Disease relevance of Hypothermia

• CONCLUSIONS: Treatment with moderate hypothermia for 24 hours in patients with severe traumatic brain injury and coma scores of 5 to 7 on admission hastened neurologic recovery and may have improved the outcome [1].
• Influence of scalp hypothermia on doxorubicin related alopecia [2].
• Effects of hypothermia on brain glucose metabolism in acute liver failure: a H/C-nuclear magnetic resonance study [3].
• New insights into the pathophysiology of global ischemia have led to the potential use of early prophylactic anticonvulsants, hypothermia, barbiturate coma, glucose manipulations, calcium-blocking agents, and hemodilution [4].
• Bretylium tosylate and ventricular fibrillation in hypothermia [5].

Psychiatry related information on Hypothermia

• It neither antagonized the effects of reserpine in rats (hypothermia, ptosis) nor potentiated the effects of amphetamine (in mice and rats), nialamide or L-dopa (in mice) on locomotor activity [6].
• Repeated administration of electroconvulsive shock (5 shocks over 10 days) significantly increased CG 3509-induced hyperactivity and the degree of reversal of pentobarbitone-induced hypothermia and respiratory depression following CG 3509 administration [7].
• 2. Previous REM sleep-deprivation enhanced both delta9-tetrahydrocannabinol (THC)-induced hypothermia and nomifensine effects on aggressive behaviour [8].
• RESULTS: MDMA treatment caused a clear and consistent hyperthermia at 28 degrees C and hypothermia at 16 degrees C. Months later, rats pre-treated with MDMA at either 16 or 28 degrees C displayed increased anxiety in the social interaction and emergence tests and reduced escape attempts and increased immobility in the forced swim test [9].
• SR 58611A was active with minimal effective doses of 0.1-0.3 mg kg-1 i.p. in several models (antagonism of the hypothermia induced by apomorphine and reserpine; potentiation of the toxicity produced by yohimbine; reversal of learned helplessness), but was inactive in the tests of reserpine-induced ptosis and behavioural despair [10].

High impact information on Hypothermia

• Hypothermia did not improve the outcomes in the patients with coma scores of 3 or 4 on admission [1].
• Prevention of doxorubicin-induced hair loss with scalp hypothermia [11].
• Hypothermia and intolerance to cold induced by intracisternal administration of the hypothalamic peptide neurotensin [12].
• Ethanol-induced intoxication and hypothermia were studied in rats approximately 7 months after severe thiamine deficiency, when treated rats appeared to have recovered their physical health [13].
• Calcium, other divalent cations, and calcium antagonists were tested for their ability to alter ethanol-induced sleeping time, hypothermia, and behavioral intoxication in mice and rats [14].

Chemical compound and disease context of Hypothermia

• Mice treated with 6-hydroxydopamine before they were chronically fed phenobarbital did not develop functional barbiturate tolerance, measured by duration of the loss of righting reflex and hypothermia [15].
• GRK5-KO mice exhibited mild spontaneous hypothermia as well as pronounced behavioral supersensitivity upon challenge with the nonselective muscarinic agonist oxotremorine [16].
• In separate studies urea influx was inhibited by hypothermia (decrease from 37 degrees to 28 degrees C), by phloretin (0.1 mM in bath), by cyanide (1 mM), but not by probenecid (0.2 mM) [17].
• Brain glutamate and aspartate concentrations were respectively decreased to 60.9% +/- 7.7% and 42.2% +/- 5.9% (P < 0.01) in normothermic animals with acute liver failure compared to control and were restored to normal values by mild hypothermia [3].
• Again, these changes of lactate and alanine concentrations were prevented by mild hypothermia [3].

Biological context of Hypothermia

• Taken together, the results show that 5-HT-induced hypothermia is mediated by the 5-HT(7) receptor, and that oleamide may act through an independent mechanism as well as at an allosteric 5-HT(7) receptor site to regulate body temperature [18].
• We report that hypothermia rescues most hippocampal CA1 neurons from ischemia-induced cell death and attenuates ischemia-induced down-regulation of mRNA encoding the AMPA receptor subunit GluR2 [19].
• Similarly, the difference of P and V action potential duration was increased markedly by low K and hypothermia, and slightly by quinidine, while the slope of phase 3 was significantly decreased by all these factors [20].
• Hamsters whose lateral septum was infused with vasopressin showed almost no periods of hypothermia, whereas hamsters treated with control infusions displayed a normal hibernation pattern [21].
• In contrast, hypothermia resulted in a strikingly less pronounced CD11b upregulation during bypass [22].

Anatomical context of Hypothermia

• Thus, hyperosmolarity, but not hypothermia, can directly stimulate tachykinin release from cultured rat sensory C-fibers [23].
• Calcium depletion in rabbit myocardium. Calcium paradox protection by hypothermia and cation substitution [24].
• These findings suggest that: 1) mild hypothermia is an effective approach to the prevention of the central nervous system consequences of experimental ALF; and that 2) the beneficial effect of hypothermia is mediated via mechanisms involving reduced blood-brain transfer of ammonia and/or reduction of extracellular brain glutamate concentrations [25].
• Different effects of hypothermia on insulin and glucagon secretion from the isolated perfused rat pancreas [26].
• Pretreatment with a single injection of MK-801 (10 mg/kg) considerably attenuated the induction of hsp70 mRNA in hippocampus at 6 h of recirculation, an effect apparently mediated by persistent drug-induced hypothermia [27].

Gene context of Hypothermia

• Inasmuch as Rbm3 mRNA and protein levels are both increased in cells exposed to mild hypothermia, the activity of this IRES was evaluated at a cooler temperature [28].
• Increased activation of BDNF signaling is a possible mechanism by which mild hypothermia is able to reduce the neuronal damage typically occurring after cardiac arrest [29].
• The clinical manifestation with weight loss, hypothermia, hypoglycemia, hyperkalemia, and increased liver-derived enzymes in the blood together with hepatic necrosis and intravascular coagulation in moribund mice indicated a toxic shock-like syndrome, possibly mediated by the systemic TNF-alpha overproduction [30].
• The data suggest that TVX Q 7821 is a good presynaptic 5-HT1A antagonist in mice, as indicated by the 8-OH-DPAT-induced hypothermia and 5-HT synthesis rate studies [31].
• In rats the hypothermia induced by 8-OH-DPAT was partially antagonised by TVX Q 7821 while the behavioural "serotonin syndrome" induced by 8-OH-DPAT (a possible post-synaptic 5-HT1B-mediated effect) was unaffected by TVX Q 7821 as was the locomotion induced by RU 24969 [31].

Analytical, diagnostic and therapeutic context of Hypothermia

• Emergency treatment of neonatal hyperammonaemic coma with mild systemic hypothermia [32].
• Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children [33].
• Morphologic protection was better with higher dose nifedipine and potassium cardioplegia than with either low-dose cardioplegia or hypothermia alone [34].
• Bradykinin was measured by radioimmunoassay in blood samples obtained before, during and after profound hypothermia (to 18 degrees C) and cardiopulmonary bypass [33].
• The results show that progressive hypothermia to 22 C during calcium-free perfusion periods produced a progressive reduction of CK release and morphologic evidence of injury due to anoxia, caffeine, or DNP, which closely paralleled protection of hearts from the calcium paradox [35].

References