Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten clinically intact weaned piglets were experimentally intoxicated by intravenous injection of lipoproteide-free lipopolysaccharide endotoxin according to Westphal of E. coli O 127:B8. Severe endotoxin shock with all clinical manifestations of experimental coli-enterotoxaemia was induced in all animals and included circulatory disorder with tachycardia, intermittent pallor and/or cyanosis, symptoms of severe systemic intoxication, neurological symptoms, such as lack of coordination, hindleg staggering, spasm, paresis, paralysis, changes in respiration, such as rise in respiratory frequency and deepened breathing premortal deceleration of respiration and gasping for breath, temperature, variation, including hyperthermia and aggravating hypothermia, gastro-intestinal symptoms, such as temporary vomiting and persistent diarrhoea, leucopenia, eosinopenia, variation of haematocrit, edematisation, increased transudation, congestion, and gastro-intestinal shock lesions. Eight animals died. These experiments quite obviously have confirmed that endotoxin shock is the common pathogenetic principle behind all forms of coli-entertoxaemia (i.e, the forms of edematisation, cardiovascular failure, and gastro-intestinal processes.) Lipopolysaccharide endotoxin alone may be responsible for the development of both edemas and neurotoxic symptoms (edema disease) and diarrhoea (gastro-intestinal form of coli-enterotoxaemia). The pathogenetic relevance of additional toxins (neurotoxin and enterotoxin) is discussed under this aspect.
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PMID:[Experimental studies on the pathogenesis of Coli-enterotoxemia in swine. 4. Effect of lipopolysaccharide endotoxin on weaned piglets following parenteral administration]. 33 9

In experiments with white rats, chlorpromazine, diazepam and imirpramine injected intraperitoneally in the dose of 20 mg/kg and imipramine and diazepam in the dose of 50 mg/kg did not enhance the acute toxicity of ethanol expressed as LD50. Only chlorpromazine in the dose of 50 mg/kg i.p. increased toxicity of ethanol. However, the aforementioned drugs intensified the central action of ethanol by prolonging (except imipramine) duration of narcotic sleep and motor incoordination, and potential ethanol-induced hypothermia.
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PMID:The influence of chlorpromazine, diazepam and imipramine on the central action of ethanol. 61 4

Feruloyltyramine (FT), a new amide compound, together with p-coumaroyltyramine (p-CT) was isolated and identified in ethanol extract of cannabis seeds. FT and p-CT were also detected in the roots, leaves and resin of Cannabis sativa L. The intracerebroventricular injection of these amides caused hypothermia and motor incoordination in mice, and the maximal effects were caused 160 to 240 min after the injection. Furthermore, p-CT also exhibited cataleptogenic effect in mice, although FT did not show any effect. These results suggest that these amide compounds may be responsible for some pharmacotoxicity of marihuana.
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PMID:Analysis and pharmacotoxicity of feruloyltyramine as a new constituent and p-coumaroyltyramine in Cannabis sativa L. 180 39

In adult male Sprague-Dawley rats kept at an ambient temperature of 23-25 degrees C, ethanol was injected intraperitoneally in a dose of 4.0 g/kg to produce a clear-cut impairment of autonomic and motorial functions. Following the injection of ethanol, motor coordination, measured on a rotorod, behavioral sleep, righting reflex and colonic temperature were monitored at predetermined intervals for 5.0-7.0 hr. In the first experiment, either 1.0 mg/kg RO 15-1788 (flumazenil), a benzodiazepine (BZ), receptor antagonist, or 1.0-5.0 mg/kg diazepam, a classical benzodiazepine receptor agonist, were injected intraperitoneally either alone or concurrently with ethanol's administration. In the second study, either RO 15-1788 (1.0 or 2.0 mg/kg) or diazepam (1.0 or 5.0 mg/kg) was injected at the nadir of the fall of body temperature induced by ethanol. Although RO 15-1788 alone failed to affect the rats' temperature, it did not prevent the characteristic ethanol-induced hypothermia but rather potentiated it in a dose-dependent manner. Further, this BZ receptor antagonist exacerbated motor incoordination and other behavioral effects when given either simultaneously with ethanol or at the nadir in the animals' core temperature. Although diazepam evoked a dose-dependent hypothermia, it did not enhance ethanol-induced hypothermia when both drugs were administered simultaneously. However, diazepam augmented motor incoordination and other effects and served to delay their recovery. When given to the rats at the nadir of ethanol hypothermia, diazepam did not potentiate ethanol's thermolysis but retarded the recovery from hypothermia; it caused also a dose-dependent delay in the recovery of motor coordination and other responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential actions of RO 15-1788 and diazepam on poikilothermia, motor impairment and sleep produced by ethanol. 221 22

In the early 1970's, calcium ions were implicated in the mechanism underlying the perturbation of the "set point" for body temperature produced by a thermolytic drug. Since Ca++ is thought to be involved in the incapacitating effects of ethanol on body temperature and motor coordination, this investigation sought to compare the differential central actions of a Ca++ chelating agent with those of a Ca++ channel antagonist on ethanol-induced poikilothermia and motor functions. A chronically indwelling cannula for intracerebroventricular (ICV) injection was implanted stereotaxically in each of 25 adult male Sprague-Dawley rats. Following postoperative recovery, each rat was given ethanol in a 20% v/v solution by the intraperitoneal route in a dose of 4.0 g/kg, which was selected to insure a clear-cut impairment of autonomic and motorial functions. Colonic temperature, behavioral sleep, righting reflex and degree of motor coordination on a rotorod were monitored at selected intervals for 5.0-7.0 hr after the injection of ethanol. Two experimental designs were used: First, either 12.5, 25 or 50 micrograms ethyleneglycol-bis-(beta-amino ethyl ether) N,N'-tetra-acetic acid (EGTA), or 25 or 50 micrograms verapamil, both dissolved in an artificial CSF vehicle, were infused ICV at the same time as ethanol's administration. In the second design, the compounds were infused at the nadir of the ethanol-induced temperature decline. EGTA infused ICV in the rat together with ethanol produced a dose-dependent inhibition of ethanol hypothermia and a more rapid recovery of the animal's righting reflex, arousal and motor coordination than that following ethanol alone. Although verapamil infused ICV in the 50 micrograms but not 25 micrograms dose minimized the poikilothermic response to ethanol, it was not as efficacious as that of EGTA. When infused ICV at the point of maximum fall in the rats' temperature. EGTA entirely reversed the hypothermia induced by ethanol and evoked a thermogenic response in the rat. In contrast, verapamil infused ICV in the same doses tended only to retard the further decline in the animal's body temperature. Similarly EGTA was far more effective than verapamil in ameliorating the other physiological actions of ethanol in terms of the reversal of areflexia, behavioral sleep and motor incoordination. These results suggest that the characteristic attributes of membrane Ca++ in terms of its binding and other neuronal properties play a significant functional role in the incapacitating action of ethanol on the diverse physiological processes mediated by the brain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alcohol-induced poikilothermia, sleep and motor impairment: actions on brain of EGTA and verapamil. 251 53

The ability of the GABA(B) receptor antagonist, phaclofen to alter behavioral effects of ethanol was evaluated by loss of righting reflex (sleep time), motor incoordination (bar holding), spontaneous locomotion (open field activity) and hypothermia. Pretreatment with phaclofen significantly decreased the effects of ethanol on motor incoordination, locomotor activity and hypothermia. However, phaclofen had no effect on either pentobarbitalor diazepam-induced motor incoordination. Phaclofen slightly increased the ED50 for loss of the righting reflex but did not alter either the duration of reflex loss produced by ethanol or blood ethanol levels at awakening. Our results suggest phaclofen is rapidly inactivated resulting in difficulty in observing antagonism of long duration ethanol effects. These findings suggest that the GABA(B) system may play a role in mediating several important actions of ethanol.
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PMID:A new alcohol antagonist: phaclofen. 255 16

In 45 newly-weaned 3 to 4-week-old piglets, diarrhoea was induced by a combined infection with transmissible gastroenteritis (TGE) virus and enterotoxigenic E. coli (ETEC) strains. In untreated control animals this dual inoculation resulted in profuse diarrhoea, vomiting, hypovolaemic shock and death of 77% of the animals within five days of TGE virus inoculation. Antisecretory drugs were administered intramuscularly for three consecutive days after experimental infection. The neurolepticum chlorpromazine, at 2 mg/kg/24 h, resulted in a significant inhibition of diarrhoea and vomiting, and in an increase in weight gain and survival. Sedation and hypothermia, however, were serious side-effects. The alpha 2 agonist clonidine, at 80 micrograms/kg/12 h, induced a significant antidiarrhoeal effect and a reduction in mortality. The drug, however, provoked decreased activity of alpha 2-adrenergic excitation and incoordination. The beta-adrenergic antagonist propranolol, at 0.33 mg/kg/8 h, and the calcium channel blocker verapamil, at 2 mg/kg/8 h, had no beneficial effect on the experimentally induced diarrhoea.
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PMID:Effect of antisecretory drugs on experimentally induced weanling diarrhoea in piglets. 267 57

Three behavioral tests, namely, runway activity, horizontal dowel test and hypothermia, were used to compare the effects of Ro15-1788, a specific benzodiazepine antagonist, on the common neuropharmacological actions of chlordiazepoxide (CDP) and ethanol in C57BL/6J mice. Ro15-1788 completely reversed the CDP-induced inhibition of runway activity and incoordination on a horizontal dowel, but only partially antagonized the hypothermic effects of CDP. The latter phenomenon was likely to be due to the rapid elimination of Ro15-1788, but could also be due to the fact that hypothermia might not be a specific action of CDP. The sedative actions of ethanol were not antagonized at all by Ro15-1788. In fact, Ro15-1788 potentiated the incoordinating effect of ethanol as determined by the horizontal dowel test such that mice injected with Ro15-1788/ethanol had lower brain ethanol levels than mice injected with vehicle/ethanol when they fell off the dowel. In contrast, mice injected with Ro15-1788/CDP took longer to fall off and had significantly higher CDP levels at fall-off than mice injected with vehicle/CDP. The stimulatory effect of a low dose of ethanol on runway activity was reversed by Ro15-1788. These data are discussed in terms of the possible mechanisms of actions for CDP and ethanol.
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PMID:Differential effects of Ro15-1788 in actions of chlordiazepoxide and ethanol. 283 50

The establishment of, and sex differences in, physical dependence on methaqualone (MQ) in rats were studied by the drug-admixed food (DAF) method. Female and male rats were treated with MQ-admixed food on the same schedule of gradually increasing doses (0.5 and 1 to 6 mg of methaqualone/g of food). Only female rats showed hypothermia from MQ at 1 and 2 mg/g and motor incoordination from MQ at 4 and 6 mg/g of food. Moreover, after MQ withdrawal, severe withdrawal signs, including convulsions and death, were observed in female rats, but not in male rats. We also instituted a different schedule of graded increases in dose (1 and 2 to 10 and 12 mg/g of food) to develop physical dependence on MQ in male rats. Under this schedule male rats exhibited a hypothermia and severe motor incoordination from MQ 6 and 8 mg/g of food condition. After MQ withdrawal, various severe signs of MQ withdrawal occurred, including tremor, convulsions and death. These results demonstrate that severe physical dependence on MQ in both sexes can be established using the DAF method, and that there are marked sex differences in the physical dependence on MQ.
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PMID:Sex differences in physical dependence on methaqualone in the rat. 317 79

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system. 319 80


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