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)

2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol, hydrochloride (JO 1017) is a novel antidepressant drug. Its biochemical and pharmacological properties were investigated in mice, rats, dogs, rabbits and guinea pigs. In vitro, it selectively inhibited serotonin uptake and had a high affinity for the 3H-paroxetine and 3H-imipramine binding sites. Biochemical studies demonstrated the lack of MAO-A and MAO-B inhibition and the absence of marked affinity for muscarinic, histaminic or other conventional brain receptors. Chronic treatment with JO 1017 induced a decrease in the Bmax values for imipramine sites but did not modify the Bmax for beta-adrenergic and 5-HT2 receptors. The neuropsychopharmacological profile of JO 1017 is characterized by a decrease of the immobility times in behavioural despair tests with mice, a decrease of the escape failures in the rat learned helplessness test, a strong potentiation of L-5-HT P-induced head-twitches in mice and an antagonism of reserpine-induced ptosis in rabbits. It weakly antagonized oxotremorine-induced hypothermia and did not influence the hypothermia induced by apomorphine. In contrast to most other antidepressants, a high dose of JO 1017 induced hypermotility in mice placed in an activity meter without producing stereotyped behaviour and group toxicity. Unlike tricyclic antidepressants, JO 1017 was devoid of severe cardiotoxicity in guinea pigs and had no central anticholinergic nor antihistaminic properties. These results suggest that JO 1017 is a selective serotonin uptake inhibitor with a high safety margin. JO 1017 may have a potential clinical utility both in the treatment of depression and for indications where serotonin transmission is involved, e.g., anxiety, panic attack, obsessive compulsive disorder, obesity and alcohol consumption.
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PMID:Biochemical and pharmacological evaluation of the novel antidepressant and serotonin uptake inhibitor 2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol hydrochloride. 216 3

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component. When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 x 10(-3) mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice. These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatobiliary effects of morphine are mediated in the brain. 217 93

Cats are susceptible to poisoning by insecticidal products containing D-limonene, linalool, and crude citrus oil extracts. Signs of toxicosis include hypersalivation, muscle tremors, ataxia, depression, and hypothermia.
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PMID:Toxicology of selected pesticides, drugs, and chemicals. D-limonene, linalool, and crude citrus oil extracts. 218 Jan 84

Behavioural tests for predicting antidepressant activity in the animal provide a closer approximation than other tests of states of depression in man but are often long and costly to perform (except the behavioural despair test). The tests proposed here presuppose a pharmacological interaction (except the Porsolt test) but are simple enough to allow screening: included are antagonism of reserpine hypothermia, ptosis and akinesia; antagonism of effects induced by oxotremorine; antagonism of high-dose apomorphine; and potentiation of yohimbine toxicity. In combination with the study of motor activity in the mouse, these tests allow assessment of the specificity of antidepressant activity by establishing a ratio between the "antidepressant" dose and the "stimulant" or "sedative" dose. It can be predicted that a substance will be antidepressant and sedative or stimulant at the same dose if the ratio is close to 1; if the ratio is less than 1, at antidepressant doses the substance will be very sedative or stimulant according to the case. The specificity of the tests discussed can be debatable. Antagonism of reserpine-induced hypothermia indicates substances with direct or indirect beta-mimetic activity, ptosis antagonism, substances with alpha-adrenergic (not antidepressants) or serotoninergic (possibly antidepressants) activity; and akinesia antagonism, a direct or indirect dopaminergic activity (sometimes found in antidepressants) with psychostimulant activity. The oxotremorine test is related to the anticholinergic activity of substances, except in the case of hypothermia antagonism. The high-dose apomorphine test seems to be specific for substances inhibiting norepinephrine reuptake. The yohimbine test is simple to carry out, relatively inexpensive and does not fail to screen any molecule known to be effective to-date. The behavioural despair test is a good complement for screening except for drugs having a beta-agonist activity, it appears that this test is dependent on functional relationships between alpha 2 and serotonergic systems.
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PMID:Is it possible to predict the activity of a new antidepressant in animals with simple psychopharmacological tests? 218 84

Severe hypothermia is seldom observed in our country due to the mild climate. But it can represent a difficult medical problem. Severe hypothermia occurs when body temperature falls below 28 degrees. The victim may be unconscious with a severe depression of vital functions. All such patients should undergo vigorous cardiopulmonary resuscitation and rapid rewarming. The most efficient methods of rewarming are represented by peritoneal irrigation and esophageal thermal tube.
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PMID:[ Physiopathology and treatment of accidental hypothermia]. 219 48

Clonidine may be a source of serious toxicity when ingested by toddlers. We describe 11 cases of clonidine ingestion by toddlers (mean dose 0.15 mg/kg; range 0.01 to 0.57). The source of the clonidine was a grand-parent in six of 11 cases. Symptoms included altered level of consciousness (n = 11), miosis (n = 5), bradycardia (n = 8), hypotension (n = 5), apnea and respiratory depression (n = 6), hypothermia (n = 5) and hypertension (n = 3). Therapeutic interventions included naloxone (n = 8) and atropine (n = 4), dopamine (n = 1), fluid resuscitation (n = 4), and endotracheal intubation (n = 1). There were no deaths. Symptoms of clonidine ingestion were typically mild if the dose ingested was less than 0.01 mg/kg, while bradycardia and hypotension occurred usually with doses of greater than 0.01 mg/kg. Apnea and respiratory depression were common when the dose exceeded 0.02 mg/kg. More effective measures are needed to prevent these potentially serious intoxications.
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PMID:Critical care for clonidine poisoning in toddlers. 220 40

The aim of this study was to determine whether administration of ethanol protects rats against the preconvulsive symptoms of high pressure nervous syndrome (HPNS). Male Sprague-Dawley rats were given either saline or 0.5, 1.5 or 2.5 g/kg ethanol i.p. After injection, the animals were individually exposed to helium-oxygen at 60 atmospheres absolute (atm abs) pressure. The chamber temperature was adjusted to counteract ethanol- and helium-induced hypothermia. Several behavioral parameters were scored continuously during the first 64 min after injection. The time spent in tremor at high pressure was significantly less in the 1.5 and 2.5 g/kg ethanol-treated groups. The number of jerks was significantly lower in the 2.5 g/kg ethanol-treated group. The two highest doses of ethanol induced a characteristic pattern of unsteady locomotion, which was returned to normal in the 1.5 g/kg group at 60 atm abs. Other behavioral effects of ethanol, such as depression of total motor activity, were also reduced. These results indicate that ethanol can significantly ameliorate some of the adverse symptoms of HPNS in freely moving rats.
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PMID:Interaction of ethanol and the high pressure nervous syndrome in rats. 221 48

A study of acute alcohol influence (heavy drinker) on sudden unexpected death were analyzed as to age, sex, cause of death and along with the lethal blood alcohol content. Excess alcohol abuse by adults or middle aged women causatived acute intoxication with actual toxic depression of brainstem function (high blood levels, means 3,6 mg/g). Others (alcohol abuse) die by drowning, trauma, sudden coronary death (drinking spirits), cardiomyopathy, hypothermia or hypoglycemia (Diabetes). The autopsy findings are discussed.
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PMID:[Cause of death in severe acute ethanol intoxication]. 224 82

Individual sensitivity to alcohol may influence the severity of functional deficits due to prenatal alcohol exposure. To examine this hypothesis, Long-Sleep (LS) and Short-Sleep (SS) mice, selectively bred for differences in ethanol-induced narcosis, were intubated with either 2.9 g/kg ethanol (E) or an isocaloric amount of sucrose (S) twice per day on days 7 through 15 of pregnancy. An untreated control group (C) was maintained for each line. Offspring were fostered to lactating Rockland-Swiss mice at birth. Males and females from each litter were challenged with an acute dose of ethanol (3.8 g/kg) at 30 days of age. Measures of sleep time duration, waking blood ethanol concentrations (BEC), rectal temperatures, heart rate, and ethanol clearance were obtained to examine whether the acute effects of ethanol are altered by prenatal alcohol exposure. Prenatal alcohol exposure did not differentially affect responses to ethanol challenge within either genotype. Ethanol-induced hypothermia, heart-rate depression, and sleep time did differ between genotypes, with LS more affected than SS mice. Ethanol clearance rates were faster for SS than LS mice. These results suggest postnatal pharmacological responses to acute ethanol challenge are not altered by prenatal alcohol exposure in LS and SS mice. Prenatal alcohol-exposed offspring of both mouse genotypes showed lower average heart rate responses than controls, suggesting this measure may be a sensitive indicator of prenatal alcohol effects in mice.
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PMID:Responses to ethanol challenge in long- and short-sleep mice prenatally exposed to alcohol. 231 Apr 99

Cold exposure accelerates the firing frequency of norepinephrine (NE) neurons, enhancing NE release and leading to NE depletion in specific regions of the brain. The accelerated firing activates the enzyme tyrosine-hydroxylase, making it more tyrosine sensitive. The reduction of brain NE is accompanied by a behavioral depression on the open field test. Two experiments were performed on adult male rats. First, it was determined whether systematic lowering of core body temperature produced behavioral depression in the swim test. Second, treatment with the NE precursor tyrosine was employed in an attempt to prevent hypothermia-induced behavioral depression. In Experiment 1, two levels of hypothermia were highly effective in producing behavioral depression in rats forced to swim in a narrow cylinder. In Experiment 2, treatment with tyrosine (400 mg/kg, IP) thirty minutes prior to the hypothermia procedure completely reversed the behavioral depression found in Experiment 1. Tyrosine administration did not significantly influence the rate of deep body cooling during the hypothermia treatment.
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PMID:Tyrosine pretreatment reverses hypothermia-induced behavioral depression. 231 Sep 42


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