Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A female child with brachycephaly, hypertelorism, convergent strabismus, interstitial keratitis, analgesia on both sides of the face, absent corneal reflexes, and focal congenital alopecia of a zone of the occipital and posterior parietal scalp is presented. The patient also had generalized hypotonia in early life, and at age 4 years 9 months, she was found to be moderately mentally subnormal and to have severe cerebellar deficit consisting of gait and truncal ataxia. There was no clinical evidence of other cranial nerves being affected. It is postulated that the patient has a cerebellotrigeminal and focal dermal dysplasia due to a development arrest of the ectoderm, which gives rise to the alar plate of the rhombencephalon, the overlying epidermis, the motor nucleus of V, and the trigeminal placodes.
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PMID:Cerebellotrigeminal and focal dermal dysplasia: a newly recognized neurocutaneous syndrome. 9 27

Four pharmacologic actions of intravenous ketamine (30 mg/kg) were studied in the rat. To elucidate the mechanism(s) terminating the pharmacologic effects, animals were pretreated with ketamine and agents anticipated to modify hepatic microsomal metabolism, including phenobarbital and SKF 525A. SKF 525A pretreatment markedly prolonged ataxia, analgesia and agitation, in addition to significantly elevating brain and plasma ketamine levels subsequent to the initial 10 minutes following injection; thus hepatic metabolism appeared to play a prominent role in the termination of the posthypnotic effects of the drug. While significantly shortening the durations of the three posthypnotic events, phenobarbital and ketamine pretreatments also lowered the brain and plasma levels of ketamine. With all pretreatments, brain ketamine levels were almost identical at the cessation of hypnosis (25 mug/g of tissue) and ataxia (8-10 mug/g of tissue). No pretreatment altered either the duration of loss of righting reflex (hypnosis) or brain and plasma ketamine levels during the initial 10 minutes after injection. Approximately 70% of the injected drug was recovered from four tissues, skeletal muscle, gut, skin and liver, at 10 minutes after injection; thus redistribution from brain to other tissues appeared to play a major role in the cessation of hypnosis. Ketamine pretreatment caused a 2-fold increase in the rate of its in vitro hepatic microsomal metabolism. Brain and plasma ketamine levels 30 minutes after injection were nearly identical in rats pretreated with ketamine and phenobarbital, although phenobarbital pretreatment resulted in a 4-fold increase in in vitro ketamine hepatic metabolism.
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PMID:Biodisposition of ketamine in the rat: self-induction of metabolism. 127 Dec 78

Seven drugs administered im were evaluated to determine their efficacy in immobilizing captive agoutis. Ketamine HCl (63-83 mg/kg) and phencyclidine HCl (16.5-22.0 mg/kg) produced immobilization and analgesia. Phencyclidine administration was accompanied by numerous side effects and prolonged recovery. Xylazine HCl (3-70 mg/kg) and fentanyl-droperidol (0.28-1.11 ml/kg( produced varying degrees of ataxia and intermittent recumbency. Acetylpromazine, chlorpromazine, and promazine HCl were ineffective. Surgical anesthesia was successfully induced and maintained with halothane.
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PMID:An evaluation of sedatives and anesthetics in the agouti (Dasyprocta sp). 127 34

Intramuscular (i.m.) and intravenous (i.v.) administration of detomidine at doses of 10, 20 and 40 micrograms/kg body mass was evaluated for its sedative and analgesic properties in 15 goats (Capra hircus). The drug produced dose- and route-dependent sedation. The 10 micrograms/kg dose was effective only when administered i.v. There was no observable analgesia at this dose. Higher doses produced effective sedation and moderate analgesia of the body with either route of administration. Severe ataxia and sternal recumbency were seen in all the animals after the dose of 40 micrograms/kg. Other effects of detomidine in these goats included mild to moderate salivation, depressed respiratory rate, decreased rectal temperature, bradycardia and hyperglycaemia. Plasma concentrations of total protein, sodium, potassium and chloride were not affected.
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PMID:Evaluation of detomidine as a sedative in goats. 178 30

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pharmacologic profile of protirelin tartrate]. 212 84

Effects of physostigmine on ketamine-induced anesthesia and analgesia were studied in male Sprague-Dawley rats using behavioral tests. Rats were divided into six groups. Immediately after loss of the righting reflex following an intraperitoneal injection of ketamine 75 mg/kg, each group of rats was given an intraperitoneal injection of either physostigmine 0.05, 0.1, 0.2, 0.4, 0.6 mg/kg or saline as the control, respectively. Physostigmine 0.1 mg/kg caused the greatest antagonistic effect on ketamine anesthesia as indicated by sleeping time, duration of ataxia and motor coordination. The antagonistic effects of physostigmine were reduced by a dose of physostigmine of greater than 0.1 mg/kg. However, at no dose did physostigmine antagonize ketamine analgesia as indicated by the tail-flick latency. Physostigmine (0.4 and 0.6 mg/kg) itself had analgesic and motor-suppressive actions. It can therefore be presumed that there is a limited threshold of the dose of physostigmine which develops an antagonistic effect on ketamine anesthesia due to the motor-suppressive action. It is also confirmed that physostigmine itself produces analgesia, and does not antagonize ketamine-induced analgesia.
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PMID:Antagonistic effect of physostigmine on ketamine-induced anesthesia. 225 36

The competitive excitatory amino acid antagonist cis-4-phosphonomethyl-2-piperidine-carboxylic acid (CGS 19755) increased the latency for monkeys to remove their tails from warm water (analgesia); larger doses produced ataxia, loss of righting, salivation, and eliminated reactivity to stimulation (anesthesia). CGS 19755 decreased tidal volume and had little effect on frequency of respiration. Although longer lasting, the effects of CGS 19755 were similar to the effects of ketamine, suggesting these effects result from actions at the NMDA receptor complex.
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PMID:Analgesic, anesthetic, and respiratory effects of the competitive N-methyl-D-aspartate (NMDA) antagonist CGS 19755 in rhesus monkeys. 225 91

Xylazine (0.05 mg/kg of body weight diluted to a 5-ml volume, using 0.9% NaCl) or 5 ml of 0.9% NaCl was administered epidurally into the first caudal intervertebral space (Co1-Co2) in 8 cows (mean +/- SD body weight, 583 +/- 150 kg). Cows were observed for responses to deep needle pricking of the caudal dermatomes (S3 to Co), sedation, and ataxia. Heart rate, respiratory rate, body temperature, rate of ruminal contractions, coccygeal arterial blood pressure, pHa, blood gas tension (PaO2, PaCO2), base excess, total solids concentration, and PCV were determined before and after xylazine administration. Epidurally administered xylazine induced sedation and selective (S3 to Co) analgesia for at least 2 hours. Mild ataxia of hind limbs was observed in 6 cows, but all cows remained standing. Heart rate, respiratory rate, rate of ruminal contractions, arterial blood pressure, PaO2, PCV, and total solids concentration were significantly (P less than 0.05) decreased, and PaCO2, base excess, and bicarbonate concentration were significantly (P less than 0.05) increased after xylazine administration. Epidurally administered 0.9% NaCl did not alter sensory perception to needle pricking and did not affect any of the physiologic variables determined. Although epidural administration of xylazine induced analgesia and sedation in healthy cows, it should be avoided for epidural analgesia in cattle with heart disease, lung disease, and/or gastrointestinal disease because of its potent cardiopulmonary and ruminal depressant effects.
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PMID:Caudal epidural analgesia induced by xylazine administration in cows. 238 20

In 1988, the specific benzodiazepine antagonist, flumazenil (Anexate Roche), was introduced in clinical practice in Czechoslovakia for analgesia. A pilot study was initiated to establish whether .1 mg of flumazenil iv was capable of accelerating the psychic recovery of women after abortion. 30 healthy women aged 17-25 received a combination of .1 mg/kg-1 diazepam iv together with .88 mg/kg-1 ketamine iv. Another group of 10 women of the same age range were given .05 mg/kg-1 of midazolam iv. Flumazenil, in a dose of .1 mg iv, was administered to the women following the completion of the procedure, i.e., about 5-7 minutes after giving benzodiazepine. The effect of flumazenil became apparent 30 seconds after iv administration. The hypnotic-sedative effect of benzodiazepine set in after 30-60 seconds, and its biological half-life was 50-60 minutes. After administration of midazolam, an especially strong sedative effect was produced for operative intervention. The psychic effects of ketamine lasted only a little while and no occurrence of psychomimetic symptoms were observed as determined by an orientation test of place, time, and space. Retrograde amnesia was complete during the procedure. Partial amnesia occurred after administration of flumazenil. The lowest flumazenil doses antagonized only the hypnotic and sedative effects of benzodiazepine but did not influence the anxiolytic and amnestic effects. Systolic pressure increased by 10 torr: the pulse rate increased on the average from 74.4 - 84.8 beats/minute. Mild ataxia occurred in women who attempted to get out of bed, but 60 minutes after completion of the procedure, the patients were able to walk without ataxia. It was clearly demonstrated that the sedative-hypnotic effects of benzodiazepine can be subdued after abortion, shortening the period required for the recovery of the patient.
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PMID:[Initial experience with flumazenil (Anexate Roche) for abortion]. 250 17

The intracerebrally administered dynorphin-B produced not only an antinociceptive response but a motor dysfunction such as "barrel-rolling", circling, jumping or ataxia in mice. These two effects were observed in a same dose range. Both responses were also produced by a nonopioid fragment, des-Tyr-dynorphin-B. Bestatin, an aminopeptidase inhibitor, markedly potentiated the antinociceptive response induced by dynorphin-B but not the motor dysfunction. Bestatin did not affect the responses produced by des-Tyr-dynorphin-B. In the presence of bestatin, low doses of dynorphin-B produced an antinociceptive response without the motor dysfunction. Naloxone antagonized the potentiated antinocicpetion but had no effect on the motor dysfunction. These results suggest that dynorphin-B produced an analgesia through opioid receptors and that this peptide also induced a motor dysfunction through a nonopioid receptor.
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PMID:Bestatin potentiates the antinociception but not the motor dysfunction induced by intracerebrally administered dynorphin-B in mice. 256


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