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Yushi U Adachi

Publications and source records attributed to Yushi U Adachi.

16 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↗
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↗
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↗
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↗
PubMed2002

Halothane enhances acetylcholine release by decreasing dopaminergic activity in rat striatal slices.

The present study investigated the effect of halothane on acetylcholine (ACh) and dopamine (DA) release from the rat striatum. Halothane decreased DA release in a concentration-dependent manner, while increased ACh release. In our previous investigation, a volatile anesthetic, halothane, inhibited DA release from the rat striatal slices in a concentration-dependent manner. Although the release of ACh from cholinergic interneurons is tonically modulated by DA in the striatum, the effect of halothane on the relationship between the release of ACh and DA has not been discussed. Using double-labeled techniques, we investigated the effect of halothane on ACh and DA release simultaneously. The slices were incubated with [14C]-choline and [3H]-DA and superfused with modified Krebs solution containing 1 microM of hemicholinium-3. We applied electrical field stimulation (2 Hz, 240 shocks), and the amount of the release of radioactivity evoked by stimulation was calculated by subtraction of the basal radioactive outflow from the total outflow at the beginning of the respective stimulation periods. The effects of drugs on the release were expressed as the ratio of stimulation-evoked fractional releases (FR), measured in the presence and absence (FRS2/FRS1) of the drug. Halothane decreased DA release in a concentration-dependent manner (FRS2/FRS1=0.767+/-0.021, 0.715+/-0.026, 0.671+/-0.014 and 0.639+/-0.033 at the concentration of 0, 0.5, 2 and 4%, respectively), while ACh release showed a biphasic change in the presence of different concentrations of halothane. The release of ACh was significantly increased at the concentration of 2%, but not at 0.5 or 4%. Halothane failed to increase the release of ACh in striatal slices after lesion by 6-OH-dopamine. The application of amphetamine reduced the release of ACh and abolished the effect of halothane. These results indicate that the effect of halothane on ACh release is indirect: it increases the release by attenuating the inhibitory effect of DA released from the nigro-striatal pathway. The nonsynaptic interaction between DA and ACh release is involved in the effect of halothane on ACh release.

Acetylcholine↗
PubMed2002

Presynaptic inhibitory effects of rocuronium and SZ1677 on [3H]acetylcholine release from the mouse hemidiaphragm preparation.

It has been shown that nondepolarizing muscle relaxants may have effects on nicotinic acetylcholine receptors (nAChRs) other than those located on the skeletal muscle: some of them possess inhibitory effects on neuronal nAChRs [Anesth. Analg. 59 (1980) 935; Trends Pharmacol. Sci. 9 (1988) 16; Pharmacol. Ther. 73 (1997) 75]. It was shown that, e.g. (+)-tubocurarine and pancuronium are able to inhibit ACh release from the axon terminals of hemidiaphragm preparations and produce tetanic fade indicating their presynaptic effect. In this study rocuronium, a nondepolarizing steroidal muscle relaxant with shorter onset of action, and SZ1677 [1-(3alpha-hydroxy-17beta-acetyloxy)-2beta-(1.4-dioxa-8-azaspiro-[4,5]-dec-8-yl)-(5alpha-androstane-16beta-yl)-1-(2-propenyl) pyrrolidinium bromide], a short-acting muscle relaxant [Ann. New York Acad. Sci. 757 (1995b) 84] inhibited the release of ACh in response to axonal stimulation, while alpha-bungarotoxin failed to reduce the stimulation evoked release of ACh and did not produce tetanic fade. These results indicate that in addition to their postsynaptic effect, rocuronium and SZ1677 have presynaptic inhibitory effects on neuronal nAChRs at the neuromuscular junction. The finding that alpha-bungarotoxin does not inhibit the release and does not produce tetanic fade indicates that it possesses affinity only for the postsynaptic muscle nAChRs.

Acetylcholine↗
PubMed2002

Fentanyl attenuates the hemodynamic response to endotracheal intubation more than the response to laryngoscopy.

UNLABELLED: We examined the effectiveness of avoiding laryngoscopy in reducing the hemodynamic responses to orotracheal intubation during the induction of anesthesia. One hundred surgical patients who required orotracheal intubation were randomly allocated into four groups. The first and third groups underwent fiberoptic intubation, in which an anesthesiologist inserted the endotracheal tube into the trachea under TV monitoring through a bronchoscope, and the second and fourth groups underwent conventional orotracheal intubation using a rigid laryngoscope. The third and fourth groups were pretreated with 2 microg/kg fentanyl IV immediately before the induction of anesthesia. Blood pressure and heart rate were measured noninvasively. A significant reduction in hemodynamic response was seen in only the group treated with fentanyl and intubated using the fiberoptic technique. Without fentanyl, there was no significant difference in hemodynamic changes between the groups. We conclude that the administration of fentanyl suppresses the hemodynamic responses to endotracheal intubation more than it does to laryngoscopy. There was no significant difference in the hemodynamic responses to orotracheal intubation by fiberscopy and laryngoscopy without fentanyl pretreatment, whereas 2 microg/kg fentanyl significantly reduced the hemodynamic responses in the group intubated by fiberscopy. IMPLICATIONS: We assessed the effectiveness of avoiding laryngoscopy for orotracheal intubation. There was no significant difference in the hemodynamic responses to orotracheal intubation by fiberscopy and laryngoscopy without fentanyl pretreatment, whereas 2 microg/kg fentanyl significantly reduced the hemodynamic responses in the group intubated by fiberscopy. Pretreatment of fentanyl and fiberoptic intubation might be recommended for avoiding hyperdynamic responses.

Adult↗