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PubMed1985

Effects of a commercial soy lecithin preparation on development of sensorimotor behavior and brain biochemistry in the rat.

Pregnant rat dams and offspring were exposed to a 5 or 2% soy lecithin preparation or a control diet. Enrichment was either lifelong beginning at gestation, limited to the time preceding, or the time following weaning, or absent (constituting a "pure" control group). The most marked early sensorimotor deficits (reflex righting and swimming development) were seen in the 5% soy lecithin preparation group, although all soy lecithin preparation-exposed offspring had elevated brain/body weight ratios and choline acetyltransferase levels. Later, animals exposed to lifelong 5 or 2% soy lecithin preparations were hypoactive, had poor postural reflexes, and showed attenuated morphine analgesia. The results indicate that dietary soy lecithin preparation enrichment during development leads to behavioral and neurochemical abnormalities in the exposed offspring.

Animals↗

PubMed2005

Deletion of the alpha7 nicotinic receptor subunit gene results in increased sensitivity to several behavioral effects produced by alcohol.

BACKGROUND: The finding that most people with alcoholism are also heavy smokers prompted several research groups to evaluate the effects of ethanol on neuronal nicotinic acetylcholine receptor (nAChR) function. Data collected in vitro indicate that physiologically relevant concentrations of ethanol inhibit the functional activation of homomeric alpha7 nAChRs, which are one of the most abundant nAChR subtypes expressed in the mammalian brain. The studies outlined here used alpha7 gene knockout (null mutant) mice to evaluate the potential role of alpha7 nAChRs in modulating selected behavioral and physiological effects produced by ethanol. METHODS: Current evidence indicates that many responses to ethanol are not genetically correlated. Therefore, the authors measured the effects of acute administration of ethanol on several behaviors that are altered by both ethanol and nicotine: two tests of locomotor activity, acoustic startle, prepulse inhibition of acoustic startle, and body temperature. Ethanol-induced durations of loss of righting reflex and ethanol elimination rates were also determined. These studies used null mutant (alpha7(-/-)) and wild-type (alpha7(-/-)) mice. RESULTS: Relative to alpha7(+/+) mice, alpha7(-/-) mice were more sensitive to the activating effects of ethanol on open-field activity, ethanol-induced hypothermia, and duration of loss of the righting response. Deletion of the alpha7 gene did not influence the effects of ethanol on Y-maze crossing or rearing activities, acoustic startle, or prepulse inhibition of startle. Gene deletion did not alter ethanol metabolism. CONCLUSIONS: These results indicate that some but not all of the behavioral effects of ethanol are mediated in part by effects on nAChRs that include the alpha7 subunit and may help to explain the robust association between alcohol consumption and the use of tobacco.

Acoustic Stimulation↗

PubMed1992

A hypnotic response to dexmedetomidine, an alpha 2 agonist, is mediated in the locus coeruleus in rats.

Dexmedetomidine, the highly selective alpha 2-adrenergic agonist, produces a dose-dependent hypnotic response in rats through a central mechanism. Because the locus coeruleus (LC) contains pathways involved in the maintenance of vigilance and a high prevalence of alpha 2 adrenoceptors, we investigated the role of this brainstem nucleus in the hypnotic response to dexmedetomidine. The experimental model consisted of chronic, stereotactically cannulated rats (n = 157) in which the hypnotic response to dexmedetomidine was assessed by the duration of the loss of their righting reflex. Correct placement of the cannula was confirmed histologically at necropsy. The hypnotic response to dexmedetomidine 0.3-333.3 micrograms administered into the LC increased in a dose-dependent fashion. Dexmedetomidine 6.6 micrograms injected 2 mm lateral to the LC did not cause the animals to lose their righting response. Atipamezole 0.07 micrograms-12 micrograms, a selective alpha 2-adrenergic antagonist, blocked the hypnotic response to dexmedetomidine 6.6 micrograms when both were administered into the LC. Also, atipamezole 0.7-30 micrograms, administered into the LC, blocked in a dose-dependent manner the hypnotic response to intraperitoneal (ip) dexmedetomidine 50 micrograms.kg-1. Atipamezole injected into the LC did not block the hypnotic response to pentobarbital 40 mg.kg-1 ip. Prazosin, an alpha 1-adrenergic antagonist, 4.2 micrograms into the LC or 1.0 mg.kg-1 ip, did not alter the hypnotic response to dexmedetomidine 6.6 micrograms into the LC. The present data suggest that alpha 2-adrenergic receptors in the LC appear to be a major site for the hypnotic action of dexmedetomidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMed1989

Ontogenetic development of ketamine-induced sleeping time and electrocorticographic changes in rats.

Latency to the loss of righting reflex and sleeping time after ketamine were measured in 261 rats aged 7, 12, 18, 25 and 90 days. The sensitivity to ketamine was highest in 7-day-old animals and decreased with age. In the youngest group rats slept after the 20-mg/kg dose whereas not all adult animals lost their righting ability after a dose of 160 mg/kg. Electrocorticographic (ECoG) study demonstrated an age dependence of changes induced by ketamine. The youngest group exhibited only suppression of the originally discontinuous ECoG whereas signs of slow-wave sleep or depression appeared in older rats.

Aging↗

PubMed1994

Pharmacologic evidence that spinal muscarinic analgesia is mediated by an L-arginine/nitric oxide/cyclic GMP cascade in rats.

This study was designed to determine if the antinociception produced by intrathecally (i.t.) administered muscarinic agonists in male Sprague-Dawley rats is mediated by an L-arginine/nitric oxide/cyclic GMP cascade. Seven days after implantation of intrathecal catheters, antinociception was produced with graded doses of (+)-cis-methyldioxolane (CD). The ED50 values for CD in the hot-plate and tail-flick tests were 2.6 and 2.0 nmol, respectively. The corneal and righting reflexes, as well as stepping and negative geotaxic responses, were not affected by CD. Six-minute pretreatment with 50 nmol of the nitric oxide synthase inhibitor L-NG-nitroarginine (NNR) significantly inhibited CD-produced hot-plate and tail-flick antinociception as evidenced by 6-fold shifts to the right of the CD dose-response curves. Coadministration of 150 nmol of L-arginine with NNR reversed the NNR-induced inhibition of the antinociception produced by CD. D-Arginine was without effect. Pretreatment with 500 nmol of the guanylyl cyclase inhibitor methylene blue also antagonized the antinociception produced by CD in both the hot-plate and tail-flick tests. In parallel with CD, coadministration of L-arginine with NMR reversed the NMR-induced inhibition of (+)-muscarine-produced antinociception in both nociceptive tests. Intrathecal administration of buffer, 50 nmol of NNR, 150 nmol of L- or D-arginine or 500 nmol of methylene blue, did not alter nociceptive responses when injected alone. In contrast, i.t. administration of the membrane-permeable cyclic GMP analogs, dibutyryl cyclic GMP and 8-bromo cyclic GMP, produced antinociception in both nociceptive tests when injected alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗

PubMed1990

Hemicerebellectomy and motor behaviour in rats. I. Development of motor function after neonatal lesion.

This study was undertaken to determine the effect of a neonatal hemicerebellectomy (HCb) on the motor development of rats and to determine whether various aspects of motor behaviour were affected to a similar degree. Postnatal development of postural reflexes, locomotion and dynamic postural adjustments was examined during the first four months of life in normal and in neonatal HCbed rats. The results indicate that classes of motor responses are controlled by cerebellar networks to clearly different extents. Emergence of quadruped stance, placing reactions and swimming development were unaffected by neonatal cerebellar lesion. Righting reflexes, cliff avoidance and geotaxic reactions, pivoting and crawling all showed a delayed development although the subsequent recovery was almost complete. The complex postural adjustments required in crossing a narrow path or in suspending on a wire remained permanently impaired. Finally, some behaviours developed normally and only subsequently became defective. This "growing into a deficit" was displayed by the progressively reduced hindlimb grasping and the development of a vestibular drop response with a directional bias. An impressive finding was the shifting of postural asymmetries from the lesion side to the contralateral one occurring around the third postnatal week. These data providing a description of the effect of HCb on motor development are interpreted as indicating a progressive involvement of the archi- and neo-cerebellar structures in the motor function of the rat.

Animals↗

PubMed2003

Brain injury and neurofunctional deficit in neonatal mice with hypoxic-ischemic encephalopathy.

Birth asphyxia accounts for the majority of developmental motor and cognitive deficits. Studies were undertaken to develop a reproducible murine model of perinatal hypoxic-ischemic encephalopathy (HIE) which would permit both anatomic and neurofunctional quantification of injury. Short-term neurofunctional outcomes consisted of three developmental reflexes (righting, cliff aversion and geotaxis) assessed in 7-day-old mouse pups 24 h after unilateral carotid artery ligation followed by inhalation of 8% oxygen. Cerebral infarct volume was dependent on duration of hypoxia, being approximately 2.5-fold greater with longer (60 min) versus shorter (30 min) hypoxia exposure (P=0.001). All three sensorimotor neonatal reflexes assessed at 24 h after HIE injury correlated significantly with long-term neurofunction evaluated using a water-maze test of navigational learning and memory assessed 8 weeks later in the same animals. Cerebral atrophy, a delayed consequence of HIE in this model, also correlated strongly with water-maze performance (r=0.86, P=0.002). These data demonstrate for the first time that murine neonatal sensorimotor reflex performance can be rigorously quantified in the acute phase of perinatal HIE and has strong predictive value not only for anatomic extent of cerebral injury, but also for long-term neurofunctional outcome.

Animals↗

PubMed1992

[MRI findings of brain-stem tuberculoma in a case of tuberculous meningitis].

A 54-year-old woman developed headache and slight fever. When she consulted a physician, she could not move either of her eyes to the right. Cranial CT scan revealed no significant findings. Lumbar puncture was performed and CSF examination showed the cell count of 10,304/mm3, glucose level of 10 mg/dl, and total protein value of 270 mg/dl. Her symptoms and laboratory findings suggested meningitis and she was admitted to our hospital. Neurological examination revealed bilateral dilated pupils with sluggish light reflex, right gaze palsy, and hypesthesia of the left side of her face. A diagnosis of tuberculous meningitis was established by a positive test for acid-fast bacillus in CSF, and anti-tuberculous therapy was started at once. One month after the onset of symptoms, her main complaints were double vision and cerebellar ataxia. Both CT and MRI revealed a right brain-stem lesion. Pre-contrast CT could not clearly visualize the lesion but with contrast medium a homogeneously-enhanced circular lesion was shown. MRI on T2WI demonstrated the right brain-stem lesion to have a central bright core with hypointense periphery, which in turn was surrounded by hyperintensity. The lesion appeared isointense with cerebral white matter and the "central bright core" area was demonstrated to be slightly hypointense on T1WI. On post-contrast T1WI (with Gd-DTPA), the lesion showed strong homogeneous enhancement. The CT and MRI findings indicated a brain-stem tuberculoma, which was regarded as the cause of the ocular movement paralysis and cerebellar ataxia. As the clinical symptoms gradually resolved with anti-tuberculous treatment, the MRI appearance of the lesion also improved.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Diseases↗

PubMed1993

Assessing the neurotoxic potential of methyl ethyl ketoxime in rats.

The potential of methyl ethyl ketoxime (MEKO) to produce neurotoxicity following acute and subchronic exposure was studied in rats. A Functional Observational Battery, assessment of motor activity, and neuropathology evaluations were conducted in the context of acute and subchronic toxicity studies. Three independent studies are reported: a pilot time-effect study designed to determine the time course and time to peak effect following a single high dose of MEKO, a single-dose neurotoxicity study, and a subchronic (13-week) repeated-dose neurotoxicity study in rats. An acrylamide-positive control group was included in the acute and subchronic studies for comparison with MEKO. Following an acute oral exposure of MEKO at a dose level of 900 mg/kg, locomotor activity was decreased compared to control with maximum decreases occurring between 30 and 60 min following oral administration. In the acute study, transient treatment-related changes in ease of cage removal, ease of handling, and in posture and gait were observed 1 hr after dosing with 900 mg/kg MEKO, as were significant depressions in motor activity. Following a single 300 mg/kg dose, transient MEKO-related changes in gait and aerial righting reflex were noted 1 hr after dosing. All effects were reversible within 24 hr of dosing. The single 100 mg/kg dose of MEKO was without observable effects. No acrylamide-related behavioral effects were noted following a single 50 mg/kg dose. In the subchronic study, transient treatment-related changes in ease of cage removal, ease of handling, and in posture, gait, and aerial righting were observed at the 400 mg/kg/day dose level when assessments were conducted immediately after dose administration. No consistent behavioral effects were observed prior to daily dose administration even after 13 weeks of exposure, indicating a lack of cumulative behavioral effect. No consistent behavioral changes were noted at doses of 125 mg/kg/day and below. Significant dose-related decreases in red cell mass, and increases in methemoglobin levels, reticulocyte, leukocyte, Heinz body counts, and spleen weights occurred at subchronic MEKO doses of 40 mg/kg/day and higher. No MEKO-related neuropathological changes occurred. Animals receiving acrylamide at 20 mg/kg/day showed expected behavioral and neuropathological changes consistent with peripheral neuropathy. In conclusion, high doses of MEKO can produce transient and reversible changes in neurobehavioral function consistent with central nervous system (CNS) depression. No evidence of cumulative neurotoxicity was detected. The hematopoietic system was effected at doses which did not produce detectable changes in CNS function.

Animals↗

PubMed1988

[Ability of the opiate kappa-agonist bremazocine to facilitate the flexor reflex of the right hindlimb in spinal rats].

It has been found that bremazocine predominantly enhances the flexor reflex of the right hind limb, without affecting the left limb. The similarity of the visual data measuring the asymmetry of the pose and the asymmetry of EMG responses to painful stimulation has a high probability. No correlation between the asymmetry of the pose and EMG extensor activity has been found.

Analgesics↗

PubMedDate not supplied

Toxicity of phencyclidine and ethanol in combination.

The role of ethanol in phencyclidine-related death and loss of motor co-ordination was studied in male ICR albino mice. LD50s, and ED50s for loss of righting reflex, and for the "rotarod" test were determined for each drug in the presence of various doses of the other. Isobolograms (plots of equieffective dose combinations) of these LD50s and ED50s showed that low doses of ethanol reduced the LD50 of phencyclidine (PCP) by about 20%, while higher doses (1-3 g/kg) of ethanol were without further effect. In contrast to effects on lethality, there was synergism (potentiation) of loss of motor co-ordination. Doses of ethanol above 1 g/kg reduced the ED50 of PCP for loss of righting from about 60 mg/kg to 1-3 mg/kg. Similarly, low doses of PCP (less than 40 mg/kg) reduced the ED50 of ethanol from 3 g/kg to 1 g/kg. There was a slight but consistent synergism between the drugs in the rotarod test over the range of effective doses (0.25-2.0mg/kg PCP and 0.1-1.2 g/kg ethanol). It is concluded that consumption of ethanol does not greatly increase the risk of death from PCP overdose; however the severe adverse effects on motor co-ordination of moderate doses of PCP together with moderate doses of ethanol are greatly potentiated by doses of the other drug. It is estimated that commonly used doses could result in total loss of motor ability, which could explain the prevalence of accidental deaths (especially drowning) when PCP and ethanol have been consumed together.

Animals↗

PubMedDate not supplied

Complete recovery from fulminant hepatic failure with severe coma by living donor liver transplantation.

In Japan, living donor liver transplantation has been established as a therapeutic strategy for the rescue of terminal liver disease, including fulminant hepatic failure that shows no signs of recovery. We performed living donor liver transplantation for a subacute type fulminant hepatic failure patient, who had developed a hepatic coma of grade V (no right reflex, no response to pain stimuli). The electroencephalogram indicated almost flat waves. However, cranial computed tomography revealed that brain edema was not severe in this case. The recipient did not have hepatitis virus and had not taken medication that had been determined to cause hepatitis. The recipient was a 12-year-old boy, 165.5 cm in height and 45.5 kg in weight. The donor was his mother, who was 42 years old; her blood type, type B, was identical to that of the boy. The mother's right hepatic lobe was transplanted to her son (the recipient). The post-transplantation condition of recipient was quite excellent. He recovered consciousness 3 days after liver transplantation, and rapidly attained normal hepatic function. The donor was discharged on the 20th postoperative day without any problems. The recipient was discharged on the 79th postoperative day without any neurological deficits. This case suggests that deep coma without electroencephalogram waves may not be a contraindication for living donor liver transplantation in fulminant hepatic failure patients, if the brain edema is not severe.

Adult↗

PubMed2000

Cognitive impairment and synaptosomal choline uptake in rats following impact acceleration injury.

Traumatic brain injury is well known to cause deficits in learning and memory, which typically improve with time. Animal studies with fluid percussion or controlled cortical impact injury have identified transient disturbances in forebrain cholinergic innervation which may contribute to such cognitive problems. This study examines the extent to which water maze performance and forebrain synaptosomal choline uptake are affected one week after injury using the newly developed impact acceleration injury model. Injury or sham injury was delivered to adult male Sprague-Dawley rats under halothane anesthesia using a 500-g 2.1-m weight drop. Based on righting reflex, injured rats were divided into moderate (< or = 12 min) or severe (>12 min) groups. Water maze testing was performed on days 5-7 postinjury. On day 7, choline uptake was determined in synaptosomes from hippocampus, a parietal cortex, and entorhinal cortex. Maze learning was severely impaired in the severe injury group but not in the moderate injury group. Learning retention was slightly impaired in the moderate injury group and severely affected in the severe injury group. There was a very strong correlation between the severity of injury as determined by prolongation of righting times and disruption of maze learning at 1 week postinjury. There was no change in synaptosomal choline uptake in any of the forebrain regions in the severe injury group, but a slight (14%) decrease in the hippocampus and parietal cortex of the moderate injury group. Correlation analysis showed no relationship between synaptosomal choline uptake in any brain region and performance in either water maze learning or retention. This study shows that the impact acceleration model produces cognitive impairments equivalent to those seen with fluid percussion injury and controlled cortical impact. Compared with those models, the impact acceleration model does not produce a similar disruption of forebrain cholinergic nerve terminals.

Acceleration↗

PubMed1994

Post-freeze recovery of peripheral nerve function in the freeze-tolerant wood frog, Rana sylvatica.

We investigated the restoration in peripheral nerve function and simple neurobehavioral reflexes in the freeze-tolerant wood frog (Rana sylvatica). Thirty-two specimens, allowed to freeze for 39 h and ultimately cooled to -2.2 degrees C, were sampled at various time intervals up to 60 h after thawing at 5 degrees C was initiated. The sciatic nerves of treated frogs were initially unresponsive to stimulation, but usually regained excitability within 5 h. Except for a slight reduction in nerve excitability, characteristics of the compound action potentials of treated frogs were indistinguishable from those of control frogs. Recovery times for the hindlimb retraction and righting reflexes were 8 h and 14 h, respectively. Concentrations of the cryoprotectant glucose increased 8.2-fold in the sciatic nerve and 10.5-fold in the underlying semimembranosis muscle of treated frogs, and remained elevated for at least 60 h after thawing was initiated. These organs lost 47.2% and 15.9%, respectively, of their water during freezing, but were rehydrated within 2 h of the onset of thawing. The accumulation of glucose and the withdrawal of tissue water apparently are cryoprotective responses which enable this species to survive freezing.

Action Potentials↗

PubMed2005

Genetic dissociation between ethanol sensitivity and rapid tolerance in mouse and rat strains selectively bred for differential ethanol sensitivity.

BACKGROUND: The Inbred Long- and Short-Sleep mice (ILS and ISS) and the Inbred High- and Low-Alcohol-Sensitive rats (IHAS and ILAS) were selectively bred for differential alcohol sensitivity with use of the duration of loss-of-righting-reflex test (LORR), with the IHAS and ILS animals being much more sensitive than the ILAS and ISS animals, respectively. The current study was undertaken to determine whether acute sensitivity in these strains is genetically correlated to a rapid tolerance to alcohol, a form of tolerance that is evident 24 hr after a single alcohol dose. METHODS: Separate groups of animals were administered a single pretreatment dose of alcohol (0-6 g/kg for the mice; 0-4 g/kg for the rats). Alcohol sensitivity was tested 24 hr later with the LORR test, and blood ethanol concentration was tested at regain of righting (BECRR). Alcohol-induced hypothermia also was determined in the mice. Independently derived replicate rat strains were used for all experiments (IHAS1, ILAS1; IHAS2, ILAS2); no such replicates exist for the ILS and ISS strains. RESULTS: Alcohol pretreatment caused a dose-dependent decrease in LORR duration accompanied by an increase in BECRR in the ILS strain, but LORR increased in the ISS strain with no effect on BECRR. Both strains became hypothermic during the LORR test on day two, but the only significant effect of alcohol pretreatment was in the ISS strain, in which alcohol-induced hypothermia was enhanced. Alcohol pretreatment caused a significant dose-dependent decrease in LORR duration accompanied by an increase in BECRR in the IHAS1 but not in the IHAS2 strain. In contrast, ILAS1 and ILAS2 strains both showed a significant increase in LORR duration and also a significant increase in BECRR. CONCLUSIONS: Alcohol pretreatment caused a dose-dependent decrease in LORR duration and an increase in BECRR in the IHAS1 and ILS strain, suggesting the development of functional rapid tolerance. In contrast, LORR duration increased in the ILAS1, ILAS2, and ISS groups, but BECRR either increased (ILAS1, ILAS2) or did not change (ISS). These observations suggest that central nervous system sensitivity was decreased in the ILAS1 and ILAS2 groups (i.e., rapid functional tolerance) or unchanged in the ISS strain, but that some pharmacokinetic property also was altered in these strains. Overall, the results do not support a genetic relation between alcohol sensitivity and the development of rapid tolerance.

Alcoholism↗

PubMed2006

Neurodevelopmental effects of perinatal fenarimol exposure on rats.

Knowledge about the potential toxic effects of fenarimol, a widely used fungicide, is still limited. Fenarimol is an aromatase inhibitor and therefore can affect estrogen/androgen levels in vivo in rodents. In view of these facts, the aim of the present work was to study the effects of fenarimol maternal exposure during different critical phases in the development of central nervous system in rat pups, on early physical and neurobehavioral endpoints essential to their development. For that, the effects of the fungicide fenarimol (150 and 300 mg/kg) were examined at three different developmental stages in the rat: during the first 6 days of gestation, prenatal (15-21 days), or first 6 days of lactation. Three categories of the impact of fenarimol on neonatal growth and neurobehavioral development of offspring were assessed: (1) physical, (2) reflex and strength, and (3) motor coordination. Findings on the pups' physical development did not indicate any significant alterations of the postnatal age at which specific developmental milestones were observed (pinna detachment, development of the fur, eruption of the incisor teeth, opening of the ears and eyes and testes descent). However, there was a reduced rate of weight gain in pups of mothers treated during lactation related to the earlier testing time periods (1-23 days of life). The study of the functional state of the rat pup nervous systems at different stages of postnatal development revealed some neurodevelopmental delays in righting reflex, climbing and grip response and locomotion (20-90 days of life) in the treated groups. Taken together, findings of this study emphasize that, as a result of fenarimol maternal exposure, some neuromuscular and behavioral deficits in nursing pups may occur principally during the last gestational period and lactation. These results could be the basis for further studies on molecular actions of fenarimol in order to predict better the biological consequences of this fungicide.

Abnormalities, Drug-Induced↗

PubMed2000

The use of sevoflurane in a 2:1 mixture of nitrous oxide and oxygen for rapid mask induction of anaesthesia in the cat.

An inhalational technique for rapid induction of anaesthesia in unsedated cats using sevoflurane and nitrous oxide is described. Using a pliable, tight-fitting, face mask, sevoflurane (7.5-8%) was delivered from an out-of-circuit precision vaporiser connected to a coaxial non-rebreathing system using a fresh gas flow of 1 l oxygen and 2 l nitrous oxide per min. Cats were restrained with gentle but firm pressure applied by scruffing the dorsal cervical skin until the righting reflex was lost and the patient could be positioned in lateral recumbency. Typically, cats could be positioned on their side in a light plane of anaesthesia within 1 min of applying the mask, at which time the sevoflurane concentration was reduced to 5% or less. A similar protocol, using a lower initial concentration of sevoflurane, is recommended for old or debilitated patients. Maintenance of light sevoflurane (2-4%) anaesthesia by mask permitted minor interventions to be performed readily, including blood collection, intravenous chemotherapy, abdominal palpation, radiography and ultrasonography. More painful procedures, such as bone marrow aspiration, required a deeper plane of anaesthesia. Cats were sufficiently deep to be intubated, if this was required, about 3 min after commencing the induction. Recovery from sevoflurane/nitrous oxide anaesthesia was smooth and rapid, with most cats being able to right within 5 min of discontinuing the agents. This protocol for rapid inhalational induction and recovery is particularly suited to feline practice, where rendering an uncooperative patient unconscious greatly facilitates the completion of many minor diagnostic and therapeutic procedures, especially when these must be performed on successive days or when peripheral vascular access is limited. For longer procedures, isoflurane may be substituted for sevoflurane for maintenance of anaesthesia in order to minimise cost.

Anesthesia Recovery Period↗

PubMed1983

Sleeping times evoked by alpha adrenoceptor agonists in two-day-old chicks: an experimental model to evaluate full and partial agonists at central alpha-2 adrenoceptors.

The ability of a series of alpha adrenoceptor agonists to induce a sleep-like state (as measured by the time interval between the loss and regaining of the righting reflex) has been assessed in 2-day-old chicks in order to understand their pharmacological profile better. Guanabenz, guanoxabenz, UK-14,304, guanfacine and xylazine produced dose-related increases in sleeping time, the highest dose of these agonists causing the chicks to sleep for over 120 min. In contrast, the dose-response curves to tiamenidine and clonidine were flatter and bell-shaped with maxima of 30 and 60 min, respectively. The effects of all these compounds were antagonized by idazoxan (RX781094) and yohimbine (two selective alpha-2 adrenoceptor antagonists) but were moderately enhanced or unaffected by prazosin (a selective alpha-1 adrenoceptor antagonist) confirming that the state of arousal in chicks can be depressed by stimulation of alpha-2 adrenoceptors. In particular, idazoxan displaced significantly the guanoxabenz dose-response curve to the right without affecting its slope and apparent maximum and blocked the sleep induced by clonidine. However, idazoxan failed to affect the sleep evoked by ethanol, etorphine or pentobarbital. Naloxone antagonized the effects of etorphine but not those of guanoxabenz, ethanol or pentobarbital. The relatively selective alpha-1 adrenoceptor agonist, cirazoline, given in doses up to 20 mg/kg i.m., produced in chicks behavioral manifestations suggestive of enhanced arousal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗