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PubMed1976

[Acute toxicity and the central effect of 1-(m-chlorophenyl)-3-N,N-dimethylcarbamoyl-5-methoxypyrazole (PZ-177)].

In a previous paper, we reported that PZ-177 had potent anti-inflammatory and analgesic activities. In the present work, acute toxicity and action of PZ-177 on the central nervous system were tested in comparison with PZ-222, one of metabolites of PZ-177, and mepirizole. Acute toxicity of PZ-177 was slightly less than that of aminopyrine and the same as that of mepirizole in mice and rats. PZ-177 produced from sedation to loss of righting reflex with the increase of dose. At a low dose with which the righting reflex was hot lost, PZ-177 decreased spontaneous locomotion of mice in the Animex test, produced muscle relaxation in rotarod and inclined screen tests, produced sleeping-pattern in electroencephalogram of rabbit, potentiated hypnosis of barbiturates and exerted an anti-convulsive effect in mice. In these depressive effects on the central nervous system, PZ-222 was very much lower and mepirizole slightly lower than PZ-177. It would thus appear that PZ-177 has more potent analgesic, antipyretic and anti-tussive actions than do PZ-222 and mepirizole.

Acute Disease↗
PubMedDate not supplied

Evidence for site specific ethanol actions in the CNS.

The diverse behavioral and biochemical effects induced by ethanol suggest that ethanol exerts differential effects on the CNS. When the neuroactive amino acids, glycine, glutamate, aspartate, GABA and taurine, were measured in the cortex, striatum, hippocampus, midbrain, and brain stem of acute or chronic ethanol-treated rats, site specific changes were observed for glutamate, glycine, and aspartate. No changes were found for GABA or taurine. Upon in vivo application, it was found that the microinjection of thyrotropin-releasing hormone (TRH, 500 ng) into the medial septum significantly shortened ethanol's impairment of the righting reflex, while microinjection of muscimol (30 ng) markedly potentiated ethanol's impairment of the righting reflex. When these studies are combined with previous work showing that microinjection of muscimol (30 ng) into the inferior colliculus blocks audiogenically induced seizures in ethanol-withdrawn rats, the convergence implies that specific sites in the CNS may modulate certain actions of ethanol. Therefore, we propose that the medial septum and inferior colliculus can be used as in vivo models to study the acute and chronic actions of ethanol, respectively.

Amino Acids↗
PubMed2005

Altered dose-to-effect of propofol due to pharmacokinetics in rats with experimental diabetes mellitus.

Pathology related alterations in the pharmacokinetics or the pharmacodynamics of propofol could contribute to the observed large variability in the hypnotic dose. We have tested the influence of diabetes mellitus on the induction dose and the pharmacokinetics and pharmacodynamics of propofol in rats. Diabetes was induced in rats by administration of streptozotocin (60 mg kg(-1), i. p.) while control rats received vehicle intraperitoneally. All animals had glucose, cholesterol, triglycerides and albumin levels measured. In-vitro protein binding was determined by ultrafiltration. Rats were randomly split into set 1 (dose-concentration-effect study) with control and streptozotocin rats, and set 2 (pharmacokinetic study), with control and streptozotocin rats. Rats in the effect set received either a variable infusion of 6 mg kg(-1) min(-1) propofol until onset (induction dose) of the hypnotic effect (loss of the righting reflex), or a 15 mg kg(-1) bolus to assess offset time (recovery of the righting reflex). Blood (C(blood)) and brain (C(brain)) propofol concentrations at onset and offset were assayed by HPLC. In the pharmacokinetic study, propofol was administered intravenously at 6 mg kg(-1) min(-1) for 2 min. Arterial blood samples were collected between 0.5 and 540 min and assayed for propofol. A mixed effects compartmental pharmacokinetic modelling method (NONMEM) was used to analyse the observations and variabilities. The dose necessary for onset differed between streptozotocin and controls, and so did the pharmacokinetics with two- and three-compartment descriptions, respectively. C(blood) and C(brain) at onset and offset were similar, possibly rejecting changes in pharmacodynamics. The total and unbound volume of distribution was significantly lower in the streptozotocin group with no differences in clearance (CL) between streptozotocin and controls, (mean (inter-animal CV%)) CL = 0.026 (17%) and 0.025 (62%) L min(-1), respectively. Individual Bayes Vd(ss) (volume of distribution at steady state) were different, (mean (s. d.)) Vd(ss) = 7.7 (2.67) and 1.11 (0.09) L, respectively. The pharmacokinetic model was validated by comparison with the data from set 1. Simulations of total and unbound C(blood), for both groups, at the hypnotic dose for the controls, revealed differences throughout the time course of the pharmacokinetics. The difference observed in the induction dose of propofol to streptozotocin and control rats was due to alterations in the pharmacokinetics, secondary to the pathology.

Anesthetics, Intravenous↗
PubMed1989

Analysis of standing posture in patients with bilateral loss of labyrinthine excitability.

The forward-backward and right-left sways in the upright standing posture were examined using stabilometry and analysis with a 5-dimensional feedback model. The forward-backward sway was found to have a fast, hidden periodicity, composed of sways due to a loss of the labyrinthine righting reflex upon the head and interaction between the head and knee sways. Furthermore, on the basis of our previous investigation, the forward-backward sway was found to depend on the increased spinal reflexes caused by a loss of labyrinthine inhibitory control upon the antigravity muscles. The right-left sway is slow and irregular, being mainly produced by disturbance of the head righting reflex.

Feedback↗
PubMedDate not supplied

[Diagnostic role of vestibular recruitment and nystagmic parameters].

Electronystagmographic examination of 45 patients with peripheral and 22 patients with central lesions of the vestibular system was performed, using graded caloric and rotatory stimulation of labyrinths. It was demonstrated that functional and topical diagnosis of vestibular problems can be made with the aid of righting reflexes and vestibular recruitment. In this situation, it is important not only to detect the righting reflex but also to determine the nystagmic parameters, in which it is manifested, and to identify the pattern of nystagmic asymmetry and the stage of compensation of vestibular dysfunction.

Adult↗
PubMed1990

Body temperature differentially affects ethanol sensitivity in both inbred strains and selected lines of mice.

Offsetting ethanol-induced hypothermia in five inbred strains of mice changed ethanol sensitivity within strains and markedly reduced differences between strains in brain sensitivity to hypnotic ethanol doses. The present study extended this work to mice selectively bred for sensitivity and resistance to ethanol-induced loss of righting reflex (LORR) and hypothermia. In all experiments LORR duration and ethanol concentrations at return of righting reflex were measured after i.p. hypnotic ethanol doses and exposure to 22 or 34 degrees C. In experiment 1, C57BL/6J, A/HeJ, 129/J, LS/lbg and SS/lbg mice were given 4.2 g/kg ethanol. In experiment 2, the same mouse genotypes were tested with different ethanol doses (2.5-4.9 g/kg) selected to produce an equivalent degree of impairment (60 min LORR duration). In experiment 3, HOT and COLD lines of mice were given 4.0 g/kg ethanol. In agreement with previous work, offsetting hypothermia reduced differences between genotypes in ethanol sensitivity. Comparisons within genotypes indicated that ethanol sensitivity in C57, A/He, SS, HOT and COLD mice increased as body temperature increased. In contrast, ethanol sensitivity in 129 and LS mice decreased as body temperature increased. These results extend previous findings indicating that body temperature during intoxication contributes to differences between genotypes in ethanol sensitivity. The present findings also suggest that there are qualitative differences in the effects of temperature on ethanol sensitivity within genotypes.

Animals↗
PubMed1984

Xylazine-induced sedation in chicks is inhibited by opiate receptor antagonists.

The sedative effect of xylazine and its interaction with antagonists of alpha-adrenoceptors or opiate receptors was examined in chicks. The duration of the sleep-like behavioral state induced by xylazine was determined by measuring the time interval during which the chicks failed to exhibit the righting reflex. In these chicks, intramuscular administration of xylazine (0.3-4.8 mg/kg) induced a loss of the righting reflex, the duration of which was dose-dependent. Both alpha-adrenoceptor antagonists of the alpha2 type, i.e. yohimbine (0.1-1.0 mg/kg) and compound 170150 (0.1-1.0 mg/kg) (a benzodioxane derivative), and opiate receptor antagonists, i.e. naloxone (0.4-1.6 mg/kg) and nalorphine (3.0-30.0 mg/kg), effectively inhibited the sedative effect of xylazine while prazosin (0.1-10.0 mg/kg), an alpha 1-adrenoceptor antagonist, failed to antagonize xylazine-induced sedation. These findings suggest that in addition to the stimulation of central alpha 2-adrenoceptors, activation of an endogenous opiate mechanism may be involved in the sedative effect of xylazine.

Adrenergic alpha-Antagonists↗
PubMed2006

Gender specific effects of ethanol in mice, lacking CCK2 receptors.

Neuropeptide cholecystokinin (CCK) has been reported to suppress ethanol intake, but there is contradictory evidence about the role of CCK(2) receptors. In the present study anxiolytic, hypolocomotor and sedative effects of acute ethanol administration, but also voluntary ethanol consumption were studied in male and female mice, lacking CCK(2) receptors (-/-). Ethanol (1.0 and 2.0 g/kg) induced a significant reduction of anxiety-related behaviours in the elevated plus-maze, but this effect was statistically significant only in female homozygous mice (-/-). In male mice, lacking CCK(2) receptors (-/-), but not in their wild-type littermates (+/+), the suppression of vertical locomotor activity was caused by ethanol at a dose 0.5 g/kg. The highest dose of ethanol (2.0 g/kg) produced statistically significant reduction of horizontal locomotor activity only in female wild-type (+/+) mice, but this effect was related to increased basal activity when compared to female mutant (-/-) mice. Duration of the loss of righting reflex was not significantly affected by genotype or gender, but blood ethanol levels at regain of righting reflex were significantly lower in female homozygous mice (-/-) compared to their wild-type (+/+) littermates, indicating increased sensitivity to the sedative effect of ethanol. Ethanol intake, but not preference, at concentration 10% was significantly increased in female mice, lacking CCK(2) receptors (-/-). The present study revealed an altered response to the acute effects of ethanol in CCK(2) receptor deficient mice (-/-). These changes are gender-specific and could be attributed to the altered activity of dopaminergic system in male mice and increased activity of GABA-ergic system in female mice as established in our previous studies.

Alcohol Drinking↗
PubMed1989

Diazepam--morphine hypnotic synergism in rats.

The effect of diazepam-morphine combination on the righting reflex was studied in rats. Doses of the drugs given alone and in combination that block righting reflex (RR ED50) were determined with a probit procedure. Brain concentrations following equieffective doses of the drugs administered separately and in combination were determined by radioimmunoassay. Equieffective intravenous doses and corresponding brain concentrations for the agents were compared with fractional (algebraic) and isobolographic analyses. Interaction between diazepam and morphine was found to be synergistic. It is not likely to be pharmacokinetic in nature.

Animals↗
PubMed1996

[Montirelin hydrate (NS-3), a TRH analog, improved the disturbance of consciousness caused by head concussion and pentobarbital in mice].

Effects of a novel TRH analog, montirelin hydrate (NS-3), on the coma caused by head concussion and narcosis induced by pentobarbital were compared with those of TRH in mice. Head concussion caused a behavioral comatose state with loss of the righting reflex and spontaneous motor activity. NS-3 shortened the latent periods to the recovery of the righting reflex (0.03-0.1 mg/kg, i.v.) and spontaneous motor activity (0.1 mg/kg, i.v.) following the head concussion. In the case of TRH, higher doses were needed to induce such effects. NS-3 (0.1-0.3 mg/kg, i.v.) reversed the pentobarbital-induced narcosis in a dose-dependent manner. A similar effect was elicited by 30- to 100-fold higher doses of TRH than NS-3. The analeptic effect of NS-3 in the pentobarbital-narcotized mice was antagonized by SCH23390, a dopamine D1 antagonist or by the combined treatment with prazosin and scopolamine, while neither prazosin nor scopolamine alone antagonized the analeptic effect of NS-3. Taken together with the finding that NS-3 did not bind to dopamine, adrenaline or muscarine receptors, it is suggested that NS-3 may restore the disturbance of consciousness by activating the brain dopamine, noradrenaline and acetylcholine neurons without stimulating these receptors directly.

Anesthesia↗
PubMed1964

THE ACTION OF SODIUM 4-HYDROXYBUTYRATE ON SPINAL REFLEXES.

The actions of sodium 4-hydroxybutyrate, gamma-aminobutyric acid and meprobamate have been studied in unanaesthetized animals, in local anaesthetic tests, on isolated organ preparations, on convulsions induced by picrotoxin and strychnine, and on monosynaptic (patellar) and polysynaptic (plantar) reflexes of the spinal cord. Sodium 4-hydroxybutyrate induced a sleep-like state with three unusual features: the righting reflex was remarkably persistent, respiration was good throughout and recovery was abrupt. gamma-Aminobutyric acid was inactive and meprobamate caused flaccid paralysis with loss of the righting reflex. None of the agents affected the responses of the rat diaphragm either to direct stimulation of the muscle or to indirect stimulation through the phrenic nerve. Only meprobamate reduced the responses of theguinea-pig isolated ileum preparation, showed local anaesthetic action and had an anticonvulsant action. All three compounds were capable, after intravenous or topical application, of blocking plantar reflexes in doses which did not affect the patellar reflex. The spinal animal responded in the same way, to the same dose of sodium 4-hydroxybutyrate, as the decerebrate preparation. Topical application to the motor cortex had no effect on spinal reflexes. We conclude that sodium 4-hydroxybutyrate acts preferentially on the internuncial neurones in the spinal cord but differs from meprobamate in its other actions. The similarity between the actions of sodium 4-hydroxybutyrate and of gamma-aminobutyric acid provides furtherevidence in support of the hypothesis that sodium 4-hydroxybutyrate is involved in the gamma-aminobutyric acid metabolic pathways.

Aminobutyrates↗
PubMed1997

[A case of superficial siderosis of the central nervous system with bilateral vestibular dysfunction].

A 58-year-old woman developed slowly progressive hearing loss, anosmia, and unsteady gait. She had neither repeated episode of headache nor a past history of neurosurgical operation or head injury. Neurological examination revealed anosmia, moderate degree of sensorineural hearing loss. She showed loss of caloric response bilaterally. No nystagmus was found. Romberg sign was present. No cerebellar ataxia was noted in the finger-to-nose or the heel-to-knee test. No adiadochokinesis was noted. Deep tendon reflexes were increased in both upper and lower extremities. Sensation was intact. She showed disturbance of the righting reflex in the tilt-table examination. CSF were under normal pressure, xanthochromic with siderophages. CSF total protein and ferritin level were elevated. T2-weighted image (TE4000/TR100) of high field strength magnetic resonance imaging (MRI) showed marginal hypointensity of the brain stem, the Sylvian fissures, the tips of temporal lobes, anterior cerebellar surfaces and the entire spinal cord. Angiography of the cerebral vessels and spinal arteries failed to identify the source of bleeding. It seemed likely that she had lost bilateral vestibular and auditory functions caused by hemosidelin deposition to her eighth nerves which are often affected by this disorder. Her disturbance of gait and station was apparently similar to cerebellar ataxic gait, however, she did not have limb ataxia. The electronystagmogram revealed marked degree of vestibular dysfunction (VOR) and relative sparing of cerebellar function (OKN). Her disturbance of the righting reflex in the tilt-table examination and the characteristic feature of her Romberg sign with directional preponderance also indicate that the bilateral loss of vestibular functions, i.e., vestibular ataxia caused her dysequilibrium syndrome. It is our impression that vestibular ataxia might precede cerebellar ataxia commonly reported so far.

Brain↗
PubMed1999

Effects of ginseng on ethanol induced sedation in mice.

The effects of ginseng, ginsenosides, coffee, and caffeine on 75% ethanol induced sleeping in mice were examined. Mice treated with ethanol lost their righting reflex within 30 min and this lasted for about 4 h. The onset time of lose of righting reflex (LR) in mice pre-treated with ginseng, ginsenosides, coffee or caffeine 10 min before ethanol was significantly delayed; whereas the duration of sleep was not affected by all treatments. Administration of these agents 10 min after ethanol was ineffective in counteracting the LR effect of ethanol. Coffee and caffeine produced central stimulation and increased locomotor activity. Ginseng and ginsenosides were found to enhance exercise endurance and reduced the plasma level of ethanol. Gastric emptying was slowed by ginseng, ginsenosides or ethanol administration. An additive effect was observed when the mice were pre-treated with ginseng or ginsenosides 10 min before ethanol administration. It is suggested that ginseng decreased plasma ethanol concentration by delaying gastric emptying and this may be partly due to the effect of the ginsenosides.

Animals↗
PubMed1997

Role of NMDA receptors in pentobarbital tolerance/dependence.

Effects of continuous pentobarbital administration on binding characteristics of [3H]MK-801 in the rat brain were examined by autoradiography. Animals were rendered tolerant to pentobarbital using i.c.v. infusion of pentobarbital (300 micrograms/10 microliters/hr for 7 days) by osmotic minipumps and dependent by abrupt withdrawal from pentobarbital. The levels of [3H]MK-801 binding were elevated in rats 24-hr after withdrawal from pentobarbital while there were no changes except in septum and anterior ventral nuclei in tolerant rats. For assessing the role of NMDA receptor in barbiturate action, an NMDA receptor antagonist (MK-801, 2.7 femto g/10 microliters/hr) was co-infused with pentobarbital. The pentobarbital-infused group had a shorter duration of pentobarbital-induced loss of righting reflex (sleeping time) than that of the control group, and MK-801 alone did not affect the righting reflex. However, co-infusion of MK-801 blocked hyperthermia, and prolonged the onset of convulsions induced by t-butylbicyclophosphorothionate (TBPS) in pentobarbital withdrawal rats. In addition, elevated [35S]TBPS binding was significantly attenuated by co-infusion with MK-801. These results suggest the involvement of NMDA receptor up-regulation in pentobarbital withdrawal and that the development of dependence can be attenuated by the treatment of subtoxic dose of MK-801.

Animals↗
PubMed1993

Pentobarbital-morphine anesthetic interactions in terms of intensity of noxious stimulation required for arousal.

BACKGROUND: Previous reports suggest that the outcome (synergism, antagonism, summation) of opioid-barbiturate interactions may depend on the depth of anesthesia. One aim of the present study was to determine whether pentobarbital, alone and in combination with morphine, blocks awakening caused by noxious stimulation in a dose-related manner: the more intense the noxious stimulation, the more pentobarbital is required to suppress the response. A second aim of the study was to determine whether the pentobarbital-morphine anesthetic interaction depends on the depth of anesthesia measured in terms of intensity of noxious stimulation required for behavioral arousal (recovery of the righting reflex). METHODS: Experiments were performed on rats, with the measure of anesthetic effect being suppression of the righting reflex. The noxious stimulus was pressure on the tail at four levels of intensity: 0.0, 0.25, 2.5, and 3.3 kg, generated with an Analgesy-Meter. Pentobarbital and morphine were injected intravenously via chronically implanted catheters. Dose-response curves for pentobarbital given alone and in combination with morphine were determined (by probit analysis) separately for each of the pressure levels. RESULTS: Pentobarbital, alone and in combination with morphine, blocked awakening caused by noxious stimulation of different intensities in a dose-related fashion so that more anesthetic was required to block awakening with more intense stimulation. The pentobarbital ED50 values were: 12.0, 19.5, 22.7, and 24.3 mg/kg for 0.0, 0.25, 2.5, and 3.3 kg pressure, respectively. The addition of morphine (1 mg/kg) reduced the pentobarbital ED50 values for 0.0, 0.25, and 2.5 kg pressure by 34% (P < 0.0001), 39% (P < 0.0001), and 21% (P < 0.005), respectively. No change was seen in the pentobarbital ED50 value at the maximal (3.3 kg) pressure level. CONCLUSIONS: The results suggest that the depth of anesthesia can be measured in terms of intensity of noxious stimulation required for arousal and that the outcome of barbiturate-opioid anesthetic interaction depends on the depth of anesthesia.

Anesthesia↗
PubMed1995

Antagonism of ethanol by pretreatment or posttreatment with RO 15-4513 and indomethacin alone or in combination.

RO 15-4513, an inverse agonist at the GABA/benzodiazepine receptor Cl- channel complex, antagonizes multiple effects of ethanol. Prostaglandin synthesis inhibitors, such as indomethacin, also antagonize several effects of alcohols. However, prostaglandin synthesis inhibitors and RO 15-4513 each provide only partial antagonism of ethanol, typically seen as a dose-related effect with a maximum efficacy of approximately 50%. The purpose of this study was to: (1) compare the relative efficacy of these compounds for antagonizing ethanol; (2) compare the effectiveness of preethanol treatment versus postethanol treatment with each drug; and (3) compare the effect of RO 15-4513 and indomethacin in combination with the effects of each drug alone. The results show that indomethacin significantly decreased duration of loss of the righting reflex when administered either pre- or postethanol. Conversely, RO 15-4513 decreased duration of loss of the righting reflex only when given preethanol. When coadministered, RO 15-4513 and indomethacin did not show additive or synergistic effects. Compounds from these two drugs classes should continue to prove useful in elucidating ethanol's mechanisms of action.

Alcoholic Intoxication↗
PubMed1975

Biopharmaceutical factors influencing LD50. Part II: Particle size.

The effect of particle size on the time elapsing between administration and loss of righting reflex and % of deaths by determining the LD50 has been studied in mice. The drug used was pentobarbituric acid. In one preparation the particle size was less than 44 mum and in the other preparation it was greater than 297 mum and less than 420 mum. For both preparations a 1% sodium carboxymethylcellulose solution was used as suspending medium. It was found that both the curve for loss of righting reflex and the log dose-response curve, and hence the LD50, were significantly shifted to the right. There is a reflex LRR between the suspended pentobarbituric acid and the equivalent amount of sodium pentobarbital, both in 1% sodium carboxymethylcellulose solution. In reporting LD50 data it is essential not only to state the exact composition of the vehicle (viscosity factor) but also to state the exact particle size or particle size range, because by using increasing particle size the LD50 decreases.

Absorption↗