6 and 7).



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  		Figure 6. Effects of halothane and sevoflurane on phorbol 12-myristate-13-acetate (PMA)-induced glucose uptake in neonatal rat cardiomyocytes. 10 µmol/L PMA was incubated for 30 min before exposure to halothane and sevoflurane. [3H]2-Deoxyglucose uptake into cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar.

 


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  		Figure 7. Effects of halothane and sevoflurane on LiCl-induced glucose uptake in neonatal rat cardiomyocytes. 10 mmol/L LiCl was incubated for 30 min before exposure to halothane and sevoflurane. [3H]2-Deoxyglucose uptake into cardiomyocytes was measured for 5 min of incubation. Data are means ± SEM. n = 8 for each bar.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
We showed that halothane or sevoflurane alone had no effect on glucose uptake. However, these inhaled anesthetics inhibited NE-induced glucose uptake in neonatal cardiomyocytes, and the inhibition may be associated with the inhibition of {alpha}1-adrenergic receptors. {alpha}1-Adrenergic agents, but not {alpha}2- and ß-adrenergic agents stimulate glucose uptake in cardiomyocytes (5). Stimulation of glucose uptake by catecholamine occurs at a different pathway from that of insulin (5). Rattigan et al. (2) suggested that stimulation may be linked at least partially to contraction-dependent mechanisms, because the stimulation of glucose uptake by {alpha}1-adrenergic agents is dependent on the extracellular Ca2+ concentration and is decreased by Ca2+ channel blocker. On the other hand, Fischer et al. (5) proposed that the action of catecholamine on glucose uptake is not necessarily linked to the contraction-dependent action and involves a different mechanism from glucose uptake, triggered by insulin and insulinomimetic agents. Thus, the mechanism by which catecholamine regulates glucose uptake in cardiomyocytes is still incompletely understood. Inhaled anesthetics depress positive inotropic effect by {alpha}-adrenergic stimulation (9,13). Halothane and isoflurane reduce the pressor response to both {alpha}1- and {alpha}2-adrenergic receptor stimulation (13). Fairhurst and Liston (9) demonstrated that halothane decreases {alpha}-adrenergic binding by increasing membrane fluidity. In contrast, halothane and sevoflurane can potentiate the positive inotropic effects of {alpha}-adrenoceptor stimulation (14). Thus, NE-induced glucose uptake inhibited by halothane and sevoflurane appears to involve complicated mechanisms.

Contraction stimulates glucose transport in cardiac muscle. Goodyear et al. (15) demonstrated that the increase in glucose transport by contraction is independent of activation of phosphatidylinositol-3-kinase and tyrosine phosphorylation of insulin receptor substrate-1, which are intermediators of the insulin signaling pathway. Thus, cardiac muscle contraction and insulin are likely to stimulate glucose transport by separate pathways. Henriksen et al. (16) proposed that glucose transport by contraction is stimulated by phospholipase C. Phospholipase C can cause the release of inositol 1,4,5-trisphosphate and diacylglycerol which, in turn, trigger the activation of PKC and increase the intracellular Ca2+ concentration. Westfall and Sayeed (17) found that a calcium channel agonist with BAY K 86644 could increase the basal glucose transport, and that the effect could be blocked by calcium channel blockers with nifedipine and diltiazem. Youn et al. (4) also found that W7, which induces calcium release from the sarcoplasmic reticulum, caused an increase in glucose transport and that the effect was inhibited by dantrolene, which blocks calcium release from the sarcoplasmic reticulum. Our results indicate that W7-induced glucose uptake was blocked by halothane and sevoflurane. This finding suggests that halothane and sevoflurane inhibit glucose uptake through a decrease in intracellular calcium concentration. Inhaled anesthetics depress contractile function by reducing intracellular Ca2+ concentration and inhibiting sodium-calcium exchange (18). However, the contribution of inhibition of sodium-calcium exchange to anesthetic-induced depression of myocardial contractility has not been adequately defined. Alterations of intracellular Ca2+ regulation are likely to play an important role in depression of myocardial contractility. In addition, we showed that verapamil inhibited NE-induced glucose uptake. This indicates that NE-induced glucose uptake involves modulation of intracellular calcium. Thus, the decrease in NE-induced glucose uptake caused by sevoflurane and halothane appears to be associated with an alteration of intracellular calcium levels. Neonatal myocardium is more sensitive to extracellular calcium concentrations than is adult myocardium. This is associated with poorly developed sarcoplasmic reticulum of neonatal myocardium (19). In addition, neonatal cardiomyocytes are more sensitive to the negative inotropic effects of inhaled anesthetics than adult cardiomyocytes. Because inhaled anesthetics depress contractile function by reducing intracellular Ca2+ concentration, less release of calcium from sarcoplasmic reticulum appears to lead to greater depression of contraction in neonatal myocardium. Therefore, our results in neonatal cardiomyocytes may overestimate as compared with adult cardiomyocytes.

PKC plays an important role in the stimulation of glucose transport regulation. The action of insulin involves activation of PKC (3). PMA, which is a PKC agonist, stimulates glucose transport in cardiomyocytes (3), and PKC inhibitors with staurosporine inhibit the effects of insulin on glucose transport. Responses to {alpha}1-adrenergic receptor stimulation are linked to PKC (20). Thus, we studied whether the inhibition of glucose uptake by halothane and sevoflurane involves PKC. In this study, neither halothane nor sevoflurane had significant effects on PMA-induced glucose uptake. In addition, the two inhaled anesthetics did not affect insulin-induced glucose uptake. Because halothane is uncoupled from PKC in the presence of {alpha}1-adrenergic stimulation in cardiomyocytes (21), the inhibition of NE-induced glucose uptake by these anesthetics involves a pathway different from PKC.

Lithium has an insulinomimetic effect on skeletal muscle. Lithium treatment improves glucose tolerance in manic-depressive patients and in laboratory investigation (22). The effect of lithium on glucose transport in skeletal muscle may mimic the persistent effects of exercise rather than those of insulin, suggesting that a pathway different from insulin is involved in the action of lithium (22). Lithium inhibits the degeneration of inositol phosphates, which are signaling products generated by phospholipase C. However, the stimulatory effects of lithium on glucose transport may not involve phosphatidylinositol metabolism (22). In addition, lithium-induced glucose uptake is not inhibited by dantrolene. Lithium has been shown to modulate GTP-binding protein (23). GTP analogs stimulate glucose transport. Thus, it is possible that lithium acts on the glucose transport pathway via GTP-binding proteins. The present study indicated that lithium-stimulated glucose uptake was not modulated by halothane and sevoflurane. The myocardial depressant effect of halothane does not involve pertussis toxin-sensitive GTP-binding proteins (14). In addition, halothane does not involve an interaction with GTP-binding proteins in the presence of {alpha}1-adrenergic stimulation in cardiomyocytes (21). Thus, a pathway different from the action of lithium would be involved in the regulation of cardiac glucose transport by halothane and sevoflurane.

Fatty acids become the primary energy source of the heart with aging. The adult heart can use fatty acid as the sole energy substrate, whereas newborn hearts require the presence of glucose to sustain mechanical function rather than fatty acid (24). For neonatal cardiomyocytes, glucose plays a more important role as an energy source than a fatty acid. Large concentrations of fatty acid seen after cardiac surgery are associated with a decrease in glucose use (25). Glucose uptake is suppressed in the presence of fatty acid (24). In this study, fatty acid was not involved in the medium. Thus, glucose uptake in this study might be enhanced, compared with clinical conditions.

We conclude that halothane and sevoflurane probably decrease NE-stimulated glucose uptake. Inhibition is associated with a decrease in intracellular calcium levels.


   Acknowledgments
 
The authors thank Professor Dr. E. G. Erdos (Department of Pharmacology, University of Illinois College of Medicine at Chicago) and Dr. S. F. Rabito (Department of Anesthesiology and Pain Management, Cook County Hospital, Chicago) for their support of this research, and for their critical comments. We thank Dr. Elisabeth F. Lanzl for correction of English grammar and syntax.


   References
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 Methods
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 Discussion
 References
 

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Accepted for publication July 10, 2000.




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A. Kudoh, H. Katagai, and T. Takazawa
Sevoflurane Increases Glucose Transport in Skeletal Muscle Cells
Anesth. Analg., July 1, 2002; 95(1): 123 - 128.
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2000 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press