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

The effects of a dopamine antagonist (pimozide) and an alpha-adrenergic receptor blocking agent (phenoxybenzamine) on caffeine-induced changes in oxygen consumption. body temperature, blood glucose and non-esterified fatty acids (NEFA) were studied in mice. Both drugs had no effect on the increase of the oxygen consumption produced by caffeine. The decline of the body temperature induced by caffeine was not significantly influenced by pimozide, while phenoxybenzamine accentuated the hypothermic effect of caffeine. The results indicate that alpha-adrenergic and dopamine receptors do not play an essential role in the caffeine-induced stimulation of overall metabolism and hypothermia.
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PMID:Failure of phenoxybenzamine and pimozide to diminish changes in oxygen consumption and body temperature produced by caffeine. 48 30

An ergolene derivative having a piperazine-phenyl side chain instead of a peptide side chain causes rotational behavior in experimental rats and appears to activate mainly limbic DA receptors when given in vivo, in contrast to amino acid ergot alkaloids, which appear to activate all DA receptors when given systemically. Theophyllamine and caffeine were found to cause considerable enhancement of the action of DA formed from DOPAP AND DA receptor agonists such as apomorphine, piribedil, and amino acid alkaloids on supersensitive DA receptors. Many DA receptor agonists such as apomorphine, piribedil, and CB 154 have in common the property to induce hypothermia in mice, an effect that may be related to actions on limbic DA receptors. Many DA receptors agonists such as apomorphine, piribedil, ergocornine, and CB 154 are able to block ovulation in immature rats treated with PMS. It is likely that this blockade is related to activation of a DA receptor in the median eminence controlling LRF secretion. DA receptor agonists antagonize sexual activity in the female rat, whereas DA receptor blocking agents enhance it. DA neurons may therefore subserve an inhibitory role in the control by hormones of sexual behavior. It is of considerable interest that there appear to exist inhibitory DA receptors with regard to both LRF secretion and sexual behavior.
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PMID:Action of dopamine receptor agonists in forebrain and hypothalamus: rotational behavior, ovulation, and dopamine turnover. 114 54

Caffeine and other methylxanthines induce a dose-dependent reduction in core body temperature in mice. These experiments investigated the effects of neurotransmitter and neuromodulator antagonists on caffeine-induced hypothermia. Pretreatment with the alpha 2-adrenoceptor antagonist, atipamezole; the beta-adrenoceptor antagonist, propranolol; the dopamine antagonist, haloperidol; or the benzodiazepine receptor antagonist, flumazenil had no intrinsic effects on core body temperature nor did they interact significantly with the hypothermic effects of caffeine. The alpha 1-adrenoceptor antagonist, prazosin and the 5-HT receptor antagonist, metergoline significantly enhanced the hypothermic effects of caffeine, probably involving a combined effect with their intrinsic hypothermic actions. Pretreatment with the opiate receptor antagonist, naloxone (3 mg/kg i.p.), had no intrinsic effect on core body temperature but attenuated the hypothermic effect of caffeine reflected in a parallel shift to the right in the caffeine dose-effect curve. The naloxone-induced attenuation of the hypothermic effects of caffeine was also seen to be dose-dependent. The results reveal that opiate receptors (but not adrenoceptors, 5-HT, dopamine or benzodiazepine receptors) may play a role in modulating the hypothermic action of caffeine and possibly other methylxanthines.
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PMID:Opioid receptor mediation of the hypothermic response to caffeine. 133 37

The effect of a mild hypothermia (30 degrees C) on sarcoplasmic reticulum (SR) Ca2+ content and release has been evaluated in single cardiac cells loaded with the fluorescent indicator, indo-1. SR Ca2+ content, assessed by rapid caffeine application, is more pronounced at 30 than at 37 degrees C. However, hypothermia reduces the occurrence of spontaneous SR Ca2+ oscillations. In fact, following electrical stimulation, the time to onset of first SR Ca2+ oscillation was increased and their frequency reduced. Since spontaneous SR Ca2+ releases are implicated on the genesis of certain forms of ventricular arrhythmias, the protection provided by a mild hypothermia may be dependent on the modulation of intracellular Ca2+ homeostasis.
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PMID:[Myocardial protection in hypothermia depends on the modulation of intracellular Ca2+ homeostasis]. 148 82

Isometric contraction of isolated guinea-pig taenia caeci was induced with acetylcholine (ACh) and 5-hydroxytryptamine (5-HT) at 37 and 30 degrees C to investigate the effect of hypothermia on the response of smooth muscle to neurotransmitters. Lowering the temperature increased the amplitude of contraction in response to 10(-6) M ACh. Contraction in response to 10(-6) M 5-HT was also greater at 30 degrees C. 5-HT-contraction was not inhibited by atropine, but was inhibited by ketanserin. Calcium-contraction was also induced in an isosmotic high potassium solution. The amplitude of the contraction elicited by 5 x 10(-3) M Ca was significantly greater at 30 degrees C, and was inhibited by verapamil. The amplitude of the contractile response to 5 x 10(-3) M caffeine was also greater at 30 degrees C than at 37 degrees C. The finding that both calcium- and caffeine-contraction were enhanced at low temperature raises the possibility that intracellular calcium participate in cold-induced enhancement of contraction.
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PMID:Hypothermia enhances contractile responses of the guinea pig taenia caeci to acetylcholine, 5-hydroxytryptamine, caffeine and calcium. 157 74

Caffeine induces a dose-dependent decrease in core body temperature in mice and the hypothermia induced by a 100 mg/kg dose of caffeine was seen to persist for greater than 160 min. Other alkylxanthines including theophylline, enprophylline, isbutylmethylxanthine and 1,3-dipropyl-7-methylxanthine also showed dose-dependent reductions in body temperature. The dose of these drugs required to reduce body temperature by 2 degrees C was calculated and correlated with the affinities for the compounds at adenosine A1 and A2 receptors and their activities in inhibiting calcium dependent and independent phosphodiesterases. Significant relationships were found between the 2 degrees C hypothermic dose (HD2) and soluble and membrane calcium-independent phosphodiesterase inhibiting activity (r2s = 0.950 and 0.940, respectively). No significant relationship was seen between HD2 and soluble calcium-dependent phosphodiesterase inhibiting activity or with A2 adenosine receptor affinity. The relationship between HD2 and A1 adenosine receptor affinity (r2 = 0.739) did however almost reach statistical significance. These results would suggest that phosphodiesterase inhibition, instead of or in addition to adenosine receptor blockade, may play an important role in the effects of alkylxanthines on body temperature.
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PMID:Hypothermic effects of alkylxanthines: evidence for a calcium-independent phosphodiesterase action. 180 62

Hypothermic enhancement of the lethal effect of 3.5 Gy of 220-kV X rays in the absence of caffeine as well as in its presence (4 mM) was examined at temperatures between 10 and 34 degrees C in monolayer cultures in the G1 phase of the cell cycle. Correction has been made for the toxicity of low temperatures, and of caffeine at low temperatures, by concomitantly measuring cell killing in unirradiated cells. In the absence of caffeine, incubation of irradiated cells for up to 34 h at temperatures in the range 15 to 30 degrees C (or possibly 34 degrees C) enhances killing compared to that observed at 38 degrees C; the amount of enhancement is about the same throughout this range, but is nil at 10 degrees C. The enhanced killing induced by caffeine at 38 degrees C decreases as the temperature is lowered to 15 degrees C; there is no enhancement at 10 degrees C. Less killing is manifested in the range 15 to 25 degrees C in the presence of caffeine than in its absence. Recovery (loss of sensitivity to caffeine) and fixation of potentially lethal damage were studied in late-S/G2-phase cells at reduced temperatures by delaying treatment with caffeine for increasing times after irradiation. As the temperature is progressively lowered to 20 degrees C, less recovery is manifested after 5 h of incubation; no recovery is detected in the range 10 to 20 degrees C. Despite extensive recovery at 34 degrees C, no fixation is observed at that (or any lower) temperature in G2-phase cells: the cells are able to recover essentially fully when returned to 38 degrees C. In addition, responses of unirradiated control series to incubation at low temperatures appear to differ from those reported by others for longer treatment times of different cell systems.
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PMID:The action of caffeine on X-irradiated HeLa cells. IX. Hypothermic effects. 235 81

Administration of adenosine and agonists of the adenosine receptors to rats results in hypoactivity, hypothermia, muscle relaxation and antinociception. In the present study, we found that the adenosine ligand, N6-R-phenylisopropyladenosine (R-PIA), increased food intake in rats at a time in the day when rats normally eat very little food or none at all. Feeding was not reliably stimulated upon the first exposure to R-PIA, but was clearly increased following repeated administration of this agonist. Other adenosine agonists, namely 2-chloradenosine and 5'N-ethylcarboxamide adenosine, failed to alter feeding after a single injection or after repeated exposure. The adenosine antagonist, caffeine, did not block R-PIA's effect on food intake, whereas the opioid antagonist, naloxone, blocked R-PIA-induced eating. These data suggest that R-PIA stimulates feeding independent of the A1 or A2 adenosine receptors.
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PMID:The adenosine agonist N6-R-phenylisopropyladenosine (R-PIA) stimulates feeding in rats. 270 88

Morphine-induced analgesia, and the development of morphine-induced tolerance and dependence was determined in mice which had drunk caffeinated water (1 mg/ml) for 14 days or in mice which had received (-)-N6-(phenylisopropyl)-adenosine (PIA) 1 mg/kg i.p. for 14 days. Analgesia was assessed by the tail flick assay. The development of dependence was assessed by determining the ED50 of naloxone to precipitate withdrawal jumping (3 h after 100 mg/kg morphine pretreatment or 72 h after s.c. implantation of a morphine 75 mg pellet) and by determining the extent of naloxone-precipitated hypothermia in morphine-implanted animals. In mice chronically administered caffeine, the ED50 for morphine-induced analgesia was significantly decreased while the naloxone ED50 for withdrawal jumping increased by 2-fold after both types of morphine pretreatment. In control animals (tap water for 14 days), doses of 1 and 10 mg/kg of naloxone caused significant hypothermia in morphine-implanted animals. Doses of naloxone up to 100 mg/kg did not cause significant hypothermia in morphine-implanted animals which had received chronic caffeine. The development of tolerance was determined by computing the morphine potency ratio for the tail flick assay (tolerant ED50/control ED50). In mice chronically administered caffeine, the potency ratio was decreased significantly in morphine-implanted animals when compared to control. Morphine-induced analgesia, tolerance and dependence was not changed significantly in animals chronically administered PIA. Neither the distribution of morphine to the brain nor the opioid receptor binding parameters for [3H]etorphine and [3H]naltrexone were altered in mice chronically administered caffeine or PIA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of chronic administration of caffeine on morphine-induced analgesia, tolerance and dependence in mice. 300

Experiments were performed to determine whether the expression and/or repair of potentially lethal damage could be observed in mammalian cells exposed to hemataporphyrin derivative (HPD) photodynamic therapy (PDT). Photodynamic therapy was combined with posttreatment protocols known to inhibit the repair of potentially lethal damage in cells treated with X-rays, ultraviolet radiation, or alkylating agents. Potentiation of lethal damage from photodynamic therapy was induced by hypothermia (4 degrees C) following short (1 h) or extended (16 h) HPD incubation conditions. Caffeine potentiated the lethal effects of PDT only when cells were incubated with HPD for extended time periods. However, 3-aminobenzamide had no effect on the cytotoxic actions of PDT following either short or extended HPD incubations. Recovery from potentially lethal damage expressed by posttreatment hypothermia was complete within 1 h, while recovery from potentially lethal damage expressed by posttreatment caffeine required time periods of up to 24 h. The lack of effect of 3-aminobenzamide on expression of potentially lethal damage following photodynamic therapy may be related to direct inhibition of adenosine diphosphoribose transferase by photodynamic therapy. These results indicate that the expression and repair of potentially lethal damage can be observed in cells treated with PDT and will vary as a function of porphyrin incubation conditions.
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PMID:Expression of potentially lethal damage in Chinese hamster cells exposed to hematoporphyrin derivative photodynamic therapy. 301 Dec 47


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