Biomedical subjects

Y Uchihashi

Publications and source records attributed to Y Uchihashi.

At least 37 records · Page 2Linked to original sources

PubMed1999

Excessive release of [3H]noradrenaline and glutamate in response to simulation of ischemic conditions in rat spinal cord slice preparation: effect of NMDA and AMPA receptor antagonists.

In the present study we investigated the effects of NMDA and non-NMDA glutamate receptor antagonists on the ischemia-evoked release of [3H]noradrenaline from rat spinal cord slices. An in vitro ischemia model (oxygen and glucose deprivation) was used to simulate the ischemic conditions known to cause neuronal injury. Spinal cord slices were loaded with [3H]noradrenaline and superfused with Krebs solution in a micro-organ bath. Both axonal stimulation and ischemia increased the release of [3H]noradrenaline, but the release in response to glucose and oxygen deprivation was [Ca2+]o independent. Dizocilpine (MK-801), an NMDA receptor antagonist, suppressed the release of [3H]noradrenaline produced by ischemia, while it enhanced the release of [3H]noradrenaline evoked by electrical field stimulation. In contrast, LY300168 (GYKI-53655) [(+/-)-3-N-methylcarbamyde-1-(4-aminophenyl)-4-methyl-1.8-methylen e-dioxy-5H-2.3-benzodiazepine] and its (-)isomer LY303070 (GYKI-53784) [(-)-3-N-methylcarbamyde-1-(4-aminophenyl)-4-methyl-1.8-methylene- dioxy-5H-2.3-benzodiazepine] AMPA receptor antagonists, had no effect on the release of [3H]noradrenaline evoked by either electrical stimulation or ischemia. Desipramine, a noradrenaline uptake inhibitor, potentiated the release of [3H]noradrenaline evoked by ischemia, while in the absence of [Ca2+]o but under conditions when [3H]noradrenaline release was further increased, it reduced the release. Dizocilpine also decreased glutamate and aspartate release, measured by high performance liquid chromatography, during ischemia. It is concluded that glutamate release and NMDA receptors, but not AMPA receptors, are involved in the acute effect of oxygen and glucose deprivation on the excessive release of noradrenaline and that this release is not related to physiological axonal conduction.

Animals↗

PubMed1999

[The effect of sevoflurane and isoflurane on striatal dopamine of awake freely moving rats observed in an in vivo microdialysis study].

We investigated the effect of sevoflurane and isoflurane on the level of interstitial dopamine of in vivo awake, free moving rats brain striatum using microdialysis techniques. Rats were implanted with a microdialysis probe to the right striatum of the brain and administered with 1.2 MAC of each volatile anesthetics for 1 hour, and dialysates from the probe were determined every 20 minutes. Both anesthetics reduced the amount of dopamine derived from dialysate, and increased the efflux of dopamine with pretreatment of nomifensine 10mg. kg-1 i.p. The change of metabolites of dopamine during anesthesia was increased. No significant difference was found between sevoflurane and isoflurane. We hypothesized that these anesthetics might have special actions on interactions between metabolism and re-uptake of dopamine in rats striatum during anesthesia.

Anesthetics, Inhalation↗

PubMed1999

[Urinary retention as a transient neurologic symptom after accidental total spinal anesthesia with mepivacaine hydrochloride].

We report a patient in whom urinary retention as a transient neurologic symptoms (TNS) developed after accidental total spinal anesthesia with mepivacaine hydrochloride. Mepivacaine, an amide local anesthetic, has been used for spinal anesthesia and considered one of the best for spinal anesthesia for its low incidence of TNS. However, we suggest that TNS associated with mepivacaine might not be a rare complication in spinal anesthesia.

Adult↗

PubMed1998

Na+ channel block prevents the ischemia-induced release of norepinephrine from spinal cord slices.

The principal finding of the present study with rat spinal cord slices was the novel demonstration of the [Ca2+]o-independent effect of ischemia on norepinephrine release and its antagonism by tetrodotoxin and low temperature (10 degrees C). Our finding that tetrodotoxin antagonized the effects of glucose deprivation on norepinephrine release in a [Ca2+]o-independent way suggests that Na+ channel block alone, i.e., the prevention of Na+ accumulation, may account for the protective action. Low temperature completely prevented the effect of ischemia on norepinephrine release but did not change the release associated with axonal activity. This finding is in good agreement with the observation that small changes in brain temperature critically determine the extent of neuronal injury from ischemia and suggests that both [Ca2+]o-independent release and cell injury are associated with the norepinephrine membrane carrier. It is suggested, therefore, that drugs able to attenuate the increase in [Na+]i during ischemia may be useful agents to protect against ischemic damage if given before the insult.

4-Aminopyridine↗

PubMed1998

[The effects of low-doses of fentanyl, buprenorphine and pentazocine on circulatory responses to endotracheal intubation].

This study evaluates the effects of low-doses i.v. fentanyl, buprenorphine and pentazocine on circulatory responses of endotracheal intubation in 70 scheduled surgical patients. Patients were allocated to 5 groups randomly and 2 (n = 11) or 4 (n = 13) micrograms.kg-1 of fentanyl, 0.5 mg.kg-1 of pentazocine (n = 13), 5 micrograms.kg-1 of buprenorphine (n = 10) and saline as a control (n = 23) were administered 5 minutes before the administration of thiopental, respectively. Then, patients were intubated with 0.1 mg.kg-1 of vecuronium. Blood pressure and heart rate were recorded. Only 4 micrograms.kg-1 of fentanyl diminished circulatory responses of systolic blood pressure on the stimuli of endotracheal intubation.

Adjuvants, Anesthesia↗

PubMed1996

Age-dependent induction and maintenance of sensitization to methamphetamine-induced hyperactivity in mice.

Repeated administrations of methamphetamine (2 mg/kg, s.c.), 10 times at 3-day intervals, induced ambulatory sensitization in all groups of mice that were 13-, 15-, 19-, 23- and 36-week-old at the start of methamphetamine administration. The most prominent sensitization was observed in the 19-week-old mice. Among five groups of mice, even though the mice of 36 weeks old showed the highest sensitivity to methamphetamine at the first administration, they exhibited the lowest sensitization during the latter stage of repeated methamphetamine administration. Methamphetamine sensitization once established was well reproduced by the post-sensitization period of 8 weeks. Furthermore, the group of mice given methamphetamine with post-sensitization interval of 8 weeks (19-week-old mice) exhibited further enhancement of the sensitization. In contrast, the groups of mice given methamphetamine with post-sensitization intervals of 12 and 25 weeks (the 23- and 36-week-old, respectively) showed a significant reduced sensitization, and the latter group failed to reach the level of sensitization previously established. These results suggest that the induction of and maintenance of methamphetamine sensitization are dependent on the age of the mice, and that methamphetamine sensitization once established completely persists for up to 8 weeks.

Age Factors↗

PubMed1996

Differential effects of morphine-6-glucuronide, an active metabolite of morphine, and morphine on locomotor activity in mice: involvement of the opioid receptor.

Subcutaneous administration of morphine (2.5 to 20 mg/kg) or an active metabolite of morphine, morphine-6-glucuronide (2.5 to 20 mg/kg), increased the locomotor activity of mice in a dose-dependent manner. Fifteen mg/kg of morphine and 20 mg/kg of morphine-6-glucuronide were almost equipotent. Subcutaneous administration of the universal opioid antagonist, naloxone, but not the delta-selective antagonist, naltrindole, significantly suppressed the hyperlocomotion induced by morphine (15 mg kg). On the other hand the subcutaneous administration of relatively higher doses of naloxone or naltrindole significantly reduced the hyperlocomotion induced by morphine-6-glucuronide (20 mg/kg). These findings suggest that agonistic actions at the opioid receptors, especially at the delta- and mu-receptors, contribute to the morphine-6-glucuronide-induced hyperlocomotion.

Animals↗

PubMed1996

[Rhabdomyolysis induced by succinylcholine chloride and sevoflurane in an elderly man].

An 81-year-old man was scheduled for cervical lymph node biopsy. His laboratory data were within normal ranges. After induction of anesthesia with thiopental 175 mg and succinylcholine chloride (SCC) 40 mg, moderate masseter spasm was observed. Anesthesia was maintained with nitrous oxide, oxygen and sevoflurane. After the operation he had severe muscle pain and CK was elevated up to 81,400IU.l-1. The body temperature was not elevated above 37.2 degrees C during and after the operation. The skinned fiber examination, performed one month later, showed his calcium-induced-calcium-release (CICR) to be within normal ranges. We diagnosed him as rhabdomyolysis induced by coadministration of SCC and sevoflurane, especially SCC. We concluded that even in an elderly man, SCC should be administered cautiously.

Aged↗

PubMed1995

Repeated ketamine administration produces up-regulation of muscarinic acetylcholine receptors in the forebrain, and reduces behavioral sensitivity to scopolamine in mice.

To study the effects of repeated ketamine administration on central muscarinic acetylcholine receptors (mAchRs), ddY male mice were administered subcutaneous doses of 25 mg/kg ketamine every 3 days for a total of five times. Receptor binding assays of mAchR were carried out in the forebrain (FB), cerebellum (CB) and brainstem (BS), using [3H]quinuclidinyl benzilate ([3H]QNB) as a ligand. In addition, we examined whether repeated ketamine (12.5, 25 and 50 mg/kg) or saline (five times) could modify the hyperlocomotion induced by scopolamine (0.5 mg/kg, SC) (a muscarinic antagonist), using a behavior-pharmacological technique. Repeating the ketamine administration resulted in a significant increase in the receptor density value (Bmax) for [3H]QNB only in FB, dependent on the numbers of administrations (1270 +/- 33 fmol/mg protein for a single dose, 1620 +/- 59 for four treatments, 1738 +/- 70 for five treatments without any change in apparent affinity (defined as the reciprocal of the dissociation constant) (Kd). A competitive inhibition study of repeated (5 times) administration of ketamine failed to detect any subtype-specific changes in mAchRs. Repeated ketamine administration reduced the scopolamine-induced hyperlocomotion in a dose-related way, and the changes were significant at 50 mg/kg. Our results suggest that repeated ketamine administration produces an up-regulation of mAchRs, and this change may be associated with altered Ach transmission in the central nervous system.

Animals↗

PubMed1995

Delayed effects of ethanol, caffeine and nicotine assessed by wheel-running and drinking in mice.

Effects of ethanol, caffeine and nicotine, pleasurable substances, on wheel-running and drinking in mice that were housed under a 12 : 12-hr light-dark schedule (lighting period ; 6 : 00-18 : 00) were investigated. All drug administrations were carried out at 11: 00, a mid-light period. Although ethanol (0.8-2.4 g/kg p.o.) scarcely changed both the wheel-running and drinking during the light period, it was followed by a strong suppression of both behaviors during the coming dark period (18 : 00-6 : 00). The same treatment with caffeine (1-10 mg/kg s.c.) produced significant increase in the drinking during the light period, but suppression of the wheel-running during the dark period. Nicotine (0.1-1 mg/kg s.c.) significantly suppressed the wheel-running, but not drinking, during the dark period. The coadministration of nicotine (0.1-1 mg/kg) with ethanol (2.4 g/kg) reduced the behavioral suppression during the dark period. Whereas nicotine (0.1-1 mg/kg) reduced the increased drinking during light period by caffeine (10 mg/kg), but enhanced the caffeine-induced behavioral suppression during the dark period. These results indicate that the administration of pleasurable substances in the mid-light period results in a delayed effect which is characterized by a suppression of either and/or both wheel-running and drinking during the coming dark period starting 7 hr after the administration, and that nicotine acts to antagonize the effect of ethanol, but contrally to enhance the effect of caffeine.

Animals↗

PubMed1995

[Anesthetic management of a patient with microcephaly associated with cerebral atrophy].

We describe the management of a 35-year-old female with microcephaly, cerebral atrophy especially in frontal lobes, dwarfism and severe mental retardation. The patient underwent open reduction of fracture of the humerus neck suffered from traffic accident. Authors could not find any article on the anesthetic management of microcephaly but could locate some about mentally retarded patients claiming the difficulty in anesthetic induction as well as emergence and frequent incidence of convulsions. We anesthetized the patient with modified NLA with nitrous oxide-oxygen and interestingly very small doses of fentanyl (1.7 micrograms.kg-1) were required. The anesthetic and surgical courses were uneventful. The patient emerged immediately with intravenously administered naloxone and flumazenil with no excitement nor convulsion. We conclude that fentanyl is the drug of choice for mentally retarded patient with microcephaly and smaller doses per kg.weight are sufficient for orthopedic surgery.

Adult↗

PubMed1995

Evaluation of acute and sub-acute effects of cocaine by means of circadian variation in wheel-running and drinking in mice.

The effects of cocaine on wheel-running and drinking activities in mice, housed under a 12-h light-dark schedule (lighted period; 6:00-18:00 h), were investigated through long continuous observation. Cocaine (20 and 40 mg/kg, sc), administered at 11:00 h, acutely increased wheel-running and drinking, but it was followed by a sub-acute suppression of the spontaneous increment in both of these behaviors during the coming dark period (18:00-6:00 h). Such behavioral accelerating and suppressing effects of cocaine did not change throughout the whole course of administration, which was repeated five times at 3- to 5-day intervals. In addition to these findings, wheel-running and drinking spontaneously increased during the light period and decreased during the dark period on the day after the drug administration. On the other hand, the repeated administration of cocaine at 18:00 h never increased, but rather acutely suppressed both behaviors during the dark period, and no trends in the behavioral changes on the next day were clearly shown. These results suggest that the effects of cocaine on wheel-running and drinking differ depending on the time of day of the administration.

Animals↗

PubMed1995

[Effects of systemic lidocaine, mepivacaine and bupivacaine on passive avoidance learning in mice].

The effects of local anesthetics on learning were assessed in mice through one trial step-through passive avoidance performance. Lidocaine HCl (10, 20 or 40 mg.kg-1), mepivacaine HCl (15, 30 or 60 mg.kg-1) or bupivacaine HCl (2.5, 5 or 10 mg.kg-1) were injected subcutaneously 10 min before acquisition training. Lidocaine, but not mepivacaine and bupivacaine, reduced the latency in the retention trial conducted 24hr after the training in a dose-dependent manner. However, lidocaine did not alter the latency when it was given 10 min before the retention trial. These results suggest that lidocaine impairs acquisition, but not retention or retrieval phase in the memory process.

Anesthetics, Local↗

PubMed1994

The disruptive effects of ketamine on passive avoidance learning in mice: involvement of dopaminergic mechanism.

The involvement of dopaminergic mechanisms in ketamine-induced disruption of one trial step-through passive avoidance performance was assessed through the coadministration with the dopamine D1 antagonist SCH 23390, the dopamine D2 antagonist YM-091512 and the dopamine autoreceptor agonist at low doses, apomorphine, in mice. Pretraining (10 min before) administration of ketamine (0; saline, 2.5, 5 and 10 mg/kg SC) dose-dependently reduced the latency in the retention trial conducted 24 h after the training. However, ketamine did not affect the retention latency when administered immediately after the training or prior to retention. YM-09151-2 (0.01 and 0.03 mg/kg SC) and apomorphine (0.01 and 0.03 mg/kg SC), but not SCH 23390 (0.01 and 0.03 mg/kg SC), ameliorated the impaired reduction by ketamine (10 mg/kg) in a dose-dependent manner. These results suggest that ketamine obstructs the acquisition of the passive avoidance task, and that this effect is induced by stimulation of dopamine D2 receptors through dopamine release from the presynaptic terminals.

Animals↗

PubMed1994

Effects of dopamine antagonism on methamphetamine sensitization: evaluation by ambulatory activity in mice.

SCH 23390 (SCH: 0.001-0.03 mg/kg SC) and YM-09151-2 (YM: 0.001-0.03 mg/kg SC), the selective dopamine D1 and D2 antagonists, respectively, reduced dose-dependently the ambulation-increasing effect of methamphetamine (MAP: 2 mg/kg SC) in mice. The sensitization to MAP was inhibited when it was administered in combination with SCH (0.003-0.03 mg/kg) or YM (0.003-0.03 mg/kg) in the repeated administration regimen. The inhibitory action of YM on the MAP sensitization was more prominent than that of SCH. However, the repeated treatment with either SCH or YM could not ameliorate the established MAP sensitization. Rather, the repeated treatment with the highest dose of YM (0.03 mg/kg) increased the MAP sensitivity in both the MAP-sensitized and drug-naive mice. SCH had no such action. The present results suggest that the dopamine D2 receptors are more intimately involved than the dopamine D1 receptors in the increased sensitivity to MAP induced by the repeated treatment with MAP itself, behavioral sensitization, or dopamine antagonists, denervation supersensitivity.

Animals↗

PubMed1994

Long-continuous observation of the effects of methamphetamine on wheel-running and drinking in mice.

1. Effects of methamphetamine (MAP) on wheel-running and drinking in mice, housed under 12-hr light-dark schedule (light period; 06:00-18:00), were investigated through long-continuous observation. 2. MAP (1, 2 and 4 mg/kg, s.c.) acutely increased the wheel-running and drinking for 2-4 hr in a dose-dependent manner after the administration at 11:00, midpoint of light period. 3. MAP administered at 11:00 sub-acutely suppressed the spontaneous increment during dark period (18:00-06:00) in both the behaviors. 4. Many factors, such as the time-of-day and interval of the administration as well as the dose administered, affected the behavioral suppression induced by MAP. 5. In addition to these findings, the wheel-running and drinking during the light period increased even on the days without MAP administration. 6. These results suggest that MAP have not only acute stimulant and sub-acute depressant effects, but also long-lasting effects.

Animals↗

PubMed1994

Interactions of opioids with caffeine: evaluation by ambulatory activity in mice.

Morphine (up to 10 mg kg-1), buprenorphine (up to 0.1 mg kg-1), pentazocine (30 mg kg-1) and caffeine (up to 10 mg kg-1), significantly increased mouse ambulation. The combination of morphine, buprenorphine and pentazocine with caffeine generally enhanced the effect. Dopamine D1- and D2-receptor bockade, depletion of stored dopamine, and inhibition of dopamine synthesis could reduce the ambulation increased by single administration of morphine, buprenorphine and caffeine, and by combined administration of morphine and buprenorphine with caffeine. Although naloxone (0.1-3 mg kg-1) itself did not change mouse ambulation, at 3 mg kg-1, it reduced the effect of caffeine. The repeated administration of morphine (10 mg kg-1) induced a sensitization to the ambulation-increasing effect, and was inhibited by the combination of caffeine (10 mg kg-1) in the repeated administration schedule. The repeated administration of caffeine (10 mg kg-1) with buprenorphine (0.3 mg kg-1) resulted in a decrease in the effect to the level of caffeine alone. The development of cross-sensitization to morphine (10 mg kg-1) by the repeated treatment with buprenorphine (0.3 mg kg-1) was inhibited by caffeine (10 mg kg-1). Our results suggest that the dopaminergic systems are involved in the enhanced interaction of opioids having agonistic action on mu- or sigma-receptors with caffeine. However, it is also considered that, following the repeated administration, caffeine acts to reduce the sensitivity to the ambulation-increasing effect of opioids, probably inducing up-regulation of adenosinergic systems.

Animals↗

PubMed1993

Effects of haloperidol on the methamphetamine sensitization: assessment by ambulatory activity in mice.

Haloperidol (HPD: 0.0063, 0.025, 0.1 and 0.4 mg/kg, s.c.) reduced dose-dependently the ambulation-increasing effect of methamphetamine (MAP: 2 mg/kg, s.c.) in mice. The repeated administration of MAP elicited a sensitization to its ambulation-increasing effect, and the development of sensitization was inhibited when MAP was administered in combination with HPD in the repeated administration schedule. However, any dose of HPD could not ameliorate the established MAP sensitization. Whereas, the mice experienced the repeated treatment with HPD 0.4 mg/kg showed an increase in the MAP sensitivity. The present results suggest that HPD, at comparatively higher doses, produces a denervation supersensitivity of postsynaptic dopamine receptors, and shows protective action on the development of MAP sensitization. However, it is also suggested that the established MAP sensitization is irreversible even after the treatment with HPD.

Animals↗