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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic morphine treatment has been suggested to cause the development of supersensitive dopamine receptors. This increase in sensitivity was detected as a hypersensitivity in direct-acting dopamine agonists and as an increase in the affinity of dopamine receptors. However, these binding studies were performed in animals which had been withdrawn from morphine for a period of 24-48 h prior to killing. In the present study mice were implanted with pellets containing 75 mg of morphine free base. The pellets were left in situ in all experiments. One group of mice exhibited an increased sensitivity to apomorphine 72 h following pellet implantation as evidenced by a decrease in the ED50 of apomorphine for inducing cage climbing behavior. A second matched group of mice was found to have a significant increase in whole brain [3H]spiroperidol binding sites. These results suggest that chronic morphine treatment can cause the development of central supersensitive dopamine receptors. Lithium administered concurrently with the morphine attenuated the increased sensitivity to apomorphine and the increase in the number of [3H]spiroperidol binding sites. Concurrent lithium treatment also facilitated the degree of analgesic tolerance, and naloxone-induced withdrawal hypothermia. The ability of lithium to enhance analgesic tolerance while simultaneously attenuating the increase in dopamine receptors suggests that alterations in dopamine receptors might modify the degree of analgesic tolerance which develops to chronic morphine administration, or might modify the animal's response to thermal stimuli. The mechanism by which lithium enhanced naloxone-induced hypothermia is presently unknown.
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PMID:Chronically administered morphine increases dopamine receptor sensitivity in mice. 369 94

Pauling and Miller have independently proposed that the presence of an anesthetic gas in tissue induces a cage-like arrangement of hydrogen-bonded water molecules. The theories recognize that most gas-hydrate crystals would not form at the temperature and pressure that exist during anesthesia and propose that other components of tissue such as protein should have a stabilizing effect. Measurements of the behavior of water, rather than the anesthetic agent, would provide alternative information about the likelihood of hydrate crystal formation and this information could be such as to be applicable to body temperature and to pressures used for anesthesia. If the number of hydrogen-bonded water molecules in tissue is increased, then the movement of an average water molecule should be hindered. Movement of water through the tissue may be measured by tagging it with tritium and the anesthetic gas should then slow the movement of tritiated water through the tissue. The flux of tritiated water through rat cecum is indeed slowed when the cecum is exposed to the anesthetic gas, xenon, which can participate biochemically only by virtue of its van der Waals interaction. The decrement in water flux is in reasonable agreement with what could be expected theoretically from calculations based on the activation energy for the self-diffusion of water and the degree of hypothermia necessary to produce narcosis.
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PMID:Anesthetic gases and water structure. The effect of xenon on tritiated water flux across the gut. 572 84

Six receptor blockers were compared in mice for their ability to alter hypothermia induced by the dopamine agonist N-n-propylnorapomorphine (NPA). The dopamine antagonist haloperidol inhibited NPA-induced hypothermia whereas phentolamine, propranolol, sotalol, atropine, cyproheptadine, or naloxone (alpha-adrenergic, beta-adrenergic, muscarinic cholinergic, serotonergic, and opiate antagonists, respectively) failed to inhibit it. The degree of antagonism of the hypothermic effect of NPA induced by haloperidol pretreatment suggests that the hypothermic response may serve as a useful model of specific dopaminergic activity of aporphines. Hypothermia induced by NPA and other aporphines may supplement the measure of aporphine-induced stereotypic cage-climbing previously reported to be specifically dopaminergic.
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PMID:Hypothermic effects of N-n-propylnorapomorphine in mice: antagonism by neurotransmitter receptor blockers. 610 42

The effectiveness of temporal and environmental cues in eliciting conditioned hypothermia and hyperthermia was studied in male Wistar rats using as an unconditioned stimulus an IP injection of 20 mg/kg of morphine sulfate. The relevance of temporal stimuli was minimized in Experiment 1 by administering morphine at irregular times on alternate days. For one group (Cond) morphine injections were preceded and followed by periods in distinctive environments. Group Pseudo animals, though exposed to the environments, received morphine on the intervening days in the home cage; group Saline received only saline. All animals receiving morphine showed a non-specific hypothermia when not under the direct influence of morphine. A "conditioned hyperthermia" was evident in group Cond animals in the distinctive environments. In Experiment 2, in which animals remained in their home cages at all times, the relevance of temporal cues was emphasized by administering morphine at exactly 24 h intervals. These animals became hypothermic only around the time of the expected injection. Animals in another group that received morphine at irregular times showed the non-specific hypothermia seen previously. There was no evidence for a conditioned hyperthermia in this second experiment.
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PMID:Temporal and environmental cues in conditioned hypothermia and hyperthermia associated with morphine. 678 4

Three groups of male Wistar rats received daily IP injections of either 1, 2 or 5 mg/kg amphetamine at 11:15 h; a fourth group received saline injections throughout. Rectal temperature was measured in the home cage, in a pre-injection environment in which animals were placed for a period of time before the daily injection, and in an injection environment in which animals remained following the injection. Conditioned hyperthermia, a response that mimicked the unconditioned effect of amphetamine, was elicited by cues of the injection environment both during conditioning and after the drug-free period. During conditioning, hypothermia occurred at 10:30 h regardless of where the animals were, but could not be elicited at other times of day. The results with amphetamine parallel those found previously with morphine (Eikelboom and Stewart 1979, 1981).
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PMID:Conditioned temperature effects using amphetamine as the unconditioned stimulus. 679 68

Ascorbic acid (100 mg/ml) and sodium bisulfite (0.5 and 20 mg/ml) prevented more than 10% oxidation of apomorphine hydrochloride in water maintained at room temperature over 1-3 days. Refrigeration at 5 degrees prevented oxidation of apomorphine hydrochloride in aqueous solutions for 1 week. Neither ascorbic acid nor sodium bisulfite affected murine stereotyped cage climbing or hypothermia induced by apaomorphine.
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PMID:Stability of apomorphine in solutions containing ascorbic acid and bisulfite and effects of antioxidants on apomorphine-induced cage climbing and hypothermia in mice. 740 Sep 50

Sleep deprivation is associated with poor cognitive ability and impaired physical health, but the ways in which the brain and body become compromised are not understood. In sleep-deprived rats, plasma total T4 and T3 concentrations decline progressively to 78% and 47% below baseline values, respectively, brown adipose tissue 5'-deiodinase type II activity increases 100-fold, and serum TSH values are unknown. The progressive decline in plasma thyroid hormones is associated with a deep negative energy balance despite normal or increased food intake and malnutrition-like symptoms that eventuate in hypothermia and lethal systemic infections. The purpose of the present experiment was to evaluate the probable causes of the low plasma total T4 during sleep deprivation by measuring the free hormone concentration to minimize binding irregularities and by challenging the pituitary-thyroid axis with iv TRH to determine both 1) the pituitary release of TSH and 2) the thyroidal response of free T4 (FT4) and free T3 (FT3) release to the TSH increment. Sleep-deprived rats were awake 91% of the total time compared with 63% of the total time in yoked control rats and 50% of the total time during the baseline period. Cage control comparison rats were permitted to sleep normally. Sustained sleep deprivation resulted in a decline from baseline in plasma FT4 of 73 +/- 6% and FT3 of 45 +/- 12%, which were similar to the declines in total hormone concentrations observed previously; nonstimulated TSH was unchanged. In the yoked and cage control groups, FT4 also declined, but much less than that of the sleep-deprived group. The relative changes in free compared with total hormone concentrations over the study were also less parallel than those in the sleep-deprived group. The plasma TSH response to TRH was similar in all groups across experimental days. The plasma FT4 and FT3 concentrations in sleep-deprived rats increased after TRH-stimulated TSH release to an extent comparable to control values. Taken together, low basal FT4 and FT3 hormone concentrations and unchanged TSH and thyroidal responses to TRH suggest a pituitary or hypothalamic contribution to the hypothyroxinemia during sleep deprivation.
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PMID:Pituitary and peripheral thyroid hormone responses to thyrotropin-releasing hormone during sustained sleep deprivation in freely moving rats. 789 53

Emissions of ultrasonic vocalizations (USVs) by rat pups (Rattus norvegicus) during hypothermia have consequences for recovery and warming. We investigated the effects on dam behavior of USVs emitted by 3- to 11-day-old pups during hypothermia at rectal temperatures between 18 and 22 degrees C. Rat dams were tested in a Y maze with the home cage as a start box. Dams were given, in one condition, a choice between a hypothermic pup emitting USVs or a hypothermic, silent (anesthetized) pup and, in the other, a choice between 2 hypothermic, silent pups. Although differing in some acoustic properties from normal isolation calls, USVs emitted by hypothermic pups both elicited maternal search behavior and acted as directional cues for dams, in comparisons with control dams exposed only to silent pups. Thus USVs of pups recovering from extreme hypothermia have communicative as well as physiological significance.
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PMID:Hypothermic vocalizations of rat pups (Rattus norvegicus) elicit and direct maternal search behavior. 792 60

Interactions between central 5-HT1A receptors and the enantiomers of LY-41, a 2-aminotetralin derivative related to 8-OH-DPAT (8-hydroxy-2-(dipropylamino)tetralin), were studied. Both enantiomers of LY-41 behaved as potent 5-HT1A receptor agonists in rats, inducing the 5-HT behavioural syndrome, decreasing body temperature and inhibiting the cage-leaving response. The behavioural syndrome and the hypothermia were antagonized by the 5-HT1A receptor antagonist, (S)-UH-301. The LY-41 enantiomers also reduced brain 5-HTP accumulation in rats treated with a decarboxylase inhibitor. The pharmacology of the enantiomers of LY-41 appeared similar to that of 8-OH-DPAT. However, it is noteworthy that the stereoselective interaction of 5-HT1A receptors with LY-41 was opposite to that of 8-OH-DPAT. Thus, (R)-8-OH-DPAT was more potent than (S)-8-OH-DPAT, whereas (S)-LY-41 appeared to be more potent than (R)-LY-41.
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PMID:(R)- and (S)-8-acetyl-2-(dipropylamino)tetralin (LY-41): two novel 5-HT1A receptor agonists. 844 82

These experiments investigated the effect of either systemic opiate blockade by naloxone (5 mg/kg) or intracerebroventricular CRF (250 pmol), or the two treatments combined, on physiological and endocrine responses of male rats to two types of stress: restraint by itself (representing a psychological stress), and restraint combined with a tail clip (representing an additional mild physical nociceptive stress). Rats were restrained in a plastic container for 15 min, with or without a tail clip. Heart rate, body temperature, and serum corticosterone were measured. The first experiment showed that restraint induced marked tachycardia, maximal at 5 min, and declining thereafter. There was also a pronounced hypothermia, maximal at 10 min, and serum corticosterone was elevated 10 min after the end of the period of restraint. The presence of a tail clip increased the cardioaccelerator response, but had no effect on hypothermia. Naloxone had no effect on heart rate during restraint or on postrestraint corticosterone, but accentuated hypothermia. The effects of naloxone occurred independently of the presence of a tail clip. A subsidiary experiment showed that rats transferred to an unfamiliar cage showed a marked hyperthermic response, as described by others. The second experiment showed that CRF (250 pmol ICV) did not modify the tachycardiac response to restraint, but reduced hypothermia. This also occurred irrespective of the presence of a tail clip. The third experiment investigated the interaction between naloxone and CRF, and showed that the ameliorative effects of ICV CRF on restraint-induced hypothermia were prevented by systemic naloxone, but that neither tachycardia nor corticosterone responses were altered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions between corticotropin-releasing factor and endogenous opiates on the cardioaccelerator, hypothermic, and corticoid responses to restraint in the rat. 848 94


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