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)

Taurine (10 and 20 micrograms) injected unilaterally into the lateral ventricle of rats caused an increase in core temperature. Bilateral injection of taurine 2.5 and 5 micrograms into the preoptic region of the anterior hypothalamus induced a dose-related hyperthermia: higher doses (10 micrograms) caused hypothermia. Intrahypothalamically taurine-induced hyperthermia was blocked by prior injection of strychnine hydrochloride (5 and 15 micrograms); doses which alone had no effect on core temperature. Of the other inhibitory amino acids injected intrahypothalamically hypotaurine also induced a hyperthermia. GABA (10 micrograms) caused hypothermia; glycine (10 micrograms) had no effect. Potassium (50 mM) stimulated release of radioactivity from superfused slices of anterior hypothalamus prelabelled with [3H]taurine in a calcium-dependent manner. A high affinity uptake mechanism with a Km of 8.5 microM was demonstrated with [3H]taurine into slices of anterior hypothalamus. Taurine may have a neurotransmitter role in the anterior hypothalamus but whether the body temperature effects represent physiological or pharmacological events remains to be established.
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PMID:Role of taurine as a possible transmitter in the thermoregulatory pathways of the rat. 3 17

Taurine, homotaurine, GABA and muscimol, given intraventricularly to the conscious, unrestrained rabbit cause hypothermia and a reduction in skeletal muscle tone. Taurine and homotaurine desynchronize areas of the motor and limbic cortices, with GABA and muscimol synchronize both tracings and markedly depress the arousal reaction following external stimuli.
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PMID:Homotaurine and muscimol mimic taurine and GABA effects on muscle tone and temperature regulation. 73 91

1. Intracerebroventricular (I.C.V.) injections of taurine into rabbits resting at an ambient temperature (Ta) of 10 degrees or 23 degrees C caused hypothermia but at 30 degrees C ambient temperature, rectal temperature was unchanged. 2. An I.C.V. bolus of 0=5 mg taurine immediately followed by a slow infusion of taurine (0-01--0-2 mg/min) into rabbits at 23 degrees C ambient temperature caused sedation and peripheral vasodilation and blocked the febrile response to Salmonella typhosa endotoxin (1 microng/kg i.v.). Sustained fevers, characteristic of fevers caused by central administration of pyrogens, developed after taurine infusions were stopped. Control infusions of taurine at the same rates in the same rabbits when they were afebrile had little effect on rectal temperature. 3. An I.C.V. injection of 0-5 mg taurine reduced the hyperthermia caused by prostaglandin E1 (PGE1; 2 microng) given I.C.V. A dose of 5-0 mg not only blocked PGE1 hyperthermia but also caused marked hypothermia. 4. Bilateral injections of taurine into the preoptic/anterior hypothalamic region, at sites where injections of Salmonella typhosa endotoxin caused long-lasting fevers, had no effect on rectal temperature. Similar injections into the reticular substance of the medulla oblongata, in the region believed to be concerned with a secondary temperature control function, were also without effect on body temperature. 5. Taurine (0-5 and 5-0 mg, I.C.V.) had no consistent effect on hyperthermia induced by amphetamine (2 mg/kg, I.V.) 6. We conclude that the hypothermic effect of taurine is not due to an action on the central neurone pool or pools concerned with the integrative control of thermoregulatory effectors. This amino acid appears to inhibit neuronal activity in efferent pathways which control peripheral vasomotor tone and heat production and to depress the level of arousal. Taurine delays the onset and extends the duration of endotoxin-induced fever, perhaps by two separate action: by inhibiting activity in central thermoregulatory pathways and by promoting accumulation of endogenous pyrogen in the brain.
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PMID:Intracerebroventricular taurine in rabbits: effects of normal body temperature, endotoxin fever and hyperthermia produced by PGE1 and amphetamine. 85 4

Taurine, given intracerebroventricularly to the consciou unrestrained rabbit, causes hypothermia and a reduction in skeletal muscle tone. Evidence has been produced that the latter effect is of a central, supraspinal origin.
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PMID:Muscle relaxation induced in the rabbit by intracerebroventricular taurine injection: a supraspinal effect. 100 46

Taurine may function in brain as a neuroinhibitor, and intracerebroventricular taurine has the capacity to induce hypothermia. Its antiepileptic properties have been observed in animals and humans. On the basis of these data, we studied taurine concentration in the cerebrospinal fluid of 32 children with simple febrile convulsions (16 +/- 6 months) and of 25 children with acute hyperthermia without neurologic signs (13 +/- 8 months). Taurine concentration in cerebrospinal fluid was similar in febrile convulsion children (8 +/- 4 mumol/l) compared to a control group (7.8 +/- 3 mumol/l).
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PMID:[Taurine in the cerebrospinal fluid in febrile convulsions in children]. 279 96

Taurine and glutamine are the most abundant intracellular free amino acids in mammalian hearts where changes in their intracellular concentrations are likely to influence a number of cellular activities. In this study we investigated the effects of ischaemia and reperfusion on the intracellular concentrations of taurine and glutamine in the hearts of patients undergoing coronary artery bypass surgery using cold crystalloid or cold blood cardioplegic solutions. Ischaemic arrest (30 min), using cold crystalloid cardioplegic solution (n = 19), decreased the intracellular concentrations (micromol/g wet weight) of taurine (from 9.8 +/- 0.8 to 7.7 +/- 0.7, P < 0.05) and glutamine (8.7 +/- 0.5 to 7.2 +/- 0.6). After 20 min of normothermic reperfusion the fall in taurine and glutamine was maintained (7.5 +/- 0.5 and 7.4 +/- 0.7 for taurine and glutamine respectively). Myocardial ischaemic arrest with cold blood cardioplegic solution (n = 16) did not cause a significant fall in tissue taurine or glutamine. However, on reperfusion there was a marked fall in the intracellular concentrations of taurine (9.4 +/- 0.5 to 6.5 +/- 0.7) and glutamine (8.0 +/- 0.7 to 5.8 +/- 0.4). The fall in amino acids was associated with a fall in ATP and a rise in tissue lactate. This work demonstrates that irrespective of the cardioplegic solution used to arrest the heart, there is a marked fall in tissue taurine and glutamine which may influence the extent of recovery following surgery. The fall in taurine is largely due to efflux whereas changes in glutamine are due to both transport and metabolism. Ischaemia, hypothermia and changes in the transmembrane concentration gradients are the likely factors responsible for the changes in tissue amino acids.
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PMID:Effect of ischaemia and reperfusion on the intracellular concentration of taurine and glutamine in the hearts of patients undergoing coronary artery surgery. 909 9

(1) Taurine and GABA are recognized as endogenous cryogens. In a previous study, some structural analogues of taurine, namely 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and (+/-)cis-2-aminocyclohexane sulfonic acids (CAHS) have been shown to displace [(3)H]taurine binding from rabbit brain synaptic membrane preparations, without interacting either with GABA-ergic systems, nor with taurine uptake mechanism, thus behaving like direct taurinergic agents. (2) To answer the question whether the role of taurine as an endogenous cryogen depends on the activation of GABA receptors or that of specific taurine receptor(s), taurine or the above structural analogues were injected intracerebroventricularly in conscious, restrained rabbits singularly or in combination and their effects on rectal (RT)- and ear-skin temperature and gross motor behavior (GMB) were monitored. (3) Taurine (1.2 x 10(-6)-4.8 x 10(-5) mol) induced a dose-related hypothermia, vasodilation at ear vascular bed and inhibition of GMB. CAHS, at the highest dose tested (4.8 x 10(-5) mol) induced a taurine-like effect either on RT or GMB. On the contrary ISE, injected at the same doses of taurine, induced a dose-related hyperthermia, vasoconstriction and excitation of GMB. AEA and TAG caused a dose-related hyperthermia, but at doses higher than 1.2 x 10(-7) mol caused death within 24 h after treatment. (4) CAHS (4.8 x 10(-5) mol) antagonized the hyperthermic effect induced by TAG (1.2 x 10(-6) mol), AEA (1.2 x 10(-8) mol) or ISE (4.8 x 10(-5) mol). (5) In conclusion, these findings may indicate the existence of a recognition site specific for taurine, responsible for its effects on thermoregulation.
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PMID:A specific taurine recognition site in the rabbit brain is responsible for taurine effects on thermoregulation. 1278 8

The second most abundant cerebral amino acid, taurine, is widely consumed in the so-called "energy drinks". Therefore, its possible actions on the brain are of great interest. In the present experiments taurine was given intraperitoneally to rats in order to study if it can be administered systemically in large enough amounts to alter cerebral dopaminergic transmission or to induce hypothermia. In addition, the effects of subcutaneously administered lipophilic taurine analogue, N-pivaloyltaurine, were studied. The extracellular striatal taurine and dopamine concentrations were estimated using in vivo microdialysis in awake and freely moving rats, and the rectal temperatures were measured. Taurine at the total dose of 45 mmol/kg i.p. led to a maximally 8-fold increased striatal extracellular taurine concentration, induced a long-lasting hypothermia, and significantly reduced the striatal extracellular dopamine concentration. The latter effect was strengthened by co-treatment with reuptake inhibitor nomifensine. N-pivaloyltaurine (15 mmol/kg in total, s.c.) only slightly elevated the striatal extracellular taurine concentration, failed to alter the rectal temperature, and in contrast to taurine somewhat elevated the striatal extracellular dopamine concentration suggesting a different mechanism or locus of action from that of taurine. Finally, our experiments using brain microdialysis confirmed the earlier findings that taurine is slowly eliminated from the brain. The results clearly indicate that systemically given taurine enters the brain in concentrations that induce pharmacological effects.
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PMID:The effects of systemically administered taurine and N-pivaloyltaurine on striatal extracellular dopamine and taurine in freely moving rats. 1289 27