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)

In the rat dorsal hippocampus and dorsal raphe nucleus, the microiontophoretic application of ergotamine and 5-HT suppressed the firing activity of CA3 pyramidal neurons and 5-HT neurons, an effect antagonized by selective 5-HT1A receptor antagonists. Co-application of ergotamine prevented the inhibitory action of 5-HT on the firing activity of CA3 pyramidal neurons but not of 5-HT neurons, indicating that ergotamine acted as a partial 5-HT1A receptor agonist in the dorsal hippocampus and as a full agonist at 5-HT1A autoreceptors. Ergotamine decreased, in a concentration-dependent manner, the electrically evoked release of [3H]5-HT in preloaded rat and guinea pig hypothalamus slices; this effect was prevented by the nonselective 5-HT receptor antagonist methiothepin but not by the selective 5-HT1B/1D receptor antagonist GR 127935 or the alpha 2-adrenoceptor antagonist idazoxan. Although body temperature in humans remained unchanged following inhaled ergotamine, in the rat, subcutaneously injected ergotamine produced a hypothermia that was prevented by a pretreatment with the 5-HT1A/1B receptor/beta-adrenoceptor antagonist pindolol. Finally in humans, ergotamine did not alter prolactin or adrenocorticotropic hormone levels, but increased growth hormone level, which was prevented by pindolol. Cortisol level was increased in humans by ergotamine, but this enhancement was unaltered by pindolol. In conclusion, the present results suggest that ergotamine acted in the rat brain as a 5-HT1A receptor agonist and as an agonist of terminal 5-HT autoreceptor of a yet undefined subtype. In humans, ergotamine also displayed some 5-HT1A receptor activity but, probably because of lack of receptor selectivity, it did not present the same profile as other 5-HT1A receptor agonists.
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PMID:Effect of ergotamine on serotonin-mediated responses in the rodent and human brain. 977 59

Products containing gamma-butyrolactone (GBL) are marketed for many claimed purposes, including to induce sleep, release growth hormone, enhance sexual activity and athletic performance, relieve depression, and prolong life. GBL is converted by the body into gamma-hydroxybutyrate (GHB), a drug banned outside of clinical trials approved by the Food and Drug Administration (FDA). Recognized manifestations of GHB toxicity include bradycardia, hypothermia, central nervous system depression, and uncontrolled movements. This report describes seven cases of GBL toxicity involving the product "Revivarant," which is labeled as containing 1.82 g of GBL per fluid ounce, reported from two hospital emergency departments (EDs) in Minnesota during October-December 1998 and summarizes an additional 34 cases of GBL toxicity reported to poison centers in New Mexico and Texas during October 1998-January 1999.
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PMID:Adverse events associated with ingestion of gamma-butyrolactone--Minnesota, New Mexico, and Texas, 1998-1999. 1007 58

Serotonergic receptors of the 5-HT1A subtype have been suggested to play a pivotal role in the mechanism of action of antidepressant drugs, including specific serotonin reuptake inhibitors (SSRIs). We examined the effect of clinical doses of the SSRI, fluoxetine, on 5-HT1A receptor function in 15 normal volunteers. Hypothermic and hormone responses to the 5-HT1A receptor agonist, ipsapirone (0.3 mg per kg, per os) were examined after two weeks of placebo and again, after the subjects had been receiving fluoxetine for four weeks. On fluoxetine, the hypothermic response to ipsapirone was significantly blunted, as were ACTH, cortisol and growth hormone release. Ipsapirone plasma levels were significantly increased by fluoxetine but a pharmacokinetic effect could not have accounted for the observed blunting of 5-HT1A receptor mediated effects. These findings confirm and extend previous observations in rodents and humans and indicate that both post-synaptic 5-HT1A receptors in the hypothalamus, which mediate hormone responses to 5-HT1A agonists, and pre-synaptic 5-HT1A receptors which (putatively) mediate the hypothermic response, are rendered subsensitive by chronic SSRI administration. Since fluoxetine did not have significant effects on mood and other psychological variables in these subjects, alterations in 5-HT1A receptor function induced by SSRIs may have psychotropic relevance only in the context of existing perturbations of serotonergic function which underlie the psychopathological states in which these drugs are therapeutically effective.
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PMID:5-HT1A receptor function in normal subjects on clinical doses of fluoxetine: blunted temperature and hormone responses to ipsapirone challenge. 1032 31

We have presented a new concept of brain hypoxia oriented brain hypothermia treatments. All severe brain injury patients (148 cases) were GCS < 6. The masking brain hypoxia by brain thermo pooling, catecholamine surge induced cardiac dysfunction and intestinal vasodilatation, reduction of Hb-2.3 diphosphoglyserate were major target of initial treatment. These specific brain hypoxia was only controlled by brain hypothermia (34-32 degrees C), oxygen delivery > 800 ml/min. and AT-III > 100%. 2. The brain hypothermia were very successful to prevent masking brain hypoxia, selective radical attack to A10 dopamine nervous system, and brain edema. However, metabolic shift to lipid metabolism and lower growth hormone related immune crisis were recorded as a negative factors. Clinical results were so advanced. The mortality were 44 in 148 cases (30%), good recovery were 59 in 148 cases (40%), mild disability were 20 in 148 cases (13%) and vegetate state were only 15 in 148 cases (10%). The combination of brain hypothermia and replacement of cerebral dopamine were very successful to prevent the vegetation in severe brain injury.
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PMID:[The brain hypothermia therapy for prevention of vegetation after severe brain injury]. 1048 50

Depression has been shown in some studies to be associated with a reduction in hypothalamic 5-HT(1A) receptor function, as indicated by reduced hormone and/or hypothermic responses to 5-HT(1A) agonists such as ipsapirone. The hypothermic response to ipsapirone was reduced in depressed patients treated with amitriptyline. Hormone and hypothermic responses to 5-HT(1A) agonists were reduced in normal subjects administered specific serotonin reuptake inhibitors. Effects of electroconvulsive therapy (ECT) on 5-HT(1A) receptor-mediated responses in humans have not been reported. In the present work, ten depressed patients and 15 control subjects were challenged with placebo and with 0.3 mg/kg ipsapirone, administered 48 h apart in a randomised double blind design. Hypothermic, growth hormone (GH) and cortisol responses were measured. Seven of the depressed patients were treated with a course of ECT, and placebo and ipsapirone challenges were repeated 24 and 72 h after the last treatment. The cortisol response to ipsapirone was significantly reduced in the depressed patients compared with controls. The hypothermic response to ipsapirone was totally abolished in the depressed patients. When tested after a course of ECT, the seven depressed patients again showed reduced or blunted responses. We conclude that hypothalamic 5-HT(1A) receptor function is reduced in depression. In contrast to the effects of electroconvulsive shock (ECS) on post-synaptic 5-HT(1A) receptor function in animals, which have chiefly been measured in the hippocampus using electrophysiological techniques, ECT in humans does not induce an increase in sensitivity of post-synaptic 5-HT(1A) receptors in the hypothalamus.
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PMID:Blunted temperature and cortisol responses to ipsapirone in major depression: lack of enhancement by electroconvulsive therapy. 1081 78

The metabolic changes that occur after cardiac surgery result from a complex interaction between the effects of surgery and extracorporeal circulation per se, the inflammatory response to surgical trauma and extracorporeal circulation, perioperative use of hypothermia, the cardiovascular and neuroendocrine responses characteristic to cardiac surgery, and the drugs and blood products used to support circulation during and after operation. These changes include among others increased oxygen consumption and energy expenditure and increased secretion of insulin, growth hormone, adrenocorticotrophic hormone, cortisol, epinephrine and norepinephrine. Other changes include decreased total-Trijodthyronine levels, hyperglycemia, hyperlactatemia, increased glutamate, aspartate and free fatty acid concentrations, hypokalemia, an increased production of inflammatory cytokines and increased consumption of complement and adhesion molecules. There is evidence that better control of metabolic abnormalities improves the patients' outcome.
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PMID:Metabolic changes after cardiac surgery. 1122 61

The hypothermia produced by 5-HT1A agonists had initially been claimed to be caused by the activation of cell body 5-HT1A autoreceptors resulting in decreased 5-HT transmission in laboratory animals. In order to address this issue in humans, 12 healthy volunteers underwent a dietary tryptophan depletion paradigm to decrease 5-HT availability, under double-blind conditions, during which body temperature was monitored following oral administration of the 5-HT1A agonist buspirone (30 mg). In addition, plasma prolactin and growth hormone evaluations, two responses that are mediated via the direct activation of postsynaptic 5-HT1A receptors, were determined. The hypothesis was that if responses are mediated by decreased transmission at postsynaptic 5-HT1A receptors, resulting from dampened 5-HT release as a consequence of 5-HT1A autoreceptors activation, then responses to the exogenous 5-HT1A agonist should be attenuated when 5-HT availability has been markedly decreased beforehand. Buspirone produced the same significant increase in prolactin and growth hormone in the tryptophan-depleted state as in the control condition. Similarly, the degree of hypothermia produced by buspirone was not significantly different in the two experimental conditions. In conclusion, these results strongly suggest that the hypothermia and the increases in prolactin and growth hormone produced by buspirone are attributable to the enhanced activation of postsynaptic 5-HT1A receptors, and not to a decrease in 5-HT transmission resulting from the activation of the 5-HT1A cell body autoreceptors on 5-HT neurons.
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PMID:Serotonin 1A receptor activation and hypothermia in humans: lack of evidence for a presynaptic mediation. 1209 4

Dietary dehydroepiandrosterone (DHEA) inhibits the proliferation of syngeneic bone marrow cells (BMC) infused into lethally irradiated mice. Potential mechanisms for suppression of hematopoiesis were evaluated and the findings were as follows: (i) depletion of NK, T, B or macrophage cells failed to reverse suppression by DHEA; (ii) stem cell stimulation by erythropoietin, growth hormone, interleukin-2, Friend leukemia virus, or cyclophosphamide failed to reverse suppression; (iii) supplementation of fatty acids, mevalonate, or deoxyribonucleotides, which are dependent upon glucose-6-phosphate dehydrogenase function, did not enhance BMC growth in mice fed DHEA; (iv) DHEA downstream metabolites 4-androstenedione and 17beta-estradiol, as well as the synthetic steroid, 16alpha-chloroepiandrosterone (but not testosterone or 5-androstene-3beta,17beta-diol), also inhibited BMC growth. Tamoxifen antagonized the effects of 17beta-estradiol but not DHEA; (v) dietary DHEA causes hypothermia, but housing of DHEA-fed mice at 34 degrees C to maintain normal body temperature did not reverse suppression; (vi) DHEA leads to a decrease in food intake in rodents. Pair-feeding control diet to mice fed DHEA mimicked the effects of dietary DHEA; (vii) adrenalectomy and orchiectomy decrease the levels of stress and sex hormones, respectively. Neither procedure affected the ability of food restriction or DHEA feeding to inhibit hematopoiesis; (viii) growth of GR-3 NM pre-B leukemia cells in unirradiated mice was also suppressed by DHEA or food restriction. We conclude that DHEA, by reducing food intake in mice, inhibits bone marrow and leukemia cell growth. The precise mechanism(s) by which reduced food intake per se inhibits hematopoiesis is not known, but may involve an increased rate of cellular apoptosis.
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PMID:Dietary dehydroepiandrosterone inhibits bone marrow and leukemia cell transplants: role of food restriction. 1468 46

Ghrelin is an orexigenic peptide with prokinetic effects in the rat. We investigated the effect of ghrelin and growth hormone-releasing hormone 6 (GHRP-6) on gastric emptying and transit in control and septic mice. Mice were injected i.p. with lipopolysaccharides (LPS) or saline (control). After 16-17 h mice were pretreated with saline, ghrelin or GHRP-6 1 h before intragastric administration of Evans blue. Fifteen minutes later, after assessment of the behaviour scale, mice were killed and gastric emptying, transit and rectal temperature were measured. In control mice, ghrelin (100 microg kg(-1)) and GHRP-6 (20-100 microg kg(-1)) accelerated gastric emptying, whereas ghrelin and GHRP-6 failed to increase transit significantly. Septic mice developed a delay in gastric emptying and transit, hypothermia and a deterioration of the behaviour scale. In septic mice, ghrelin (20 microg kg(-1)) accelerated gastric emptying without effect on transit while GHRP-6 significantly accelerated gastric emptying dose-dependently and failed to increase transit significantly. Ghrelin and GHRP-6 had no effect on the endotoxin-induced hypothermia or deterioration of behaviour scale. Therefore, the beneficial prokinetic effect of ghrelin but mainly of GHRP-6 offers potential therapeutic options in the treatment of septic gastric ileus.
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PMID:Effect of ghrelin and growth hormone-releasing peptide 6 on septic ileus in mice. 1530 99

Intrauterine or fetal growth restriction is best defined by using customised birth weight percentiles based upon the growth potential for an individual infant. Growth restriction in utero may be classified as asymmetric or symmetric depending upon the duration of the process. Asymmetric growth restriction is caused by placental insufficiency, maternal hypertensive conditions, long-standing maternal diabetes, smoking, living at altitude or multiple gestation. Symmetric growth restriction may be due to congenital infections, chromosomal or other abnormalities, fetal alcohol syndrome, low socioeconomic status or be constitutional. The underlying cause of growth restriction often predicts the potential adverse effects on the foetus and newborn and later effects in childhood and adulthood. With placental insufficiency, there may be chronic or acute on chronic fetal hypoxia with birth asphyxia and hypothermia, neonatal hypoglycaemia, polycythaemia and coagulopathy. Management is directed at prevention or early treatment of these conditions. In contrast, symmetrically growth-restricted infants should be examined carefully to look for congenital infections and malformations that may need specific interventions. Infants with constitutional short stature generally do not need any specific management. Feeding of growth-restricted infants is important to overcome deficiencies incurred in utero. Most infants show catch-up growth although about 10% do not. Those with excessive catch-up growth may be at greatest risk of developing insulin resistance in adulthood leading to diabetes, obesity and heart disease. The so-called fetal origins of disease may actually have a postnatal onset related more to excessive weight gain in infancy. There is still controversy over the indications for growth hormone treatment in growth-restricted infants who remain of short stature in early childhood. Intrauterine growth restriction is also associated with a five- to seven-fold increased risk of cerebral palsy probably due to chronic placental insufficiency.
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PMID:Neonatal management and long-term sequelae. 1963 99


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