[A Case of Left Vertebral Artery Aneurysm Showing Evoked Potentials on Bilateral Electrode by the Left Vagus Nerve Stimulation to Electromyographic Tracheal Tube].

Previously, we reported a case of brainstem cavernous hemangioma showing false positive responses to electromyographic tracheal tube (EMG tube). We concluded that the cause was spontaneous respiration accompanied by vocal cord movement. We report a case of left vertebral artery aneurysm showing evoked potentials on bilateral electrodes by the left vagus nerve stimulation to EMG tube. An 82-year-old woman underwent clipping of a left unruptured vertebral artery-posterior inferior cerebellar artery aneurysm. General anesthesia was induced with remifentanil, propofol and suxamethonium, and was maintained with oxygen, air, remifentanil and propofol. We monitored somatosensory evoked potentials, motor evoked potentials, and electromyogram of the vocal cord. When the manipulation reached brainstem and the instrument touched the left vagus nerve, evoked potentials appeared on bilateral electrodes. EMG tube is equipped with two electrodes on both sides. We concluded that the left vagus nerve stimulation generated evoked potentials of the left laryngeal muscles, and they were simultaneously detected as potential difference between two electrodes on both sides. EMG tube is used to identify the vagus nerve. However, it is necessary to bear in mind that each vagus nerve stimulation inevitably generates evoked potentials on bilateral electrodes.

[A Case of Brainstem Cavernous Hemangioma Showing False Positive Response to Electromyographic Tracheal Tube].

Brainstem cavernous hemangioma is a complex lesion associated with hemorrhage and neurological deficit. The damage of the vagus nerve is a devastating surgical complication. Therefore, intraoperative anatomical and functional evaluation of this nerve is crucial. We used electromyographic tracheal tube (EMG tube)to monitor electromyogram from the vocal cord. We report a case of brainstem cavernous hemangioma showing false positive response to EMG tube. A 66-year-old woman underwent resection of cavernous hemangioma in the pontine tegmentum. General anesthesia was induced with remifentanl, propofol, and suxamethonium, and was maintained with oxygen, air, remifentanil and propofol. We monitored somatosensory evoked potentials, motor evoked potentials, and electromyogram of the vocal cord, orbicularis oculi, orbicularis oris and lateral rectus. When the manipulation reached brainstem, slight spontaneous respiration (SR) appeared on capnogram. Simultaneously, an alarm rang. Exposed nerves were stimulated electrically. However, there was no electromyographic response on the vocal cord. We concluded that the cause was SR accompanied by vocal cord movement. Remifentanil was increased up to 1 µg x kg(-1) x min(-1). SR did not disappear. Remifentanil was not increased any more without hindering the operation. Her operative course was uneventful. It is necessary to pay attention to false positive response caused by SR with EMG tube.

[Monitoring of Somatosensory Evoked Potentials during Foramen Magnum Decompression of Chiari Malformation Type I Complicated with Syringomyelia: A Report of Two Cases].

Few reports exist on anesthetic management for foramen magnum decompression (FMD) of Chiari malformation type I (CM I) complicated with syringomyelia. In two such cases we monitored somatosensory evoked potentials (SEP). Case 1 : A 40-year-old woman presented with occipital headache and nuchal pain for 2 months; numbness and muscular weakness of bilateral upper limbs for a month. Magnetic resonance imaging (MRI) scan showed CM I complicated with syringomyelia. Case 2 : A 32-year-old man presented with numbness and muscular weakness of bilateral upper limbs for 5 months; numbness and muscular weakness of lower limbs for 2 months. MRI scan showed CM I complicated with syringomyelia. They underwent FMD. In both cases, general anesthesia was induced with remifentanil, propofol and rocuronium, and was maintained with oxygen, air, remifentanil and propofol. Moreover, we monitored SEP. Their operative courses were uneventful. In case 1, SEP latency became shorter after FMD. Her preoperative neurologic symptoms disappeared on first postoperative day. In contrast there was no change of SEP latency after FMD in case 2. His preoperative neurologic symptoms showed no change on fifth postoperative day. SEP monitoring may be a useful index for prediction of early recovery of neurologic symptoms after FMD.

[Investigation of the neck swelling due to accumulation of irrigation fluid during shoulder arthroscopy in the beach-chair position].

BACKGROUND: The primary purpose of this study was to investigate the degree of neck swelling by accumulation of irrigation fluid during shoulder arthroscopy in the beach-chair position. METHODS: Twenty-one patients undergoing shoulder arthroscopy in the beach-chair position were included in this study. There were 16 male and 5 female patients, with a mean age of 58.7 +/- 16.1 years. All patients' weight and neck circumference were compared pre- and postoperatively and correlated to each other. RESULTS: There was a strong correlation between the increase rate of weight and the increase rate of neck circumference (r = 0.69, P < 0.05). CONCLUSIONS: Pre- and postoperative measurement of the neck circumference might be an easy and useful measure for prediction of postoperative airway obstruction.

[Seven cases of parathyroidectomy for secondary hyperparathyroidism using methylene blue: suggestion for the method of methylene blue infusion].

BACKGROUND: Intraoperative staining of the parathyroid glands with intravenously administered methylene blue is well described and has been demonstrated as an effective and safe method to facilitate parathyroidectomy. However, there have been several literatures of the development of postoperative neurological toxicity in patients who received methylene blue infusion during parathyroidectomy. We report the method of methylene blue infusion during parathyroidectomy at our institution. METHODS: Seven adult patients who had undergone parathyroidectomy for secondary hyperparathyroidism associated with chronic renal failure were included in this study. Methylene blue was administered at a constant rate of 4 mg x kg(-1) x hr(-1) with a 1% solution just before the start of operation. The infusion was stopped after the first parathyroid gland was identified. RESULTS: The mean dose of methylene blue used was 2.2 +/- 0.8 mg x kg(-1). Consequently, the dose of methylene blue by this method could be decreased to less than half of the previously administered dose (6 mg x kg(-1)) at our institution. CONCLUSIONS: The dose of methylene blue used should be kept to the minimum required to identify the parathyroid glands in each case.

[Monitoring of jugular venous oxygen saturation during superficial temporal artery-middle cerebral artery anastomosis under intraaortic balloon pumping: a case report].

A 77-year-old man scheduled for coronary artery bypass grafting underwent left superficial temporal artery-middle cerebral artery anastomosis (STA MCA). Before anesthesia, we planned to insert an intraaortic balloon pump as a perioperative circulatory assist. In addition, a fiberoptic catheter was inserted in the proximity of the right jugular bulb to monitor jugular venous oxygen saturation (Sjv(O2)) as an index of the balance between cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). Continuous infusion of nicorandil was started prior to induction of anesthesia. General anesthesia was induced with remifentanil, propofol and rocuronium, and was maintained with oxygen, air, remifentanil and propofol. After induction of anesthesia, blood pressure decreased from 160/70 mmHg to 100/50 mmHg. There was no abnormality of electrocardiogram. However, Sjv(O2) decreased from 58% to 40%. Ephedrine was immediately injected and continuous infusion of dopamine was started. Blood pressure increased and Sjv(O2) was improved to > 55%. Thereafter, his operative course was uneventful. Sjv(O2) is normally approximately 55-75%. If Sjv(O2) is < 50%, therapy (s) directed at increasing CBF and/or decreasing CMRO2 should be initiated. Sjv(O2) monitoring can be used to determine the minimal blood pressure that should be maintained to avoid cerebral ischemia in the case of STA-MCA.

[Investigation of the neck swelling caused by accumulation of irrigation fluid during shoulder arthroscopy in the beach-chair position: second report].

BACKGROUND: Previously, we reported that pre- and postoperative measurement of the neck circumference might be an easy and useful measure for prediction of postoperative airway obstruction in shoulder arthroscopy. However, it is suggested that airway pressure to cause a cuff leak around the tracheal tube in a cuff deflated condition (cuff leak pressure) is a predictor of postoperative airway obstruction. We studied a correlation between the neck circumference and the cuff leak pressure. METHODS: Forty patients undergoing shoulder arthroscopy in the beach-chair position were included in this study. There were 30 male and 10 female patients. All patients' neck circumference and cuff leak pressure were compared pre- and postoperatively and with each other. RESULTS: There was a strong correlation between the increase of neck circumference and the increase of cuff leak pressure. CONCLUSIONS: The rate of increase in neck circumference shows the swelling of external tissue of the neck. However, it may not reflect the swelling of the internal tissue containing pharynx, larynx and retrotracheal space. Alternatively, pre- and postoperative measurement of the cuff leak pressure could be a more substantial predictor of postoperative airway obstruction than the rate of increase in neck circumference.

Dexmedetomidine inhibits muscarinic type 3 receptors expressed in Xenopus oocytes and muscarine-induced intracellular Ca2+ elevation in cultured rat dorsal root ganglia cells.

Dexmedetomidine, an alpha(2)-adrenoceptor agonist, has been approved for clinical use, although the mechanism of dexmedetomidine action has not been fully elucidated. Several studies have shown that G protein-coupled receptors (GPCRs) are recognized as targets for anesthetics and analgesics. Therefore, it is of interest to determine whether dexmedetomidine affects the function of GPCRs other than the alpha(2)-adrenoceptor. We examined the effects of dexmedetomidine on M(1), M(3), 5-HT(2C), substance P, and orexin 1 receptors in Xenopus oocytes expressing individual receptors. In addition, we investigated the effects of dexmedetomidine on muscarinic receptor-mediated changes in [Ca(2+)](i) in the dorsal root ganglia (DRG) of 3-week-old Wister rats. Dexmedetomidine did not affect the 5-HT(2C)-, or substance P-induced Cl(-) currents and had little inhibition on the orexin A-induced current in oocytes expressing the respective receptors. The compound also had little effect on the acetylcholine (ACh, 1 microM)-induced Ca(2+)-activated Cl(-) currents in Xenopus oocytes expressing M(1) receptors. In contrast, dexmedetomidine inhibited the ACh-induced currents in Xenopus oocytes expressing M(3) receptors; 1 nM, 10 nM, 100 nM, and 1 microM dexmedetomidine reduced the current to 66.5 +/- 4.8, 51.3 +/- 12, 34.6 +/- 11, and 26.8 +/- 6.4% of the control value, respectively (EC(50) = 3.5 +/- 0.7 nM). Dexmedetomidine reduced the ACh-induced Cl(-) currents after treatment with the selective protein kinase C inhibitor GF109203X. Moreover, the compound inhibited the muscarinic receptor-mediated increases in [Ca(2+)](i) in cultured DRG cells in a concentration-dependent manner. Dexmedetomidine inhibits the function of M(3) receptors, in addition to its agonistic effects on alpha(2)-adrenoceptors, which provides further insight into the pharmacological properties of dexmedetomidine.

Effects of anesthetics on the function of orexin-1 receptors expressed in Xenopus oocytes.

Neurons in the hypothalamus containing the neuropeptide orexin have been implicated in the control of sleep and wakefulness and in the pathology of narcolepsy. In this study, we investigated the effects of volatile anesthetics, ethanol and intravenous anesthetics on orexin-A-induced Ca2+-activated Cl- currents using Xenopus oocytes expressing orexin-1 receptors (OX1Rs). The volatile anesthetics isoflurane, enflurane and halothane inhibited Cl- currents elicited by 1-micromol/l orexin-A. Ethanol and the intravenous anesthetics pentobarbital and ketamine also inhibited the action of orexin-A. The inhibitory effects of all of the compounds tested were shown to be caused by the inhibition of OX1R function. These results may, at least in part, explain their hypnotic effects.

[Anesthesia for a patient with polyarteritis nodosa who has a history of multiple drug allergies].

There has been little information about anesthesia for a patient with a history of multiple drug allergies. We gave anesthesia for a 32-year-old woman with polyarteritis nodosa and history of multiple drug allergies. She was scheduled to undergo bilateral tonsilectomy. We could not perform the preoperative screening of the drugs using a dermal test because of a high risk of anaphylactic shock. Anesthesia was induced with sevoflurane and nitrous oxide and maintained with sevoflurane, nitrous oxide, and fentanyl. The intra- and postoperative course was uneventful. It is important to inquire history of allergies adequately for preoperative recognition of allergens. General anesthesia with sevoflurane would be useful for a patient with history of multiple drug allergies.

The tramadol metabolite, O-desmethyl tramadol, inhibits 5-hydroxytryptamine type 2C receptors expressed in Xenopus Oocytes.

PURPOSE: Tramadol is widely used clinically as an analgesic, yet the mechanism by which it produces antinociception remains unclear. O-Desmethyl tramadol, the main metabolite of tramadol, is a more potent analgesic than tramadol. We reported previously that tramadol inhibits the 5-hydroxytryptamine (5-HT) type 2C receptor (5-HT(2C)R), a G-protein-coupled receptor that is expressed widely within brain and that mediates several effects of 5-HT, including nociception, feeding, and locomotion. The effects of O-desmethyl tramadol on 5-HT(2C)R have not been studied. In this study, we investigated the effect of O-desmethyl tramadol on 5-HT(2C)R expressed in Xenopus oocytes. METHODS: We examined the effect of O-desmethyl tramadol on 5-HT(2C)R using the Xenopus oocyte expression system. Furthermore, we investigated the effects of O-desmethyl tramadol on the binding of [(3)H]5-HT by 5-HT(2C)R. RESULTS: O-Desmethyl tramadol, at pharmacologically relevant concentrations, inhibited 5-HT-evoked Ca(2+)-activated Cl(-) currents in oocytes that expressed 5-HT(2C)R. The inhibitory effect of O-desmethyl tramadol on 5-HT(2C)R was overcome at higher concentrations of 5-HT. Bisindolylmaleimide I (GF109203X), a protein kinase C inhibitor, increased 5-HT-evoked currents but had little effect on the inhibition of 5-HT-evoked currents by O-desmethyl tramadol. O-Desmethyl tramadol inhibited the specific binding of [(3)H]5-HT by 5-HT(2C)R expressed in oocytes. O-Desmethyl tramadol altered the apparent dissociation constant for binding of [(3)H]5-HT by 5-HT(2C)R without changing maximum binding, which indicated competitive inhibition. CONCLUSION: These results suggest that O-desmethyl tramadol inhibits 5-HT(2C)R, which provides further insight into the pharmacological properties of tramadol and O-desmethyl tramadol.

Effects of anesthetics on mutant N-methyl-D-aspartate receptors expressed in Xenopus oocytes.

Alcohols, inhaled anesthetics, and some injectable anesthetics inhibit the function of N-methyl-d-aspartate (NMDA) receptors, but the mechanisms responsible for this inhibition are not fully understood. Recently, it was shown that ethanol inhibition of NMDA receptors was reduced by mutation of residues in the transmembrane (TM) segment 3 of the NR1 subunit (F639A) or in TM4 of the NR2A subunit (A825W), suggesting putative ethanol binding sites. We hypothesized that the actions of other anesthetics might also require these amino acids and evaluated the effects of anesthetics on the NMDA receptors expressed in Xenopus oocytes with two-electrode voltage-clamp recording. Effects of hexanol, octanol, isoflurane, halothane, chloroform, cyclopropane, 1-chloro-1,2,2-trifluorocyclobutane, and xenon were reduced or eliminated in the mutant NMDA receptors, whereas the inhibitory effects of nitrous oxide, ketamine, and benzene were not affected by these mutations. Rapid applications of glutamate and glycine by a T-tube device provided activation time constants, which suggested different properties of ketamine and isoflurane inhibition. Thus, amino acids in TM3 and TM4 are important for the actions of many anesthetics, but nitrous oxide, benzene, and ketamine seem to have distinct mechanisms for inhibition of the NMDA receptors.

[Anesthetic management of a patient in whom one-lung ventilation occurred due to an incorrectly positioned stent].

Stents are inserted for severe stenosis of the trachea owing to malignant tumors, but an incorrectly positioned stent can cause airway obstruction. Here, we report the anesthetic management of a patient undergoing removal of an incorrectly positioned stent. A 56-year-old man had a stent inserted in the trachea for stenosis caused by a tumor. One month later, he was scheduled for reinsertion of a stent for tracheal stenosis owing to growth of the tumor, but the stent was inserted in the left main bronchus interfering ventilation to the right lung. Therefore, removal of the stent under general anesthesia was scheduled. As the stent was to be removed from an incision in the cricoid, we had to maintain deep anesthesia to maintain immobility, keeping spontaneous respiration in case we could not ventilate during surgery. Since inhaled anesthetics are insufficient to maintain deep anesthesia, we anesthetized the patient with an intravenous anesthetic, sevoflurane and continuous propofol infusion. Propofol allows spontaneous respiration better than opioids. With this method we were able to anesthetize the patient maintaining spontaneous respiration and oxygenation with stable vital signs during surgery.

The effects of the tramadol metabolite O-desmethyl tramadol on muscarinic receptor-induced responses in Xenopus oocytes expressing cloned M1 or M3 receptors.

O-desmethyl tramadol is one of the main metabolites of tramadol. It has been widely used clinically and has analgesic activity. Muscarinic receptors are involved in neuronal functions in the brain and autonomic nervous system, and much attention has been paid to these receptors as targets for analgesic drugs in the central nervous system. We have reported that tramadol inhibits the function of type-1 muscarinic (M(1)) receptors and type-3 muscarinic (M(3)) receptors, suggesting that muscarinic receptors are sites of action of tramadol. However, the effects of O-desmethyl tramadol on muscarinic receptor functions have not been studied in detail. In this study, we investigated the effects of O-desmethyl tramadol on M(1) and M(3) receptors, using the Xenopus oocyte expression system. O-desmethyl tramadol (0.1-100 microM) inhibited acetylcholine (ACh)-induced currents in oocytes expressing the M(1) receptors (half-maximal inhibitory concentration [IC(50)] = 2 +/- 0.6 microM), whereas it did not suppress ACh-induced currents in oocytes expressing the M(3) receptor. Although GF109203X, a protein kinase C inhibitor, increased the ACh-induced current, it had little effect on the inhibition of ACh-induced currents by O-desmethyl tramadol in oocytes expressing M(1) receptors. The inhibitory effect of O-desmethyl tramadol on M(1) receptor was overcome when the concentration of ACh was increased (K(D) with O-desmethyl tramadol = 0.3 microM). O-desmethyl tramadol inhibited the specific binding of [(3)H]quinuclidinyl benzilate ([(3)H]QNB) to the oocytes expressed M(1) receptors (IC(50) = 10.1 +/- 0.1 microM), whereas it did not suppress the specific binding of [(3)H]QNB to the oocytes expressed M(3) receptors. Based on these results, O-desmethyl tramadol inhibits functions of M(1) receptors but has little effect on those of M(3) receptors. This study demonstrates the molecular action of O-desmethyl tramadol on the receptors and may help to explain its neural function.

Gargling with sodium azulene sulfonate reduces the postoperative sore throat after intubation of the trachea.

Postoperative sore throat (POST) is a complication that remains to be resolved in patients undergoing endotracheal intubation. In this study, we investigated whether preoperative gargling with sodium 1,4-dimethyl-7-isopropylazulene-3-sulfonate monohydrate (sodium azulene sulfonate, Azunol) reduces POST after endotracheal intubation. Forty patients scheduled for elective surgery under general anesthesia were randomized into Azunol and control groups. In the Azunol group, patients gargled with 4 mg Azunol diluted with 100 mL tap water (40 microg/mL). In the control group, patients gargled with 100 mL of tap water. After emergence from general anesthesia, the patients with POST were counted and POST was evaluated using a verbal analog pain scale. There were no significant differences between the two groups by age, height, body weight, gender distribution, or duration of anesthesia and surgery. In the control group, 13 patients (65%) complained of POST, which remained 24 h later in nine patients (45%). In the Azunol group, five patients (25%) also complained of POST, which completely disappeared by 24 h later. The incidence of POST and verbal analog pain scale scores in the Azunol group decreased significantly compared with the control group. We demonstrated that gargling with Azunol effectively attenuated POST with no adverse reactions.

The effects of the neurosteroids: pregnenolone, progesterone and dehydroepiandrosterone on muscarinic receptor-induced responses in Xenopus oocytes expressing M1 and M3 receptors.

The neurosteroids pregnenolone, progesterone, and dehydroepiandrosterone (DHEA) occur naturally in the nervous system. They act on neural tissues, participate in neuronal signaling, and are reported to alter neuronal excitability via nongenomic mechanisms. Muscarinic receptors have important roles in neuronal functions in the brain and autonomic nervous system. In this study, we investigated the effects of pregnenolone, progesterone, and DHEA on M(1) and M(3) muscarinic receptors using the Xenopus oocyte expression system. Pregnenolone and progesterone inhibited the acetylcholine (ACh)-mediated responses of M(1) and M(3) receptors expressed in Xenopus oocytes, whereas DHEA did not. The half-maximal inhibitory concentrations (IC(50)) for pregnenolone inhibition of M(1) receptor- and M(3) receptor-mediated currents were 11.4 and 6.0 microM respectively; the IC(50) values for progesterone inhibition of M(1) receptor- and M(3) receptor-mediated currents were 2.5 and 3.0 microM respectively. The selective protein kinase C (PKC) inhibitor GF109203X had little effect on the pregnenolone or progesterone inhibition of the ACh-induced currents in Xenopus oocytes expressing M(1) or M(3) receptors. The inhibitory effects of pregnenolone and progesterone were overcome at higher concentrations of ACh. Pregnenolone and progesterone inhibited the [(3)H]quinuclidinyl benzilate (QNB) binding to M(1) and M(3) receptor expressed in Xenopus oocytes, and Scatchard plot analysis of [(3)H]QNB binding revealed that pregnenolone and progesterone altered the K(d) value and the B(max), indicating noncompetitive inhibition. In conclusion, pregnenolone and progesterone inhibited M(1) and M(3) receptor functions noncompetitively by the mechanism independent of PKC and by interfering with ACh binding to the receptors.

[Complications related to anesthesia method in the University of Occupational and Environmental Health Hospital].

BACKGROUND: Complications related to anesthesia remain a problem. We studied the incidence of complications during anesthesia in 2758 patients who had undergone anesthesia in the University of Occupational and Environmental Health Hospital. METHODS: We checked the anesthesia records retrospectively and analyzed the collected data for the incidence of complications during anesthesia. RESULTS: The total incidence of complications during anesthesia was 12.2%. The incidences of complication are estimated to be 13.4% in inhalation anesthesia, 11.9% in inhalation anesthesia plus epidural, spinal or conduction block, 8.9% in CSEA, zero % in epidural anesthesia and 7.5% in spinal anesthesia. CONCLUSIONS: The incidence of complications in inhalation anesthesia was almost as same as that in inhalation anesthesia plus epidural, spinal or conduction block. More study should be necessary to prevent complications related to anesthesia.

The inhibition of aortic smooth muscle cell proliferation by the intravenous anesthetic ketamine.

Smooth muscle cell (SMC) proliferation has been recognized as central to the pathology of both major forms of vascular disease, atherosclerosis and hypertension. Recently, we reported that ketamine inhibits rat mesangial cell proliferation, suggesting that ketamine inhibits cell growth. Although the IV anesthetic ketamine has been widely used clinically, the exact effects of ketamine on vascular SMC proliferation have not been studied. In this study, we investigated the effects of ketamine on vascular SMC proliferation. Ketamine inhibited [(3)H]thymidine incorporation and decreased the number of SMCs in a concentration-dependent manner (10-200 microM); neither propofol nor fentanyl inhibited [(3)H]thymidine incorporation into human aortic SMCs. The protein kinase C (PKC) inhibitor GF109203x abolished the ketamine-induced inhibition of [(3)H]thymidine incorporation into SMC, but the inhibition was not affected by either the protein kinase A inhibitor H-89 or the protein kinase G inhibitor KT5823. A histological analysis demonstrated the inhibitory effect of ketamine on the intimal thickening of the balloon-injured rat aorta. Based on these results, ketamine inhibits SMCs at clinical concentrations via the PKC pathway. Our results indicate that ketamine might prevent the proliferation of SMCs clinically.

Analysis of the effects of halothane on Gi-coupled muscarinic M2 receptor signaling in Xenopus oocytes using a chimeric G alpha protein.

Metabotropic G protein-coupled receptors have recently been recognized as targets for anesthetics and analgesics. In particular, G(q)-coupled receptors such as muscarinic M(1) receptors (M(1)R) and 5-hydroxytryptamine (5-HT) type 2A receptors have been reported to be targets for anesthetics. Much less is known, however, about the effects of anesthetics on G(i)-coupled receptors. Here we report a method to analyze functions of G(i)-coupled receptors in Xenopus oocytes expressing a chimeric G alpha protein. A chimeric G alpha(q) protein G alpha(qi5), which contains carboxy-terminus five amino acids of G alpha(i), enables G(i)-coupled receptors to couple to Gq-coupled receptor-mediated downstream pathways such as activation of phospholipase C. We determined acetylcholine (ACh)-induced Ca(2+)-activated Cl(-) currents in Xenopus oocytes coexpressing G(i)-coupled muscarinic M(2)receptors (M(2)R) with the chimeric G alpha(qi5). Although ACh did not induce any currents in oocytes expressing M(2)R alone, it caused robust Cl(-) currents in oocytes coexpressing M(2)R with G alpha(qi5). The EC(50) of the ACh-induced Cl(-) current mediated through G alpha(qi5) was 0.2 micromol/l, which was 2.2 times higher than that of the ACh-induced G protein-activated inwardly rectifying K(+) currents activated by G beta gamma subunits liberated from endogenously expressed G alpha(i) in Xenopus oocytes. Other G(i)-coupled somatostatin type 2, 5-HT(1A) and delta-opioid receptors, when coexpressed with G alpha(qi5) in oocytes, also caused robust Ca(2+)-activated Cl(-) currents. In oocytes coexpressing M(2)R and G alpha(qi5), a volatile anesthetic halothane inhibited M(2)R-induced Cl(-) currents in a concentration-dependent manner with the IC(50) of 1.1 mmol/l, suggesting that halothane inhibits M(2)R-induced cellular responses at clinically relevant concentrations. Treatment with the protein kinase C inhibitor GF109203X produced a 3.5-fold enhancement of the initial Cl(-) currents induced by 1 micromol/l ACh in oocytes expressing M(2)R and G(qi5). The rate of halothane-induced inhibition of Cl(-) currents elicited by ACh, however, was not changed in such oocytes pretreated with GF109203X. These findings suggest that halothane inhibits the M(2)R-induced signaling by acting at sites other than PKC activity. Collectively these findings suggest that the use of oocyte expressing G alpha(qi5) would be helpful to examine the effects of anesthetics or analgesics on the function of G(i)-coupled receptors in the Xenopus oocyte expression system.