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PubMedDate not supplied

Brain adenosine modulation of behavioral interactions between ethanol and carbamazepine in mice.

The effect of the anticonvulsive drug carbamazepine on ethanol-induced motor incoordination and loss-of-righting reflex was investigated in male CD-1 mice. The results of the investigation showed that carbamazepine significantly potentiated the motor incoordinating effect of ethanol in a dose-dependent fashion. Although carbamazepine did not alter the onset time, it significantly prolonged the duration of ethanol-induced loss-of-righting reflex. Pretreatment with theophylline significantly attenuated the carbamazepine-induced potentiation of ethanol-induced motor incoordination and loss-of-righting reflex. Results from a blood ethanol study indicated no effect of carbamazepine on the clearance of ethanol. The data suggest the involvement of nonadenosinergic mechanism in carbamazepine-ethanol behavioral interactions which is responsible for the accentuating effects of carbamazepine on ethanol-induced motor incoordination and duration of loss-of-righting reflex.

Adenosine↗

PubMedDate not supplied

Protective action of the serine protease inhibitor N-tosyl-L-lysine chloromethyl ketone (TLCK) against acute soman poisoning.

Soman-poisoned rats display cholinergic crisis, a systemic mast cell degranulation characteristic of anaphylactic reactions and an excitotoxin-like sequential seizure and neuronal degeneration. The protection of guinea pigs from soman lethality by prophylactic administration of the serine protease inhibitor suramin suggests a possible proteolytic component in soman poisoning. The present study tested the effect of N-tosyl-L-lysine chloromethyl ketone (TLCK), an inhibitor of trypsin-like serine proteases, on soman-induced toxic signs (convulsions, righting reflex) and survival time. Nine control guinea pigs receiving 2 x LD(50) (56 microg kg(-1), s.c.) of soman immediately followed by a therapeutic dose of atropine sulfate (17.4 mg kg(-1) i.m.) experienced severe convulsions, and 8/9 lost the righting reflex. Six of these nine animals expired within 65 min; the three remaining animals survived 24 h to termination of the experiment. When a second group of animals were given TLCK (12 mg kg(-1), i.p.) 30 min prior to a 2 x LD(50) soman challenge and atropine-sulfate therapy, 5/9 experienced convulsions and only 3/9 lost the righting reflex. All nine animals survived beyond 4 h, with six surviving to 24 h. Compared with soman controls, prophylaxis with TLCK significantly prevented the loss of righting reflex (P = 0.05) and enhanced 4-h survival (P = 0.005). Although, convulsions were reduced and 24-h survival was improved in TLCK-treated animals, these results were not statistically significant. The protection from soman toxicity by chemically distinct protease inhibitors such as suramin and TLCK suggests a role for pathological proteolytic pathways in soman intoxication.

Animals↗

PubMed1989

Pharmacological and metabolic interactions between ethanol and methyl n-butyl ketone, methyl isobutyl ketone, methyl ethyl ketone, or acetone in mice.

Methyl n-butyl ketone (MnBK), methyl isobutyl ketone (MIBK), methyl ethyl ketone (MEK), and acetone are widely used industrial solvents to which certain groups of workers are exposed. Pharmacological and metabolic interactions between these solvents and ethanol were explored in male CD-1 mice. The effects of these solvents on the duration of ethanol-induced loss of righting reflex and on ethanol elimination in mice were studied. The solvents were dissolved in corn oil and injected intraperitoneally 30 min before ethanol 4 g/kg ip. The four solvents prolonged significantly the duration of ethanol-induced loss of righting reflex when given in the following doses (mmol/kg): MnBK, 3.75 and 5; MIBK, 5; MEK, 5 and 10, acetone, 20 and 40. This prolongation was dose related and increased as the dose of the solvent was increased. The concentrations of ethanol in blood or brain on return of the righting reflex were similar in solvent-treated and control animals, with the exception of the group of mice treated with 40 mmol/kg acetone in which the ethanol concentrations were significantly lower than in control animals. The mean elimination rate of ethanol was markedly reduced in mice treated with MnBK 5 mmol/kg, MEK 15 mmol/kg, and acetone 40 mmol/kg. All four solvents reduced the activity of mouse liver alcohol dehydrogenase in vitro. It is concluded that enhancement of the ethanol-induced loss of righting reflex by these solvents in mice is well correlated to reduced elimination rate of ethanol.

Acetone↗

PubMed1994

Interaction between L-glutamate and ethanol on the central depressant properties of ethanol in mice.

The effect of L-glutamate to alter ethanol-induced central depression was studies in male Swiss-Webster mice. The duration loss of the righting reflex (LORR) was used as a measurement of CNS depression. Mice were injected (IP) with ethanol (4.0 g/kg), which caused them to lose the righting reflex. After mice regained the righting reflex following ethanol injection (IP), they were immediately injected (ICV) with saline or L-glutamate (1, 15, or 25 mumol/kg). L-Glutamate induced a return to the LORR within 60 s after ICV injection of drug. When L-glutamate was administered (ICV) in the absence of ethanol, no significant loss of the righting occurred. In other experiments, DL-2-amino-5-phosphonovaleric acid (APV), a competitive inhibitor of NMDA, was given ICV with L-glutamate in the presence of ethanol. APV did not significantly antagonize the interaction between ethanol and L-glutamate. When bicuculline methiodide, a GABA antagonists, was administered with L-glutamate (ICV), bicuculline methiodide reduced the effect of L-glutamate to produce a return to the LORR in the presence of ethanol. These data indicate the L-glutamate, an excitatory amino acid neurotransmitter, can enhance the central depressant action of ethanol. It appears that an interaction between the GABAergic and glutamatergic systems may be involved in ethanol intoxication.

2-Amino-5-phosphonovalerate↗

PubMed2002

The role of adenosine in the anoxic survival of the epaulette shark, Hemiscyllium ocellatum.

The epaulette shark (Hemiscyllium ocellatum) is among the few vertebrates that can tolerate extreme hypoxia for prolonged periods and, as shown here, anoxia. We examined how anoxia affected this shark's level of responsiveness, concentration of brain ATP and adenosine -- an endogenous neuronal depressant. In addition, we investigated how these variables were affected by aminophylline, an adenosine receptor antagonist. Epaulette sharks placed in an anoxic environment (<0.02 mg O2 l(-1)) lost their righting reflex after 46.3 +/- 2.8 min, but immediately regained vigilance upon return to normoxia. Then 24 h later, the same sharks were injected with either saline or aminophylline (30 mg kg(-1)) in saline and re-exposed to anoxia. In this second anoxic episode, controls sharks showed a 56% decrease in the time taken to lose their righting reflex but maintained their brain ATP levels; conversely, aminophylline-treated epaulette sharks displayed a 46% increase in the time to loss of righting reflex and had significantly lower brain ATP levels. Since anoxia also caused a 3.5-fold increase in brain adenosine levels, these results suggest that adenosine receptor activation had a pre-emptive role in maintaining brain ATP levels during anoxia. Perhaps because adenosine receptor activation initiates metabolic depression, indicated by the early loss of responsiveness (righting reflex), such a mechanism would serve to reduce ATP consumption and maintain brain ATP levels.

Adenosine↗

PubMed1985

Reserpine-induced changes in anesthetic action of fentanyl.

The effect of prior administration of reserpine on fentanyl dose-response curves for loss of the righting reflex and prevention of purposeful movement response to noxious stimulation was studied in rats. It was found that reserpine (5 mg X kg-1, 3 h before the tests) antagonized the effect of fentanyl on purposeful movement response to the tail clamp and, at the same time, strengthened its effect on the righting reflex. As a result, reserpine pretreatment reversed the order of fentanyl potency regarding these two effects. Reserpine changed fentanyl ED50 values for the purposeful movement response from 8.2 to 20.3 micrograms X kg-1 (P less than 0.0001) and for the righting reflex from 20.5 to 13.7 micrograms X kg-1 (P less than 0.0001). The results suggest that reserpine dissociates the analgesic action of fentanyl from its anesthetic action, defined as a loss of the righting reflex. This may be regarded as an indication that the analgesic action of narcotics may not adequately reflect their anesthetic potency.

Analgesics↗

PubMed1994

Perturbation of ion channel conductance alters the hypnotic response to the alpha 2-adrenergic agonist dexmedetomidine in the locus coeruleus of the rat.

BACKGROUND: The alpha 2-adrenergic agonists are members of a novel class of hypnotic-anesthetic agents that selectively bind to alpha 2 adrenoceptors in the locus coeruleus (LC) to initiate their pharmacologic action. The postreceptor molecular mechanism of the hypnotic action of alpha 2-adrenergic agonists remains unknown. In this study we addressed the role of conductance through a variety of calcium and potassium ion channels in the hypnotic action of dexmedetomidine in the LC of the rat. METHODS: Cannulas were inserted stereotactically into the LC of halothane-anesthetized rats (n = 318). After at least 48 h, rats were tested for loss of righting reflex in response to administration of the alpha 2-adrenergic agonist dexmedetomidine at a hypnotic (7.0 micrograms LC) or subhypnotic (3.5 micrograms LC) dose. To establish the mediating role of various species of calcium and potassium ion channels in the hypnotic response, rats were pretreated with the following drugs before the administration of dexmedetomidine LC:S(+)202791 (L-type calcium-channel activator), nifedipine and R(-)202791 (L-type calcium-channel blocker), SNX 111 (N-type calcium-channel blocker), SNX 230 (P-type calcium-channel blocker), quinine (calcium-activated and voltage-gated potassium-channel blocker), charybdotoxin (calcium-activated potassium-channel blocker), dendrotoxin (voltage-gated potassium-channel blocker), or glybenclamide (adenosine triphosphate-sensitive potassium-channel blocker). The drugs were used in doses not causing behavioral effects that could have confounded the interpretation of loss of righting reflex. RESULTS: SNX 230 and the dihydropyridines nifedipine and R(-)202791 produced loss of righting reflex in the presence of a subhypnotic dose of dexmedetomidine. The hypnotic-enhancing effects of the dihydropyridines could be blocked with S(+)202791, which also diminished loss of righting reflex in response to dexmedetomidine 7.0 micrograms LC. Quinine, dendrotoxin, and charybdotoxin each attenuated the hypnotic response to dexmedetomidine 7.0 micrograms LC. The hypnotic response to dexmedetomidine was not significantly altered by SNX 111 or glybenclamide. CONCLUSIONS: Inhibition of ion conductance through L- or P-type calcium channels and facilitation of conductance through voltage-gated or calcium-activated potassium channels may be involved in the mechanism of hypnotic action of alpha 2-adrenergic agonists. These changes in ion conductance were capable of producing membrane hyperpolarization and decreasing neuronal excitability. There was no evidence for the involvement of adenosine triphosphate-sensitive potassium channels or N-type calcium channels in the hypnotic response to dexmedetomidine.

Adrenergic alpha-Agonists↗

PubMed2004

Metoclopramide attenuates iminodipropionitrile-induced oxidative stress and neurobehavioral toxicity in rats.

Metoclopramide (MET) has long been used as a neuroleptic and antiemetic drug in clinical practice. Motor impairment and dyskinesia have been reported in some patients following chronic treatment with MET. Occasionally, the adverse symptoms may appear even after acute exposure to MET in more susceptible population (such as elderly individual) or due to concomitant exposure to MET and certain neurotoxins. Iminodipropionitrile (IDPN), a prototype nitrile toxin, has been shown to produce dyskinetic syndrome in rodents. This study reports the effect of concomitant exposure of rats to MET and IDPN on behavioral abnormalities in rats namely excitation, circling and chorea (ECC) syndrome. Four groups of female Wistar rats (aged 3 months) were given MET (0, 10, 40 and 80 mg/kg, i.p., for 11 days) 30 min before IDPN (100 mg/kg, i.p. for 8 days). Two additional groups of rats were treated with either saline (control group) or 80 mg/kg of MET (drug alone group). The animals were observed for neurobehavioral abnormalities including dyskinetic head movement, circling, tail hanging, air righting reflex and contact inhibition of righting reflex. Horizontal and vertical locomotor activities and fore limbs grip strength were also measured. On day 12, the animals were sacrificed and brains were collected for biochemical analysis. MET significantly and dose-dependently protected the animals against IDPN-induced ECC syndrome, motor impairment and deficiency in grip strength. MET also protected the animals against IDPN-induced oxidative stress.

Animals↗

PubMedDate not supplied

Cadmium exposure results in decreased responsiveness to ethanol.

Adult male Sprague-Dawley rats were maintained on an ad lib diet containing 100 ppm cadmium (Group Cadmium-Diet) or a control diet with no added cadmium. On Day 61, all animals (N = 10/group) were challenged with a single hypnotic dose of ethanol (3.5 g/kg IP), prepared from a 20% v/v solution of tap water and a stock solution of 95% ethanol. The latency from the time of the injection until the loss of the righting reflex was recorded, as well as the latency for recovery of the reflex. The results showed a nonsignificant trend for animals exposed to cadmium to lose the righting reflex less rapidly than controls, and Cadmium-Diet animals regained the righting reflex significantly more rapidly than controls. These findings suggest that the pharmacologic effectiveness of ethanol is altered by chronic exposure to dietary cadmium. The implications of these data for other studies of cadmium/ethanol interactions are discussed.

Animals↗

PubMed1981

The indices of potency for intravenous anaesthetics.

In rat experiments, the relative potency an safety of thiopentone, diazepam and etomidate were assessed using different indices of anaesthesia - loss of righting reflex, prevention of movement and heart rate responses to an noxious stimulus. Log-probit dose-response curves for these end-points and for lethal effect were determined. Etomidate proved to be more potent than thiopentone or diazepam; its relative potency figures varied from 5 to 18 with the use of different end-points of anaesthesia. According to the ED50 level of response for the loss of righting reflex and increased of heart rate, diazepam was more potent than thiopentone. At the same time it was less potent in the prevention of movement response. Etomidate has an extremely large standard safety margin (SSM) regarding the loss of righting reflex; with the use of movement response or heart rate response, the SSM for etomidate was close to that of thiopentone. With diazepam, SSM for movement response and heart rate response was negative (anaesthetic dose-response curve partially overlaps the lethal curve); it was positive for the loss of righting reflex. The extreme variability in assessment of relative potency and safety with different end-points of anaesthesia probably indicates that the indices used reflected various components of anaesthesia. It seems likely that for the proper assessment of the potency of intravenous anaesthetics, one index of potency is not sufficient. Several indices of potency corresponding to different components on general anaesthesia must be used.

Anesthesia, Intravenous↗

PubMed1992

Ketamine-induced anesthesia involves the N-methyl-D-aspartate receptor-channel complex in mice.

The role of the N-methyl-D-aspartate (NMDA) receptor-channel complex in ketamine-induced anesthesia was examined in mice. General anesthetic potencies were evaluated on a rating scale, which provided the data for anesthetic scores, loss of righting reflex, sleeping time and recovery time. All drugs were administered intraperitoneally. NMDA (60-300 mg/kg), an NMDA receptor agonist, dose-dependently antagonized the general anesthetic potencies of ketamine at a dose of 100 mg/kg which produced loss of righting reflex in more than 90% of the mice. On the other hand, a high dose of N-methyl-L-aspartate (400 mg/kg), a stereoisomer of NMDA, did not. A dose of 300 mg/kg of NMDA significantly shifted the dose-response curve of ketamine for loss of righting reflex to the right. A high dose of D-cycloserine (200 mg/kg), an agonist at the glycine site on the NMDA receptor complex, slightly but significantly shortened the sleeping time caused by ketamine (100 mg/kg). However, neither a critical subconvulsive dose of kainate (15 mg/kg), a kainate receptor agonist, nor a subconvulsive dose of quisqualate (120 mg/kg), an alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor agonist, reversed general anesthesia induced by 100 mg/kg of ketamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1997

[Sudeck's syndrome. Was Sudeck right?].

Reflex sympathetic dystrophy (RSD) is a syndrome affecting an extremity after a minor trauma or operation. At the moment there is no consensus about the pathogenesis of RSD. In 1942 Paul Sudeck suggested that the signs and symptoms of RSD may be provoked by an exaggerated inflammatory response to injury or operation of an extremity. His theory found no disciples, as most physicians believe that RSD is initiated by an hyperactive sympathetic system. We performed various clinical and experimental investigations, including the effects of antiinflammatory treatment. The results of these studies support the theory of Paul Sudeck.

Animals↗

PubMed2000

Quantitative trait loci affecting ethanol sensitivity in BXD recombinant inbred mice.

BACKGROUND: Genetic and environmental factors contribute to an individual's sensitivity to ethanol, although the exact genes underlying ethanol's effects are not known. Quantitative trait locus (QTL) mapping is one successful method for provisionally identifying genes participating in the mediation of a given behavior. QTL analyses seek to identify associations between a quantitative response and previously mapped marker genes across genetically diverse individuals. Many QTL analyses have been performed in BXD recombinant inbred (RI) strains of mice derived from a cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. METHODS: We conducted a QTL analysis of ethanol-induced loss of righting reflex and ataxia using a panel of 25 BXD RI strains and the progenitors B6 and D2. We measured the duration of loss of righting reflex after injection and blood ethanol concentrations upon regaining of righting reflex. Ataxia was measured as the latency to fall from a vertical screen. RESULTS: Genome-wide QTL analyses correlating strain means with allelic status at >1500 markers identified several associations (p < or = 0.01). These provisional QTLs were on all chromosomes except 2, 5, 12, 13, and X, and several map near potential candidate genes. CONCLUSIONS: These results suggest that ethanol sensitivity is determined by the actions of multiple genes and further suggest their general chromosomal map locations. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.

Alcohol Drinking↗

PubMed1985

Intraseptal microinjections of substance P and analogs potentiate pentobarbital-induced narcosis and depression of hippocampal cholinergic activity.

Intraseptal microinjection of Substance P (SP) has been shown to depress activity in the septal-hippocampal cholinergic pathway in the rat. Pentobarbital also depresses septal-hippocampal cholinergic activity, and a relationship between this depressed activity and pentobarbital-induced narcosis is suggested by a variety of studies. To examine this relationship further, we microinjected SP and its analogs, [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-SP and [D-Pro2, D-Trp7,9]-SP, intraseptally in rats pretreated with pentobarbital, and measured the duration of loss of righting reflex and change in choline uptake in hippocampal synaptosomes. The duration of pentobarbital-induced loss of righting reflex was prolonged and the pentobarbital-induced reduction of hippocampal choline uptake was enhanced by all three drugs. A negative correlation (r = -0.96, P less than .02) was seen between duration of loss of righting reflex and synaptosomal choline uptake. Thus, the two analogs of SP appear to act as SP agonists at the septum, judged by their abilities to potentiate pentobarbital narcosis and reduce septal-hippocampal cholinergic activity. This is in contrast to reported actions of these two analogs as SP antagonists in various peripheral tissues.

Animals↗

PubMed1981

Ethanol-induced changes in tyrosine hydroxylase activity in brains of mice selectively bred for differences in sensitivity to ethanol.

The effects of ethanol on tyrosine hydroxylase (TH) activity in five brain areas were analyzed in two lines of mice selectively bred for their differences in sensitivity to ethanol. Following a 4.1 g/kg dose of ethanol, intraperitoneally, short sleep (SS) mice lose their righting reflex for a duration of 20 minutes and long sleep (LS) mice fail to regain their righting reflex until 120 minutes. A significant increase in TH activity occurred in the striatum, locus coeruleus and frontal cortex in both lines of mice approximately 25 minutes following ethanol administration. A decrease in TH activity occurred in the substantia nigra of SS mice at 5 minutes following ethanol administration. However, there was no significant differences in TH activity in any of these four brain regions between LS and SS mice at any time following ethanol administration. In contrast, hypothalamic TH activity was significantly increased at 25 minutes in the SS mice and at 125 minutes in the LS mice following the administration of ethanol, times which coincided with the regaining of the righting reflex. These data suggest that activation of TH in the hypothalamus of LS and SS mice in response to ethanol is associated with arousal from ethanol induced narcosis.

Animals↗

PubMed2003

Propofol-induced anesthesia in mice is mediated by gamma-aminobutyric acid-A and excitatory amino acid receptors.

UNLABELLED: To elucidate the role of gamma-aminobutyric acid (GABA)(A) receptor complex and excitatory amino acid receptors (N-methyl-D-aspartate [NMDA] and non-NMDA receptors) in propofol-induced anesthesia, we examined behaviorally the effects of GABAergic and glutamatergic drugs on propofol anesthesia in mice. All drugs were administered intraperitoneally. General anesthetic potencies were evaluated using a righting reflex assay. The GABA(A) receptor agonist muscimol potentiated propofol (140 mg/kg; 50% effective dose for loss of righting reflex) induced anesthesia. Similarly, the benzodiazepine receptor agonist diazepam and the NMDA receptor antagonist MK-801 augmented propofol anesthesia, but the non-NMDA receptor antagonist CNQX did not. In contrast, the GABA(A) receptor antagonist bicuculline antagonized propofol (200 mg/kg; 95% effective dose for loss of righting reflex) induced anesthesia. However, neither the benzodiazepine receptor antagonist flumazenil, the GABA synthesis inhibitor L-allylglycine, nor the NMDA receptor agonist NMDA reversed propofol anesthesia. Conversely, the non-NMDA receptor agonist kainate enhanced propofol anesthesia. These results suggest that propofol-induced anesthesia is mediated, at least in part, by both GABA(A) and excitatory amino acid receptors. IMPLICATIONS: We examined behaviorally the effects of GABAergic and glutamatergic drugs on propofol-induced anesthesia in mice. The results suggest that propofol anesthesia is mediated, at least in part, by both GABA(A) and excitatory amino acid receptors.

Anesthesia, General↗

PubMed2002

The effects of NMDA and GABAA pharmacological manipulations on ethanol sensitivity in immature and mature animals.

BACKGROUND: Sensitivity to the hypnotic effects of ethanol dramatically increases with age (Silveri and Spears, 1998). Little is known regarding the neural mechanisms that might underlie this relative resistance of young animals to ethanol. The present study used a psychopharmacological approach to examine the influence of NMDA (N-methyl-D-aspartate) and GABA (gamma-Aminobutyric acid) receptor systems in modulating age differences in ethanol responsiveness between young [postnatal day (P26)] and mature (P70) female and male Sprague-Dawley rats. METHOD: Dose response curves were established for the effects of intraperitoneal (ip) administration of the NMDA antagonist (+)MK-801 (0.75, 1.0, or 1.25 mg/kg), the GABAA agonist muscimol (0.75, 1.25, or 1.75 mg/kg), or saline on loss and regain of the righting reflex and trunk blood alcohol levels following 3.5 g/kg of ethanol. RESULTS: (+)MK-801 increased time to regain the righting reflex at both ages, maintaining the age-related increase in ethanol sensitivity typically observed, although a gender effect also emerged at P70, with females being more sensitive than males to (+)MK-801-induced increases in duration of loss of the righting reflex. In contrast to the across-age similarity in responsiveness to (+)MK-801, P26 animals were considerably more sensitive to muscimol's enhancing effect on ethanol sedation than mature animals. CONCLUSION: Although modulation of either the NMDA or GABA system enhances the sedative effects of ethanol at both ages, stimulation of the GABAA receptor is a more effective means of prolonging ethanol sedation in immature than mature animals.

Age Factors↗

PubMed1981

Behavioural, electroencephalographic and histological study of the protective effect of etomidate against histotoxic dysoxia produced by cyanide.

The acute toxicity of cyanide is largely due to the inhibition of cytochrome oxidase, and the subsequent breakdown of cellular metabolism. Breakdown in cellular metabolism, leading to a disruption of cellular integrity lies at the heart of the permanent neurological damage resulting from ischemic/hypoxic brain insult. In 200 g male Wistar rats treated with 5 mg/kg KCN i.v. and ventilated until spontaneous breathing restarted, the cornea reflex, tail-pinch reaction and righting reflex disappeared for about 20 min. In curarized and artificially ventilated rats the EEG remained flat for a similar period before slowly returning. Saline treated animals which survive the KCN injection die significantly earlier than non-KCN treated animals when injected with 120 mg/kg metrazol s.c. one week later. Histological examination of KCN treated animals revealed swollen mitochondria at 20 min, and microvacuolization and ischemic cell changes at 1 week. In rats pretreated with etomidate 10 mg/kg s.c. 30 min before cyanide the cornea, tail-pinch and righting reflex were absent for the same time as in controls. The EEG was similar to that seen in saline/KCN animals, however, the time to EEG was similar to that seen in saline/KCN animals, however, the time to EEG silence was doubled. One week after the cyanide injection their reaction to the metrazol injection was similar to animals treated one week earlier with saline. Although there was evidence of swollen mitochondria 20 min after KCN, one week after KCN there was no evidence of ischemic hypoxic brain damage. These results demonstrate that under similar conditions of dysoxia, etomidate treated animals appear to be protected from the behavioural and histological sequelae of those conditions.

Animals↗