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PubMed1995

Developmental toxicity of lithium treatment at prophylactic levels.

Lithium (Li+) salts are frequently used in psychiatry and may be administered to women in their reproductive years. We have investigated the influence of chronic Li+ administration on rat offspring. Pregnant Wistar rats drank either tap water ad libitum or 10 mM LiCl, or were water restricted (paired to rats receiving LiCl) until pup weaning. Following birth, pups were fostered to form five experimental groups (N = numbers of litters): a) Control-S, stressed by water restriction (N = 21), b) Li+ during the prenatal and lactating periods (N = 18), c) Li+ during the prenatal period only (N = 22), d) Li+ during the lactating period only (N = 15), and e) Control-NS no treatment (N = 13). Prenatal water restriction or Li+ treatment impaired the performance of the righting reflex, altered the number of males born and delayed the final date of eye opening. Postnatal water restriction or Li+ treatment of the dams reduced body growth and the date of eye opening of pups. No difference was found in the time to pup earflap opening, or in the motor coordination test. The specific effect of lithium on pups included impairment of the righting reflex, an increase in the number of males born, a reduction in body weight at weaning and a delay in the eye opening date. The serum Li+ levels of the dams were maintained at approximately 0.5 mEq/l. There was an increase in serum potassium, but not sodium, concentrations. We conclude that chronic treatment of dams with Li+ in amounts similar to those used in the prophylaxis of bipolar disorders aggravated the delay in physical and behavioral development of pups produced by stress associated with limited water intake and handling.

Animals↗

PubMed1993

Pentobarbital administered intracerebroventricularly antagonizes morphine-induced antinociception in mice.

The purposes were to show that pentobarbital administered intracerebroventricularly (i.c.v.) antagonized the antinociceptive action of morphine given intrathecally in the tail-flick test in mice, determine whether this antagonistic action involved spinal release of dynorphin A (Dyn A) and demonstrate whether the mechanism involved gamma-aminobutyric acid (GABA) receptors. Previously, it was shown that midazolam given i.c.v. antagonizes morphine-induced antinociception by release of Dyn A in the spinal cord. This antagonism by midazolam is reversed by a variety of benzodiazepine/GABAA receptor complex antagonists given i.c.v. The results indicated that the antagonistic action of pentobarbital given i.c.v. was not due to release of Dyn A based on presumptive tests for Dyn A release. 1) In the tail-flick test, the opioid receptor antagonists, naloxone and nor-binaltorphimine intrathecally, did not reverse the antagonism. 2) Pretreatment with dynorphin antiserum and morphine had no effect. The effect of pentobarbital was inhibited by a benzodiazepine receptor antagonist, flumazenil, given i.c.v. but not by a GABA antagonist, bicuculline s.c. or a chloride ion channel antagonist, picrotoxin, i.c.v. In contrast, the duration of loss of the righting reflex from systematically administered pentobarbital was shortened by bicuculline and picrotoxin but not by flumazenil. These results taken together with the previous results on midazolam suggested that the antagonistic action of pentobarbital on morphine-induced antinociception appeared to involve different GABA receptors from those involved in release of Dyn A by midazolam and those involved in the pentobarbital-induced loss of the righting reflex.

Animals↗

PubMed2004

A comparison of xylazine and medetomidine in an anesthetic combination in New Zealand White Rabbits.

A comparison was made of two anesthetic protocols for cardiothoracic surgery in rabbits. Eight male New Zealand White rabbits (2.8 to 3.2 kg) were used in a double crossover study. Each rabbit received intramuscular ketamine (35 mg/kg), xylazine (5 mg/kg), and buprenorphine (0.03 mg/kg) or ketamine (35 mg/kg), medetomidine (0.5 mg/kg), and buprenorphine (0.03 mg/kg) on alternate weeks. After intramuscular injection, each rabbit was intubated and placed on 0.75% isoflurane in 1 L O2/min. Palpebral, pedal, and righting reflexes and cardiopulmonary parameters were measured every minute for the first 10 min and every 5 min thereafter. Rabbits were monitored for 20 min of spontaneous ventilation followed by 60 min of intermittent positive pressure ventilation. Intermittent positive pressure ventilation and isoflurane then were discontinued and recovery monitored. Systolic, mean, and diastolic blood pressures were higher in the medetomidine-treated rabbits. Return of the palpebral, pedal, and righting reflexes was prolonged in the medetomidine-treated rabbits. There were no differences in heart rate, respiratory rate, return to spontaneous breathing, and time to extubation between the two groups. These results indicate medetomidine can be safely used in rabbit anesthesia, provides acceptable cardiovascular parameters, and induces a longer anesthetic period than that of xylazine.

Anesthesia↗

PubMed1998

Chronic desipramine treatment desensitizes the rat to anesthetic and antinociceptive effects of the alpha2-adrenergic agonist dexmedetomidine.

INTRODUCTION: The effects of long-term administration of the tricyclic antidepressant agent desipramine on the hypnotic, antinociceptive, anesthetic-sparing, and central norepinephrine turnover suppressant action of short-term dexmedetomidine, a highly selective alpha2-adrenergic agonist, were studied in rats. METHODS: Rats were given a 3- or 4-week course of twice daily administration of desipramine, 10 mg/kg, or saline. The effect of a hypnotic dose of dexmedetomidine, 250 microg/kg given intraperitoneally, on the duration of loss of righting reflex was determined. The tail flick latency response was determined before and after 50 microg/kg dexmedetomidine. The minimum anesthetic concentration of halothane and the central norepinephrine turnover rate were determined before and after administration of 30 microg/kg dexmedetomidine. Changes in the affinity and density of the alpha2-adrenergic receptor in locus coeruleus and spinal cord also were determined. RESULTS: Treatment with desipramine decreased dexmedetomidine-induced loss of righting reflex duration by 67% and eliminated the antinociceptive effect of dexmedetomidine. Dexmedetomidine produced a 55% decrease in minimum anesthetic concentration in the control group but no reduction in desipramine-treated rats. Desipramine did not change the receptor density or binding affinity of alpha2 receptors at the site for hypnotic (locus coeruleus) or antinociceptive (spinal cord) responses. No decrement in the central norepinephrine turnover rate was noted in the locus coeruleus of dexmedetomidine after 3 weeks of treatment with desipramine. The alpha1-adrenergic antagonist prazosin at 1 or 5 mg/kg completely (minimum anesthetic concentration reduction), almost completely (antinociceptive), or partially (hypnotic) restored responsiveness to normal. CONCLUSIONS: These data indicate that treatment with desipramine induces hyporesponsiveness to the hypnotic, analgesic, and minimum anesthetic concentration-reducing, but not to the suppression of central norepinephrine turnover, properties of dexmedetomidine. The hyporesponsiveness appears to involve an alpha1-adrenergic mechanism.

Adrenergic alpha-Agonists↗

PubMed1999

Cross-sensitivity between isoflurane and diazepam: evidence from a bidirectional tolerance study in mice.

We examined in mice the effect of chronic diazepam treatment on the sensitivity to isoflurane, and that of repeated isoflurane exposure on the sensitivity to diazepam. Mice were divided into four groups: group 1, treated with diazepam, 10 mg/kg i.p. twice daily; group 2, vehicle-treated controls; group 3, exposed to 3% isoflurane for 25 min twice daily; and group 4, untreated controls. After 14 days the effect of the treatment was assessed. Twenty-four hours after the last 10 mg/kg diazepam treatment, groups 1 and 2 received diazepam, 5 mg/kg i.p., and were subjected to the horizontal wire test (HWT). All control mice but only 10% of the diazepam-treated mice failed the HWT. Groups 1 and 2 were then exposed to increasing concentrations of isoflurane. Diazepam-treated mice (group 1) lost the HWT at 0.7+/-0.7%, compared with 0.6+/-0.1% in controls (group 2) (P<0.001); the ED50 was 0.75% vs. 0.65%. Group 1 mice lost the righting reflex at 0.94+/-0.07% isoflurane vs. 0.87+/-0.06% in group 2 (P<0.01); the ED50 was 0.93% vs. 0.82%. Recovery time was 175+/-161 s in group 1 vs. 343+/-275 s in group 2 (P<0.02). Twenty-four hours after the last of the repeated exposures to isoflurane, we examined the responses of groups 3 and 4 to increasing concentrations of isoflurane. Mice in group 3 lost the righting reflex at 1.0+/-0.06% isoflurane vs. 0.9+/-0.04% in controls (group 4) (P<0.001); the ED50 was 0.96% vs. 0.85%. Recovery time was 113+/-124 s vs. 208+/-126 s in groups 3 and 4 (P<0.09). Diazepam, 3 mg/kg i.p. administered to groups 3 and 4, caused loss of the HWT reflex in 33% of group 3 mice and in 82% of controls (group 4) (P<0.001). It appears that prolonged exposure to both diazepam and isoflurane caused reduced sensitivity to each drug separately, as well as to the other drug. This finding may strengthen the theory that inhalational anesthetics may act via the same mechanism as the benzodiazepines.

Administration, Inhalation↗

PubMed2004

Behavioral characterization of acetaldehyde in C57BL/6J mice: locomotor, hypnotic, anxiolytic and amnesic effects.

RATIONALE: Acetaldehyde, the first metabolite of ethanol, was recently suggested to contribute to many behavioral effects of ethanol, although few studies have directly investigated the behavioral effects of acetaldehyde itself. OBJECTIVES: The aim of the present study was to characterize the locomotor, hypnotic, anxiolytic-like and amnesic effects of acetaldehyde in C57BL/6J mice. METHODS: Increasing doses of acetaldehyde (0-300 mg/kg) were injected intraperitoneally and their effects on a series of representative behaviors were investigated. The locomotor effects of acetaldehyde were measured in activity boxes. The duration of the loss of righting reflex was used as an index of the hypnotic effects of acetaldehyde. The anxiolytic-like effects of acetaldehyde were tested with an elevated plus-maze and the amnesic effects with the one-trial passive avoidance test. Finally, brain and blood acetaldehyde concentrations were assessed. RESULTS: Acetaldehyde induced a significant hypolocomotor effect at 170 mg/kg and higher doses. In addition, the hypnotic effects of acetaldehyde were demonstrated by a loss of righting reflex after the administration of 170 and 300 mg/kg acetaldehyde. The elevated plus-maze showed that acetaldehyde does not possess anxiolytic-like properties. Finally, acetaldehyde (100-300 mg/kg) dose-dependently altered memory consolidation as shown by a reduced performance in the passive avoidance test. CONCLUSIONS: The present results show that acetaldehyde induces sedative, hypnotic and amnesic effects, whereas it is devoid of stimulant and anxiolytic-like properties in C57BL/6J mice. However, the behavioral effects of acetaldehyde after intraperitoneal administration were apparent at very high brain concentrations. The present results also indicate that acetaldehyde is unlikely to be involved in the anxiolytic properties of ethanol in mice.

Acetaldehyde↗

PubMed2001

Role of GABA(B) receptors in the sedative/hypnotic effect of gamma-hydroxybutyric acid.

The present study was aimed at identifying the receptor systems involved in the mediation of the sedative/hypnotic effect of gamma-hydroxybutyric acid (GHB) in DBA mice. Administration of the putative antagonist of the GHB binding site, 6,7,8,9-tetrahydro-5-hydroxy-5H-benzocyclohept-6-ylideneacetic acid (NCS-382; 50-500 mg/kg, i.p.), significantly increased the duration of loss of righting reflex induced by GHB (1000 mg/kg, i.p.). In contrast, the GABA(B) receptor antagonists, (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911; 25-100 mg/kg, i.p.) and (3-aminopropyl)(cyclohexylmethyl)phosphinic acid (CGP 46381; 12.5-150 mg/kg, i.p.), completely prevented the sedative/hypnotic effect of GHB. SCH 50911 (100 and 300 mg/kg, i.p.) was also capable to readily reverse the sedative/hypnotic effect of GHB (1000 mg/kg, i.p.) in mice that had lost the righting reflex. SCH 50911 (100 mg/kg, i.p.) also completely abolished the sedative/hypnotic effect of the GABA(B) receptor agonist, baclofen. These results indicate that the sedative/hypnotic effect of GHB is mediated by the stimulation of GABA(B) receptors and add further support to the hypothesis that the GABA(B) receptor constitutes a central site of action of GHB.

Animals↗

PubMed1992

The general anesthetic potency of propofol and its dependence on hydrostatic pressure.

Although plasma concentrations of propofol during anesthesia are well known, the free concentration remains unknown because of uncertainties regarding plasma protein binding, interaction with other protein-bound substances, the level of binding to its lipid carrier, and the use of adjuvants. At elevated surrounding pressure, all general anesthetics require higher concentrations to reach adequate levels of anesthesia. To determine the anesthetic potency of propofol at equilibrium conditions and to study the effects of pressure on propofol-induced anesthesia, Rana pipiens tadpoles were exposed to different concentrations of pure, not emulsified, propofol in aqueous solution. Anesthesia was defined as loss of the righting reflex. Ten animals per concentration were used, and each experiment was conducted twice. Pressure experiments were performed with nonanesthetized tadpoles and urethane-anesthetized tadpoles as control groups. Propofol concentrations were measured spectrophotometrically. At 1 atmosphere absolute (atm abs), a semilogarithmic sigmoidal concentration-response curve was obtained with a half-maximal effect of propofol at 2.2 +/- 0.22 microM (EC50; mean +/- SE). Increased pressure shifted the concentration-response curve to the right. The EC50 increased linearly with increasing pressure up to 121 atm abs (EC50 at 121 atm abs = 4.1 +/- 0.41 microM). For pressure greater than 121 atm abs, an increased excitability of the tadpoles made it difficult to distinguish the righting reflex from involuntary movements. The saturated solubility of propofol in aqueous solution was found to be 1.0 +/- 0.02 mM (mean +/- SD), and the octanol/water partition coefficient was 4,300 +/- 280. Propofol adhered to the correlation between anesthetic potency and octanol/water partition coefficient exhibited by other general anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗

PubMed1995

[Lactitol suppresses the disturbance of consciousness caused by experimentally induced hepatic encephalopathy in rats: an EEG study].

Electroencephalographic (EEG) studies were conducted to demonstrate the ameliorating effects of lactitol and its reference drug lactulose on the disturbance of consciousness caused by severe hepatic encephalopathy in rats permanently implanted with cortical electrodes. A novel experimental animal model of combined-type human hepatic encephalopathy was prepared by portacaval shunting followed by a single treatment with dimethylnitrosamine (30 mg/kg, i.p.). Lactitol or lactulose was orally administered twice a day for seven days and once on the morning of the eighth day. Ammonium acetate (500 mg/kg) was injected into the cecum 4 hr after the final administration of the drug. In control animals not treated with either drug, but in which hepatic encephalopathy had been induced, ammonium acetate induced a comatose state defined by a loss of the righting reflex accompanied by slowing or flattening of the cortical EEG. In control animals, significant increases in delta (1-3 Hz)-activity and significant decreases in beta (13-25 Hz)-activity during coma were detected by means of EEG power spectral analysis. Lactitol at doses of 3 g/kg/day or higher or lactulose at 6 g/kg/day significantly suppressed these EEG changes. Both drugs also suppressed in a dose-dependent manner the loss of the righting reflex. Lactitol may therefore be useful for ameliorating the disturbance of consciousness in patients with hepatic encephalopathy.

Animals↗

PubMedDate not supplied

Acute toxicity (LD50 and CD50) of lidocaine and prilocaine in combination with adrenaline and felypressin.

The toxicity of the combination of vasoconstrictors to local anaesthetic solutions has been debated since its first use in the beginning of this century. A combination of two vasoconstrictors to a local anaesthetic has been proposed by some researchers. In this study they were evaluated the acute toxicity (lethal dose 50%, convulsion dose 50%) and latency times of loss of righting reflex and convulsion as well as the duration of convulsion) of 2% lidocaine or 3% prilocaine, when administered in combination with adrenaline and felypressin at various concentrations. Lethal dose 50% studies showed that for both anaesthetics the solutions with higher concentrations of adrenaline were more toxic. The opposite was observed in the convulsion dose 50% studies. No alterations were observed in the control groups. All lidocaine solutions increased the latency of loss of righting reflex. The latency of convulsion was increased in some groups, but once the convulsion was achieved there was no difference in its duration. There was no statistical difference among prilocaine groups for any of the variables studied. Based on the experimental model studied, it was concluded that there is no advantage in the association of two vasoconstrictors concerning the toxicity of lidocaine and prilocaine solutions.

Anesthesia, Dental↗

PubMed2002

Forward, relaxed, and reverse selection for reduced and enhanced sensitivity to ethanol's locomotor stimulant effects in mice.

BACKGROUND: Rarely have trait markers for alcoholism risk been identified. However, relative sensitivity to the arousing effects of ethanol and sensitivity to ethanol's sedative effects have been distinguished as potentially valuable behavioral risk factors. Both traits are genetically influenced and have been modeled in mice by measuring sensitivity to ethanol-induced locomotor stimulation and hypnosis. Reverse selection was performed to examine the hypothesis that forward selection for differential sensitivity to ethanol's locomotor stimulant effects resulted in homozygous fixation of selection trait-relevant alleles and to test the hypothesis that common genes influence ethanol's stimulant and sedative effects. METHODS: Bidirectional selective breeding was completed for enhanced (FAST mice) and reduced (SLOW mice) sensitivity to ethanol's locomotor stimulant effects. Selection was terminated (relaxed), and the lines were tested to detect genetic drift. Reverse selection for enhanced sensitivity to ethanol-induced stimulation in SLOW mice and reduced sensitivity in FAST mice was performed for 16 generations. Forward and reverse selected lines were tested for sensitivity to ethanol's sedative effects by measuring duration of ethanol-induced loss of righting reflex. RESULTS: Differential sensitivity to the sedative effects of ethanol emerged with selection for differential ethanol stimulation, indicating a common genetic influence on these traits. SLOW mice developed greater sensitivity to ethanol's sedative effects relative to FAST mice. Reverse selection, never before reported for a pharmacogenetic trait, was effective in eliminating most of the difference in stimulant sensitivity between the FAST and SLOW lines and also eliminated the difference in loss of righting reflex duration. CONCLUSIONS: Residual heterozygosity persisted at trait-relevant loci even at the selection plateau, possibly due to heterosis, natural selection favoring heterozygosity, or epistatic phenomena involving differences in the sets of genes regulating the high- versus low-sensitivity traits. They also suggest that some common genes influence sensitivity to ethanol's locomotor stimulant and sedative effects.

Alcohol Drinking↗

PubMed1985

Inducing anesthesia with a GABA analog, THIP.

The authors have postulated previously that general anesthetic agents act via a potentiation of the inhibitory action of gamma-aminobutyric acid (GABA) at central synapses. If the hypothesis is true, GABA should induce anesthesia, however, GABA itself does not pass through the blood-brain barrier. A GABA analog was sought as a substitute to test the authors' hypothesis. A new bicyclic GABA analog, THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol) was selected because its properties are similar to GABA in vitro. THIP was found to induce anesthesia in rodents, and its behavior was compared with that of thiopental, ketamine, midazolam, and gamma-hydroxybutyrate. Complete loss of righting reflex occurred with doses of THIP and thiopental just under 100 mumol/kg, with ketamine and midazolam less than 50 mumol/kg and with gamma-hydroxybutyrate of more than 6,000 mumol/kg. Complete recovery from thiopental and ketamine occurred in less than 5 min, with midazolam recovery required about half an hour and with gamma-hydroxybutyrate and THIP it took about 1 1/2 h. THIP induced analgesia as well as sedation and loss of righting reflex. Recovery was complete, and no adverse effects were noted in these rodents.

Analgesics↗

PubMed1992

Anesthetic properties of riluzole (54274 RP), a new inhibitor of glutamate neurotransmission.

It has been suggested that some anesthetic agents could exert their hypnotic/anesthetic effects by selectively blocking receptors involved in the central excitatory neurotransmission mediated by glutamate. In the present study, we analyzed whether riluzole (54274 RP), a novel compound that inhibits both the release and some postsynaptic effects of glutamate in some brain structures, has anesthetic properties in rats. For this purpose, we investigated whether 1) riluzole administered intraperitoneally (ip) at doses ranging from 2.5 to 45 mg/kg induces loss of righting reflex (LRR); 2) riluzole (2.5 and 5 mg/kg) prolongs sleep-times induced by either ketamine (30 or 80 mg/kg ip) or thiopental (25 or 35 mg/kg ip); 3) a 5-mg/kg subanesthetic riluzole dose affects the minimum alveolar concentration of halothane (MACh). Onset of drug action was defined as the period of time from the ip injection to LRR. Sleep-time was considered the period of time from LRR to restoration of righting reflex. Riluzole at doses greater than 15 mg/kg was able to induce LRR (riluzole dose for which LRR was achieved in 50% of the rats [ED50 = 25.6 mg/kg]). A positive correlation was found between the dose of riluzole and sleep-time (r = 0.92, P less than 0.001). A 5-mg/kg (but not 2.5-mg/kg) riluzole dose significantly prolonged sleep-times induced by both ketamine (30 and 80 mg/kg) and thiopental (25 but not 35 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗

PubMed1988

Kinetics of drug action in disease states. XXVII. Effect of experimental renal failure on the pharmacodynamics of zoxazolamine and chlorzoxazone.

The purpose of this investigation was to determine whether the pharmacodynamics of the centrally acting skeletal muscle relaxants zoxazolamine (ZOX) and chlorzoxazone (CZX) are altered in renal failure. Male Lewis rats with renal failure due to bilateral ligation of ureters and sham-operated controls (ZOX and CZX), as well as rats with uranyl nitrate-induced renal dysfunction and saline-injected controls (ZOX only), received an infusion of ZOX or CZX until onset of loss of righting reflex. Drug concentrations in serum, brain and cerebrospinal fluid at that time were substantially lower in animals with renal failure or dysfunction than in normal controls. The ZOX concentrations in the cerebrospinal fluid correlated negatively with indices of renal function (serum creatinine and urea concentrations). Administration of a concentrated dialyzate of serum from rats with uranyl nitrate-induced renal dysfunction to normal animals also decreased the concentrations of ZOX at onset of loss of righting reflex. Thus, the sensitivity of the central nervous system of rats to the depressant action of ZOX and CZX is significantly increased by renal failure. This effect appears to be mediated, at least in part, by an endogenous, dialyzable substance that accumulates in the blood of rats with impaired renal function.

Acute Kidney Injury↗

PubMed1986

Activities of thiamine-dependent enzymes in two experimental models of thiamine-deficiency encephalopathy. 2. alpha-Ketoglutarate dehydrogenase.

Chronic thiamine deprivation in the rat leads to selective neuropathological damage to pontine structures. Onset of neurological symptoms of thiamine deprivation (ataxia, loss of righting reflex) was accompanied by selective decreases (of the order of 30%) in the activity of alpha-ketoglutarate dehydrogenase (alpha KGDH) in lateral vestibular nucleus and hypothalamus. Enzyme activities were decreased to a lesser extent in medulla oblongata, striatum and hippocampus and were unchanged in other brain structures. No changes in alpha KGDH occurred prior to the onset of neurological signs of thiamine deprivation. Administration of the central thiamine antagonist, pyrithiamine, results within 3 weeks in loss of righting reflex and convulsions and in more widespread neuropathological changes than those observed following thiamine deprivation. alpha KGDH activities were found to be substantially diminished in all brain regions studied following pyrithiamine treatment with most severe changes occurring in brain regions found to be vulnerable to pyrithiamine (lateral vestibular nucleus, hypothalamus, midbrain, medulla-pons). In some cases, alpha KGDH changes preceded the appearance of neurological symptoms of pyrithiamine treatment. Such decreases in alpha KGDH may explain previous findings of region-selective changes in energy metabolism and of decreased synthesis of glucose-derived neurotransmitters (acetylcholine, GABA, glutamate) in pyrithiamine-treated rat brain. Thiamine administration to symptomatic pyrithiamine treated rats resulted in reversal of neurological signs of encephalopathy and in normalisation of defective alpha KGDH activity in all brain regions. These findings suggest that the reversible neurological symptoms associated with Wernicke's Encephalopathy in man likely result from region-selective impairment of alpha KGDH.

Animals↗

PubMed1997

A comparison of sevoflurane and isoflurane for short-term anesthesia in polecats (Mustela eversmanni).

Twenty-four Siberian polecats (Mustela eversmanni) from 12 litters were anesthetized with either inhaled sevoflurane or isoflurane. With 7% delivered sevoflurane and 5% delivered isoflurane, time to loss of righting reflex (mean +/- SE) with sevoflurane (1.9 +/- 0.1 min) was significantly shorter compared with isoflurane (2.6 +/- 0.1 min). During maintenance at a light plane of anesthesia, systolic arterial pressure was significantly higher with sevoflurane (83 +/- 2 mm Hg) compared with isoflurane (66 +/- 2 mm Hg), and heart rate was significantly lower with sevoflurane (191 +/- 3 beats/min) compared with isoflurane (204 +/- 3 beats/min). There was no difference in respiratory rate jugular venous pH, pCO3, HCO3-, base excess, or recovery of righting reflex. Induction of anesthesia is more rapid and blood pressure is better maintained with sevoflurane compared with isoflurane; therefore, sevoflurane may be less stressful and safer. Inhaled sevoflurane should be an appropriate anesthetic for black-footed ferrets (Mustela nigripes) in laboratory and field conditions.

Analysis of Variance↗

PubMed1989

Possible role of alpha-2 and alpha-1 adrenoceptors in the experimentally-induced depression of the central nervous system.

The alpha-2 adrenoceptor agonists clonidine and xylazine were employed in chicks and rats to induce a loss of the righting reflex, a sign for depression of the central nervous system. These effects of clonidine and xylazine were antagonized by yohimbine, idazoxan and CH-38083 (7,8-(methylenedioxi)-14-alpha-hydroxyalloberbane HCl), compounds having alpha-2 adrenoceptor antagonist properties. Prazosin, an antagonist for alpha-1 adrenoceptors, enforced the alpha-2 adrenoceptor agonist-induced depression in both species. 6-Hydroxydopamine treatment, which reduced the norepinephrine concentrations in the rat cerebral cortex by 76%, increased the duration of the loss of righting reflex induced by xylazine indicating that central postsynaptic alpha-2 adrenoceptors might also be involved in this behavioral alteration. The electrically-stimulated tritium release was also determined from the isolated rat cerebral cortex slices which had been preloaded with 3H-norepinephrine. Clonidine and xylazine inhibited the stimulation-induced tritium release and this inhibition was counteracted by yohimbine, idazoxan or CH-38083, but not by prazosin. We have concluded from the present data that stimulation of alpha-2 adrenoceptors with pre- and postsynaptic locations or inhibition of alpha-1 adrenoceptors in the central nervous system may shift the depression/vigilance balance to the direction of depression which might be accompanied by a decreased activity of cortical noradrenergic neural transmission.

Adrenergic alpha-Antagonists↗

PubMed1983

Sensitivity to ethanol in inbred mice: genotypic correlations among several behavioral responses.

The sensitivity of several inbred strains of mice was assessed for ethanol's effects on activity, body temperature, ataxia, balance, and the righting reflex. Genotypic correlations among the mean responses for the strains were estimated as indexes of pleiotropic influences of genes on drug responses. Three major groups of genetic influence were detected: (a) hypothermic sensitivity to ethanol, (b) activity change (increase after ethanol), and (c) high basal activity. In the first group of variables, strains that had large reductions in body temperature after being given ethanol had high baseline temperatures, pronounced ataxic response to ethanol, and a long-lasting loss of righting reflex. Home cage baseline activity was negatively correlated with body temperature variables. The second group of variables was composed largely of ethanol-induced increases and decreases in activity, which were negatively intercorrelated. Strains with larger increases in activity showed more rapid loss of balance after ethanol. The third group of variables indicated that high levels of basal activity in an open field and in the home cage were determined by the action of common genes. Strains with higher basal activity levels had reduced sensitivity to ambulatory ataxia following ethanol. Thus, there were substantial pleiotropic effects of common genes on several behavioral responses to ethanol in inbred mice. Conversely, the three major groups were not systematically correlated with one another to a major extent. This suggests the influence of three reasonably distinct sets of genes on these responses to ethanol.

Animals↗