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

At ambient temperatures (Ta) of both 8 and 22 degrees C, intraventricular administration of TRH (10-80 microgram) produced a dose-dependent hypothermia in rats. The hypothermia was due to both decreased metabolic heat production and cutaneous vasodilatation. In contrast, at 30 degrees C Ta, TRH increased metabolic heat production (due to behavioral excitation) and led to hyperthermia.
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PMID:Effects of thyrotrophic-releasing hormone (TRH) on thermoregulation in the rat. 677 89

TRH and PS-24 (a TRH peptidase resistant analogue) induce different effects on body temperature and motor activity in rats kept at 4 degrees C. PS-24 induced hypothermia, but TRH did not. PS-24 induced hypermotility, while TRH induced slight hypomotility. The thermal effect of TRH in hypophysectomized rats was similar to its effect in control intact rats, but PS-24 induced marked hypothermia in hypophysectomized rats. While TRH partially blocked d-amphetamine-induced hypothermia, PS-24 induced marked hypothermia in hypophysectomized rats. While TRH partially blocked d-amphetamine-induced hypothermia were blocked in olfactory tubercle-lesioned rats. The data indicate that the thermal effects of PS-24 are mediated by the dopaminergic neurons in the nucleus accumbens and are reversible by pretreatment with haloperidol in hypophysectomized rats. In addition, no correlation between the effects of the treatments on thermoregulation and motor activity was found.
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PMID:Effects of TRH and PS-24 on colonic temperature and motor activity of rats: possible role of dopamine. 679 10

The C-terminal octapeptide of cholecystokinin (CCK-8) injected into the lateral ventricle of rats produced a lowering of body temperature. CCK-8 potentiated pentobarbital-induced hypothermia, but not the ethanol one. Thyrotropin releasing hormone (TRH) and prostaglandin E2 (PGE2) antagonized the hypothermic effect of CCK-8. Non-sulfated CCK-8 was ineffective in lowering body temperature, indicating that sulfated tyrosine in the CCK molecule is indispensable for its hypothermic action. Caerulein was found to possess rather less activity compared with CCK-8.
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PMID:Effect of cholecystokinin octapeptide on body temperature in the rat. 680 79

Intracerebroventricular (i.c.v.) injection of neurotensin (NT) induced catalepsy in mice at doses greater than or equal to 0.02 microgram. The cataleptic effect progressively increased, reaching a maximum at approx. 2 hr after injection. In contrast, the hypothermic effect of neurotensin reached a maximum 1 hr after the injection, and was declining at 2 hr. Not all mice that showed hypothermia also showed catalepsy, and some mice showed catalepsy without hypothermia. Catalepsy induced by intracerebroventricular injection of neurotensin was not significantly correlated with the hypothermia. Furthermore, oxotremorine induced hypothermia without catalepsy. Thus, several lines of evidence indicate that the catalepsy induced by neurotensin is not the consequence of the neurotensin induced hypothermia. Thyrotropin releasing hormone (TRH), injected either intracerebroventricularly with neurotensin, or intraperitoneally before neurotensin abolished the hypothermia but only diminished the catalepsy scores. The cataleptic effect of neurotensin is consistent with its other neuroleptic-like activities.
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PMID:Neurotensin induces catalepsy in mice. 681 Jan 95

Two patients who developed Wernicke's Encephalopathy with subsequent hypothermia are described. Both patients responded rapidly to thiamine administration and one later had hypothalamic-pituitary function tests performed. This patient demonstrated depressed TSH response to TRH and a sluggish early cortisol response to adequate hypoglycaemia compared to 17 control subjects. These findings may suggest that previously described hypothalmic-pituitary abnormalties in chronic alcoholics may be mediated via thiamine deficiency and may also reflect hypothalamic damage contributing to the hypothermic state. The importance of intravenous thiamine administration in cases of coma of unknown aetiology is emphasised.
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PMID:Coma and hypothermia in Wernicke's encephalopathy. 693 37

We studied 13 known or potential antidepressants, choosen in different pharmacological classes: desipramine, imipramine, nialamide, dexamphetamine, AHR 1118, amineptine, iprindole, mianserine, nomifensine, salbutamol, TRH viloxazine, zimelidine. Each of these compounds was studied on 8 psychopharmacological tests: motor activity, reserpine induced hypothermia, reserpine induced ptosis, oxotremorine induced hypothermia, oxotremorine induced tremors, high doses apomorphine induced hypothermia, potentiation of toxic effects of yohimbine, behavioural despair. Clinical active compounds are efficient on yohimbine test and at least on one model of hypothermia; with a few exceptions, easy to explain, substances with a clearly demonstrated antidepressant activity in human have some common effects; these common effects can be used to predict, from animal experiments, an antidepressant effect in man.
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PMID:[The new versus the old antidepressant drugs: a comparative study of their psychopharmacological profiles (author's transl)]. 728 51

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

1. It has been reported by several groups that thyroid status can alter ethanol preference in rats. However, results using different methods and different strains of rats have not been consistent. 2. In this study, thyroidectomy or T4 augmentation was used to produce hypothyroidism or hyperthyroidism, respectively, in adult male Fischer-344 rats. 3. Preference for weak solutions (4 or 5%) of ethanol or tap water and ethanol-induced sedation and hypothermia were compared in hypothyroid, hyperthyroid and euthyroid rats. 4. No significant differences in preference indices (the ratios of ethanol to total liquid consumed) among the three groups were observed; however, for ethanol to contribute a greater portion of total calories ingested by hypothyroid rats than by euthyroid or hyperthyroid rats. 5. The duration of sleep resulting from a single i.p. injection of 2.5 mg/kg ethanol was increased (by 34%) in hyperthyroid rats and decreased (by 16%) in hypothyroid rats compared to euthyroid controls. Only the effect of hyperthyroidism was significant at the 0.05 level. 6. Colonic temperatures differed with thyroid state (hyperthyroid > euthyroid > hypothyroid) but the decrease produced by ethanol did not differ by thyroid state. 7. Observed differences in ethanol-induced sedation are consistent with differences in brain TRH levels and effects on neurotransmitter systems associated with different thyroid states.
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PMID:Effects of thyroid state on preference for and sensitivity to ethanol in Fischer-344 rats. 847 26

The acute phase of spinal cord injury includes primary and secondary pathological patterns. Primary patterns include the effects of contusion, laceration, stretch of neural tissue and direct vascular trauma. These changes are irreversible. Secondary patterns include posttraumatic ischemic changes, loss of energy metabolism, oedema, release of cytotoxic substances such as free radicals, and electrolyte changes such as an increase in intracellular calcium ions. These changes may be reversible. This determines treatment strategies. Free-radical scavengers, opioid receptor antagonists include TRH and its analogues, calcium channel blockers, volume expander, osmotic diuretics, hypothermia, antioxidants, cycloxygenase inhibitors, serotonin antagonists and NMDA receptor antagonists were tested in experimental models during the last 4 years. The successful treatment should break the feedback loops and trails of secondary injury cascade in many places so combined treatment connected with many elements and surgery decompression is necessary.
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PMID:[The physiopathology of acute spinal cord injury and a hope for a successful treatment]. 865 40

Eleven patients with severe head injuries were treated by artificial moderate hypothermia (32.0-33.0 degrees C). Measurement of the serum levels of anterior pituitary hormones (LH, FSH, TSH, and PRL) and the response of these hormones to the respective releasing hormones was done in the 11 patients before and during hypothermia. All 11 patients were under GCS 5. Those with brain death during hypothermia were excluded. Moderate hypothermia was performed for 3-7 days and involved cooling to 32.0-33.0 degrees C (Jugular venous blood temperature). The peak value of LH, FSH, TSH and PRL to administration of TRH or LH-RH during hypothermia were significantly lower than those before hypothermia, while basal values of those hormones were not affected by this treatment. These findings suggested that anterior pituitary function were suppressed by moderate hypothermia.
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PMID:[Anterior pituitary functions in patients with severe head injuries treated with moderate hypothermia]. 904 26


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