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Hideyuki Higuchi

Publications and source records attributed to Hideyuki Higuchi.

At least 19 recordsLinked to original sources
PubMed2006

Pentobarbital inhibits L-DOPA-induced dopamine increases in the rat striatum: An in vivo microdialysis study.

Pentobarbital is reported to inhibit ketamine-induced dopamine (DA) release in the rat nucleus accumbens. The accumbens is a part of the limbic dopaminergic system in the brain, and the dopaminergic neural activity of other components may also be sensitive to pentobarbital. We investigated the effect of pentobarbital administration on DA release in the striatum known as DA-rich basal ganglia, and the interaction between pentobarbital and L-DOPA, using in vivo microdialysis techniques. Male SD rats were implanted microdialysis probe into the right striatum. The probe was perfused with modified Ringer's solution and dialysate was directly injected to an HPLC. Every group of rats was consisted of six to seven animals. In the first experiment, rats were given saline, 25 and 50 mg kg(-1) pentobarbital. The second, each rat was given a local administration of 2 and 5 microg ml(-1) of L-DOPA with perfusate. Finally, other sets of rats were given 5 microg ml(-1) of L-DOPA and 25, 50, or 100 mg kg(-1) pentobarbital. Pentobarbital anaesthesia decreased the extracellular concentration of DA, and local administration of L-DOPA significantly increased DA concentration. Pretreatment with pentobarbital diminished the L-DOPA-induced DA increase. The results of the present investigation demonstrate that administration of pentobarbital might inhibit dopaminergic neural activity not only in the nucleus accumbens but also in the rat striatum. Pentobarbital anaesthesia antagonizes DA increase induced by L-DOPA and suggests the inhibition of metabolism of L-DOPA. The results of some animal experiments on dopaminergic activity under pentobarbital anaesthesia should be reconsidered.

Adjuvants, Anesthesia↗
PubMed2006

[The effect of isoflurane anesthesia on dopamine release in rat striatum with pretreatment of imipramine].

BACKGROUND: Isoflurane anesthesia has been shown to have a possibility of inducing a biphasic effect on dopamine release in rat striatum. The current study investigated the effect of isoflurane on the extracellular concentration of dopamine in the rat striatum pretreated by a classical antidepressant, imipramine, using in vivo microdialysis techniques. METHODS: After intraperitoneal administration of 5 and 10 mg x kg(-10 of imipramine, the rats were anesthetized with 1 and 2.5% isoflurane inhalation. The control group was injected saline. Isoflurane anesthesia increased the extracellular concentration of dopamine metabolites without any change in dopamine concentration. RESULTS: Under pretreatment of 5 mg x kg(-1) of imipramine, the effect of isoflurane on the change in dopamine and its metabolites was preserved. Whereas, 10 mg x kg(-1) of imipramine pretreatment induced a marked increase in the extracellular concentration of dopamine when only 1% isoflurane was applied but not with 2.5% isoflurane. In the rat administered 10 mg x kg(-1) of imipramine, anesthesia-induced increase of 3-methoxytyramine was not found. CONCLUSIONS: Our previous investigation suggested that the isoflurane anesthesia has a biphasic effect on dopamine release in rat striatum under pargyline pretreatment. The same effect was shown in the rat administered imipramine. Isoflurane anesthesia might modify dopaminergic neural activity and release of neurotransmitters through different and complex ways.

Anesthesia, Inhalation↗
PubMed2006

[The effect of halothane or sevoflurane anesthesia on the extracellular concentration of dopamine and its metabolites examined by in vivo microdialysis techniques].

BACKGROUND: Volatile anesthetics induce changes in the extracellular concentration of dopamine (DA) metabolites in the rat striatum and their metabolism might be modified in different manners by different anesthetics. Although, we have studied DA metabolism during anesthesia using in vivo microdialysis techniques, time dimensional changes were not assessed concerning the difference between anesthetics. In the current investigation, the rats were anesthetized with halothane or sevoflurane, which has different blood solubility, and investigated the effect of anesthetics and time-related development on DA metabolism. METHODS: The rats were implanted with a microdialysis probe in the striatum and perfusate was introduced to HPLC every 20 min. Anesthesia was induced with halothane or sevoflurane for 20 or 60 min, and methamphetamine 2 mg x kg(-1) was administered during or after inhalation. RESULTS: Both anesthetic agents increased the concentration of DA metabolites, and dose and time dependency was more obvious with sevoflurane than with halothane. The increase of metabolites was prolonged after halothane anesthesia (20 min), but the effect of methamphetamine administered immediately after anesthesia on DA release was not enhanced by halothane anesthesia. Sevoflurane, not halothane anesthesia, antagonized methamphetamine-induced decrease of metabolites. CONCLUSIONS: Not only the difference of blood solubility between halothane and sevoflurane and anesthetic effect of time dependency, but also another pharmacological property affects DA metabolism, including the change in the activity of dopamine transporter during inhalation of anesthetics.

Anesthetics, Inhalation↗
PubMed2005

Isoflurane anesthesia induces biphasic effect on dopamine release in the rat striatum.

The effect of isoflurane anesthesia on changes in the extracellular concentrations of dopamine (DA) and its metabolites (3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)) modulated by pargyline, monoamine oxidase inhibitor, was studied using in vivo microdialysis techniques. A microdialysis probe was implanted into the right striatum of male SD rats. Each rat (n=5-6) was given saline or the same volume of 30 or 75 mg kg(-1) pargyline intraperitoneally with or without 1 h isoflurane anesthesia (1 or 3%). Isoflurane anesthesia increased the extracellular concentration of DA in high dose (3%) and increased the metabolite concentrations in a dose-dependent manner. Pargyline administration increased the extracellular concentration of DA and 3-MT, and decreased that of other metabolites. After 30 mg kg(-1) pargyline treatment, 1% isoflurane-induced DA release and increasing of 3-MT were preserved, whereas high dose isoflurane (3%) decreased the concentration of metabolites (DOPAC and HVA), despite of the increase by low dose isoflurane (DOPAC). When 75 mg kg(-1) pargyline was administered, isoflurane anesthesia decreased the concentration of DA and DOPAC. The isoflurane-induced 3-MT increase was preserved in all experiments. Our results suggest that isoflurane anesthesia induced biphasic effect on DA regulation probably by the potentiation of DA release and the inhibition of DA synthesis. Isoflurane might modulate DA homeostasis presynaptically.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2005

Reversal of neuromuscular effects of adenosine by specific adenosine A1-receptor antagonist in live rats.

Intravenous adenosine in-vivo was shown to potentiate the effects of non-depolarizing neuromuscular blocking agents. This study aimed to determine whether adenosine A1-receptors mediated this potentiation. The authors investigated the effects of intravenous adenosine, N6-cyclopentyladenosine, specific A1-receptor agonist, and 8-cyclopentyl-1,3-dipropylxanthine, specific A1-receptor antagonist, on neuromuscular block by vecuronium, in in-vivo rat sciatic nerve-tibialis anterior preparations. In the presence of 50% steady state block by vecuronium, adenosine, and N6-cyclopentyladenosine caused similar degree of depressions of twitch tension. Twitch tension returned to its pre-injection value more rapidly when 8-cyclopentyl-1,3-dipropylxanthine was given at the maximal block than when it was allowed to recover spontaneously. It was concluded that in in-vivo adenosine potentiated the neuromuscular effects of vecuronium through adenosine A1-receptors in rats.

Adenosine↗
PubMed2005

Effects of epidural saline injection on cerebrospinal fluid volume and velocity waveform: a magnetic resonance imaging study.

BACKGROUND: The phenomenon of epidural "top-up" (increased spread of local anesthetic due to epidural fluid injection) is explained partly by an epidural volume effect. This study was designed to investigate the change in cerebrospinal fluid (CSF) volume and velocity waveform induced by epidural saline injection. METHODS: (1) Lumbar epidural catheters were placed in 28 patients. Magnetic resonance images were obtained for measurements of lumbosacral CSF volume and velocity waveform. Saline was injected into the epidural space through the catheter to three groups of randomly assigned patients: 5-ml saline (n = 10), 10-ml saline (n = 9), and 15-ml saline (n = 9) groups. A repeat image series was performed after epidural injection to compare CSF volume and velocity waveform before and after epidural injection. (2) We also examined the time course of dural sac compression after epidural saline injection in a separate series. Seven axial images at disk levels from T11-T12 to L5-S1 were obtained before injection and 1, 3, 5, 10, 15, 20, 25, and 30 min after 10-ml saline injection to compare each dural area before and after injection. RESULTS: (1) Saline injected through the epidural catheter compressed the dural sac with variability of the extent of compression, resulting in a significantly decreased CSF volume in all patients (P <== 0.001). The mean reductions in CSF volume were 2.0 +/- 1.0 ml in the 5-ml group, 4.4 +/- 1.4 in the 10-ml group, and 7.2 +/- 2.6 in the 15-ml group. There were significant differences among the three groups (P < 0.05 approximately 0.001). After the saline injection, the synchronization between the CSF velocity waveform and the cardiac cycle disappeared in significantly more patients in the 10-ml group (7 of 9 patients) than in the other groups (P < 0.05). However, there was no significant relation between measures of CSF velocity waveform and dural area in any patient. (2) The maximum reduction of the sum of the total of seven disk areas occurred 5 min after epidural saline injection; thereafter, dural compression was gradually restored but did not return to the value before injection for 30 min. CONCLUSIONS: These findings indicate that the reduction in CSF volume was injection-volume dependent, dural compression lasted at least 30 min after saline injection, and the changes of the CSF flow dynamics did not correlate with the degree of dural sac compression.

Adult↗
PubMed2005

The effect of adenosine triphosphate on vecuronium-induced neuromuscular block.

Continuous IV adenosine triphosphate administration has been used during surgery in the expectation of analgesic and vasodilative effects. Because adenosine triphosphate inhibits neuromuscular transmission, we investigated whether the neuromuscular effect of vecuronium was enhanced by IV adenosine triphosphate in 29 patients randomly given either continuous IV adenosine triphosphate 0.1 mg.kg(-1).min(-1) or 0.9% NaCl when undergoing elective minor surgery. Anesthesia was induced and maintained with propofol. Neuromuscular monitoring was recorded from the adductor pollicis muscle using electromyography with train-of-four stimulation of the ulnar nerve. Vecuronium 25, 30, or 40 microg/kg was given and lag time, onset time, and maximum block were recorded. ED50 and ED95 values for each group were derived from least squares linear regression analysis. ED50 and ED95 values were 29 microg/kg and 44 microg/kg, respectively, for the adenosine triphosphate group and 26 microg/kg and 46 microg/kg, respectively, for the controls. Differences in lag time, onset time, and neuromuscular responses between the two groups were not statistically significant. A significantly larger number of patients in the adenosine triphosphate group showed hypotension (systolic blood pressure <80 mm Hg). Our results demonstrated that adenosine triphosphate 0.1 mg.kg(-1).min(-1) did not enhance the neuromuscular block induced by vecuronium.

Adenosine Triphosphate↗
PubMed2005

The influence of lumbosacral cerebrospinal fluid volume on extent and duration of hyperbaric bupivacaine spinal anesthesia: a comparison between seated and lateral decubitus injection positions.

UNLABELLED: We designed the present study to examine the influence of lumbosacral cerebrospinal fluid (CSF) volume on the spread and duration of hyperbaric bupivacaine spinal anesthesia when the injection is made with the patient in the lateral position compared with that when the patient is in a seated position. Seventy-four patients undergoing peripheral orthopedic or urogenital surgery with spinal block were enrolled. Lumbosacral CSF volumes were calculated from axial magnetic resonance images. Patients were randomly assigned to 1 of 2 groups: the lateral (L) and seated (S) groups (n = 37 each). Spinal anesthesia (3 mL hyperbaric 0.5% bupivacaine) was administered using a 25-gauge pencil-type needle with the needle aperture directed cephalad and the patient in the lateral decubitus position with the non-operated side up (L group) or with the patient in a seated position (S group). Patients were turned supine immediately after spinal injection (L group) or after remaining seated for 2 min (S group). Statistical correlation coefficients (rho) were assessed using Spearman's rank correlation. There were negative correlations between CSF volume and peak sensory block level in both the L (rho = -0.69, P < 0.0001) and S groups (rho = -0.68, P < 0.0001). In the S group, but not in the L group, CSF volume significantly correlated with onset time of peak sensory block level (rho = -0.48, P = 0.004), and time required for regression to L1-4 (P < 0.05-0.01). We conclude that CSF volume influences the spread of spinal anesthesia with hyperbaric bupivacaine regardless of patient position when the spinal injection is made. CSF volume influenced the duration of spinal sensory anesthesia when the injection was made with the patient in a seated position, but not in the lateral position. IMPLICATIONS: Patient position during the spinal injection does not alter the influence of cerebrospinal fluid (CSF) volume on the spread of hyperbaric bupivacaine spinal anesthesia. However, CSF volume influences the duration of spinal sensory anesthesia when the injection is made with the patient in a seated position, but not in the lateral position.

Adult↗
PubMed2004

Influence of lumbosacral cerebrospinal fluid density, velocity, and volume on extent and duration of plain bupivacaine spinal anesthesia.

BACKGROUND: The current study was designed to investigate the influence of lumbosacral cerebrospinal fluid (CSF) density, velocity, and volume on the extent and duration of plain bupivacaine spinal anesthesia. METHODS: Forty-one patients scheduled to undergo orthopedic surgery with spinal block were enrolled. Lumbosacral CSF volumes were calculated from low thoracic, lumbar, and sacral axial magnetic resonance images. CSF velocity at the L3-L4 level was derived from phase-contrast magnetic resonance images. Spinal anesthesia was performed in the lateral decubitus position. CSF (2 ml) was sampled to measure CSF density before injection of 3 ml plain bupivacaine (0.5%). Statistical correlation coefficients (rho) between CSF characteristics and measurements of spinal anesthesia were assessed by Spearman rank correlation. In addition, stepwise multiple linear regression models were used to select important predictors of measures of spinal anesthesia. RESULTS: There was a significant correlation between CSF density and peak sensory block level (rho = 0.33, P = 0.034). Lumbosacral CSF volume inversely correlated with peak sensory block level (rho = -0.65, P < 0.0001) and positively correlated with onset time of complete motor block (rho = 0.42, P = 0.008). CSF volume also inversely correlated with time required for regression of the sensory block to L1 (rho = -0.35, P = 0.026) and L2 (rho = -0.33, P = 0.039). There was a significant inverse correlation between peak diastolic CSF velocity and duration of motor blockade (rho = -0.44, P = 0.005). Multiple regression analysis revealed that weight and CSF volume significantly contributed to the peak sensory block level (R2 = 0.46). CONCLUSIONS: These findings indicate that CSF density and volume influence the spread of spinal anesthesia with plain bupivacaine and that CSF volume also influences the duration of spinal anesthesia. CSF velocity might also influence the duration of plain bupivacaine spinal anesthesia.

Adult↗
PubMed2004

Factors affecting the spread and duration of epidural anesthesia with ropivacaine.

BACKGROUND: Epidural anesthesia has an unpredictable extent and duration. Differences in the surface area of the lumbosacral dura, epidural fat volume, and epidural venous plexus velocity might explain the variability in the extent and duration of epidural anesthesia with ropivacaine. METHODS: Twenty-six healthy patients, aged 18-45 y, undergoing peripheral orthopedic surgery were enrolled. Dural surface area and posterior epidural fat volume were calculated from low thoracic, lumbar, and sacral axial magnetic resonance images obtained at 8-mm increments. Epidural venous plexus velocity at the L3-L4 disk level was derived from phase-contrast magnetic resonance images. The patients received 100 mg ropivacaine (1.0%) epidurally. The spread and duration of sensory anesthesia was assessed by pinprick, and that of motor block was assessed using a modified Bromage scale. Statistical correlation coefficients (rho) between magnetic resonance imaging and epidural anesthesia measurements were assessed by Spearman rank correlation. Stepwise multiple linear regression models were used to select important predictors of measures of epidural anesthesia. RESULTS: Dural surface area correlated with peak sensory block level (rho= -0.73, P = 0.0003) and onset time of caudal and cephalad block (rho = 0.62, P = 0.002; rho = -0.63, P = 0.002). Fat volume correlated with the regression to L5-S3 (rho = -0.44.44 to -0.54, P = 0.029 to 0.007). Epidural venous plexus velocity was significantly correlated with the regression to L3 (rho = -0.42, P = 0.038) and L4 (rho = -0.48, P = 0.017). Multiple regression analysis revealed that dural surface area was a significant predictive variable for the peak sensory block level (R = 0.61, P < 0.0001). CONCLUSIONS: These findings indicate that dural surface area influences the spread of epidural anesthesia with ropivacaine and posterior fat volume influences the duration of epidural anesthesia in healthy patients within a narrow age range. Epidural venous plexus velocity might also influence the duration of epidural anesthesia with ropivacaine.

Adipose Tissue↗
PubMed2003

Temperature and humidity of the Dräger Cato anesthetic machine circuit.

PURPOSE: The Dräger Cato anesthetic machine (Dräger, Lübeck, Germany) effectively humidifies and warms anesthetic gases, because it has a built-in hotplate to heat the breathing system, and expired gas passes through the CO2 absorbent three times during one breath. In the present study, we measured the temperature and absolute humidity (AH) of the anesthetic circuit in the Dräger Cato machine with and without heat moisture exchangers (HME), and compared them with those in another anesthetic machine, the Aestiva/5 (Datex-Ohmeda, Helsinki, Finland). METHODS: Forty-eight adult patients were randomly assigned to one of eight groups according to the anesthetic machine, fresh gas flow (FGF), and the use of HME (n = 6 each): Cato 0.51 x min(-1) without HME (group 1), Cato 1.01 x min(-1) without HME (group 2), Cato 0.51 x min(-1) with HME (group 3), Cato 1.01 x min(-1) with HME (group 4), Aestiva 0.51 x min(-1) without HME (group 5), Aestiva 1.01 x min(-1) without HME (group 6), Aestiva 0.51 x min(-1) with HME (group 7), and Aestiva 1.01 x min(-1) with HME (group 8). The temperature and AH of the anesthetic gases were measured with a Moiscope (S.K.I. Net, Tokyo, Japan), which was placed between the endotracheal tube and the Y-piece of the anesthetic circuit. The HME was placed between the Moiscope and the Y-piece of the anesthetic circuit. The temperature and AH of the anesthetic gases were measured at 5, 10, and 15 min and then every 15 min up to 150 min after tracheal intubation. RESULTS: Among the groups without HME (groups 1, 2, 5, and 6), the inspired temperatures and AH in groups 1 and 2 were significantly higher than those in groups 5 and 6 at all times during the study period (P < 0.01-0.001). The inspired temperatures and AH of the groups with HME (groups 3, 4, 7, and 8), were significantly higher than those in groups 2, 5, and 6 (P < 0.01-0.001). Among the groups with HME, the AH in group 3 was significantly higher than that in group 8 until the final study period. CONCLUSION: The present study indicates that the Dräger Cato machine was more effective in warming and humidifying respiratory gas than the Aestiva/5, and that Aestiva/5 without HME does not reach the optimal temperature and humidity ranges, even if minimal flow anesthesia (0.51 x min(-1)) is performed.

Adult↗
PubMed2003

Halothane attenuated haloperidol and enhanced clozapine-induced dopamine release in the rat striatum.

The effect of halothane anesthesia on changes in the extracellular concentrations of dopamine (DA) and its metabolites (3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA)) induced by neuroleptics was studied using in vivo microdialysis techniques. Halothane attenuated haloperidol-induced dopamine release and enhanced clozapine-induced dopamine release in the rat striatum.A microdialysis probe was implanted into the right striatum of male SD rats. Rats were given saline or the same volume of 200 microg kg(-1) haloperidol (D(2) receptor antagonist), 10 mg kg(-1) sulpiride (D(2) and D(3) antagonist), or 10 mg kg(-1) clozapine (D(4) and 5-HT(2) antagonist) intraperitoneally with or without 1-h halothane anesthesia (0.5 or 1.5%). Halothane anesthesia did not change the extracellular concentration of DA, but increased the metabolite concentrations in a dose-dependent manner. The increased DA concentration induced by haloperidol was significantly attenuated by halothane anesthesia, whereas the metabolite concentrations were unaffected. Halothane had no effect on the changes in the concentrations of DA or its metabolites induced by sulpiride. The clozapine-induced increases in DA and its metabolites were enhanced by halothane anesthesia. Our results suggest that halothane anesthesia modifies the DA release modulated by antipsychotic drugs in different ways, depending on the effects of dopaminergic or serotonergic pathways.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2003

[Sudden increase in bispectral index during propofol anesthesia in three patients].

We report 3 patients who developed a sudden unpredicted increase in bispectral index (BIS) value during propofol and fentanyl anesthesia. The patients were induced with propofol 2-mg.kg-1 and fentanyl 2-micrograms.kg-1 and muscle relaxation was obtained by vecuronium 0.12-mg.kg-1. During induction of anesthesia, BIS value went down to below 50 in all three cases, and anesthesia was maintained by continuous infusion of propofol at a rate of 5 mg.kg-1.hr-1 and intermittent administration of fentanyl. Forty to sixty min after starting the operation, BIS value increased suddenly (up to 80) and the body movement of the patients was observed. The serum concentration of propofol was approximately 2.5 micrograms.ml-1. All patients were successfully treated with increasing the infusion rate of propofol and additional administration of fentanyl. No clear recall or explicit memory during operation was observed after anesthesia, but, anesthesiologists might have to pay more attention to unpredictable changes of anesthetic depth during propofol anesthesia using target controlled infusion.

Adult↗
PubMed2003

[Determination of cotinine in human urine by gas chromatograph-mass spectrometry].

A gas chromatograph-mass spectrometric assay has been developed for the quantitation of cotinine, the major metabolite of nicotine, in human urine. Extraction or condensing procedure was not required and the method reduced time involved in sample preparation. The analytes were separated on the fused-silica capillary column. The operating conditions were: injector, 250 degrees C; detector, 280 degrees C; column, 50-250 degrees C. The total gas flow-rate of helium (carrier) was 50 ml.min-1 and the pressure of column inlet was 100-200 kPa. The retention time was 18.1 min and the limit of quantitation was 5 ng.ml-1. This method provides an easy and simple assay for the detection of cotinine in clinical settings.

Adolescent↗
PubMed2002

Flumazenil reduces the hypnotic dose of propofol in male patients under spinal anesthesia.

PURPOSE: Flumazenil has been reported to produce a partial benzodiazepine-agonist-like effect in some psychopharmacological examinations. This study investigated the effect of flumazenil on the hypnotic activity of propofol in 60 men scheduled for minor surgical procedures done under spinal anesthesia. METHODS: After a steady state of spinal anesthesia had been reached, patients were pretreated with saline or flumazenil, 5 microg.kg(-1), followed by the administration of saline or midazolam, 10 microg.kg(-1). Then, 250 microg.kg(-1).min(-1) of propofol was infused until hypnosis was achieved. Loss of response to a simple command with a slight stimulus, served as the end-point for hypnosis. Immediately after achievement of the end-point, propofol infusion was discontinued, and a 2-ml venous blood sample was obtained from the dorsal pedis vein to determine plasma propofol concentration. RESULTS: Flumazenil significantly decreased the dose of propofol required and the time required to achieve hypnosis compared with values in the control group (55 +/- 10 [mean +/- SD] vs 71 +/- 14 mg and 212 +/- 42 vs 268 +/- 48 s, respectively; P < 0.05), whereas flumazenil attenuated the effect of midazolam in reducing the plasma concentration of propofol at hypnosis (2.9 +/- 0.5 and 2.5 +/- 0.6 microg.ml(-1), respectively; P < 0.05). CONCLUSION: These results suggested that flumazenil may potentiate the hypnotic properties of propofol, despite flumazenil having an antagonistic effect on the enhanced hypnotic activity of propofol induced by the coadministration of midazolam.

Journal Article↗