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)

Habituation to a test environment following daily exposure for 5 days was examined in three genetically different strains of mice. C57 animals showed significant habituation to the new environment already on the second day. The habituation of NMRI mice was significant on the third day, whereas CBA mice showed no habituation at all during the experimental period. There was no difference between the animal strains in learning capacity in a passive avoidance test, but CBA mice displayed a significant increase in latency in their performance. When tested for sensitivity to the convulsant actions of GABAergic antagonists, picrotoxin produced seizures at lower doses in CBA as compared to NMRI and C57 mice, whereas there was no difference between the strains in the seizure activity produced by the specific GABA receptor antagonist bicuculline. When the animals were tested for sensitivity to ethanol in a horizontal wire test, ethanol (2 g/kg, IP) produced muscle relaxation in CBA mice whereas the performance of NMRI and C57 was not affected. A large dose of ethanol (4 g/kg, IP) produced a significantly longer sleeping time in CBA mice as compared to NMRI and C57 animals. Ethanol-produced hypothermia was, however, similar in all animals. Environment-dependent development of tolerance to ethanol following daily injections of ethanol for 4 days was examined. C57 mice showed the most rapid development of tolerance towards ethanol's hypnotic actions, whereas CBA mice showed no tolerance to this effect of ethanol. No difference between the strains to the development of tolerance to ethanol's hypothermic effects was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that genetic differences in habituation and GABAergic mechanisms may be related to sensitivity to ethanol and development of ethanol tolerance in mice. 174 5

Hypothermia is not and should not be a prevalent feature of diving, yet many divers become extremely cold and uncomfortable during their work. It is not difficult to provide adequate insulation to protect the torso but if movement and dexterity are to be maintained, the extremities will inevitably suffer. Free swimming divers are limited by duration in cold (5 degrees C), shallow (10 m) water. Six hours is a typical maximum before both core cooling and extremity pain or dysfunction pose a threat. Habituation to cold may be observed in some divers. Surface supplied or bell supported divers, relying on supplementary hot water, need between 500 and 3500 Watts to preserve comfort over the range 10 to 300 m depth. Deep diving, using oxyhelium gas mixtures, can result in high respiratory convective losses in excess of 300 Watts. Heat exchangers are used to prevent damage to the tract. There have been a number of cases where hypothermia has been implicated in the cause of death in diving accidents, but generally the reason is not lack of physiological knowledge but equipment failure and inadequate contingency. Recent developments in diver protection have focused on electrically heated hand wear to preserve performance and prevent the risk of non freezing injury in a relatively inactive diver.
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PMID:Diving and hypothermia. 181 77

Triadimefon is a widely used systemic fungicide, yet there is little published information on its effects in mammals. This study describes the effects of triadimefon in male and female rats using a functional observational battery (FOB), motor activity (measured in a figure-eight maze), and operant performance (responding under a fixed-interval 3-min schedule). For the FOB, Long-Evans hooded rats were tested immediately before dosing and 0.5, 4, 24, and 48 hr after IP dosing with either vehicle, 30, 100, or 300 mg/kg triadimefon. Prominent effects of triadimefon (100 and 300 mg/kg) included increased arousal, stereotypies involving repetitive sniffing, head bobbing, and pacing, and self-mutilation. Dose-related handling-induced convulsions, changes in reflexes and sensory reactivity, hypothermia, and body weight loss were also significant findings. Doses of 30, 75 and 150 mg/kg triadimefon increased figure-eight maze activity whereas 300 mg/kg decreased activity. Habituation of activity during the session as well as the spatial distribution within the maze were also affected by triadimefon. Overall rates of responding maintained by fixed-interval milk reinforcement were increased at 30 and 56 mg/kg, and decreased at 100 and 200 mg/kg. Responding within the 3-min fixed-interval was also affected, with low rates normally occurring early in the interval markedly increased. These effects on operant performance were similar to those seen following d-amphetamine, and were attenuated by pretreatment with chlorpromazine (0.5 mg/kg). On many measures, female rats appeared to be somewhat more sensitive than males. Recovery was evident in some measures the day after dosing, but the effects of high doses (greater than or equal to 100 mg/kg) were typically prolonged (several days). Thus triadimefon produced a unique neurotoxic syndrome which is similar in many aspects to that produced by CNS stimulants.
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PMID:Neurobehavioral effect of triadimefon, a triazole fungicide, in male and female rats. 275 25

The irreversible muscarinic agonist, BM123 (63 mu moles kg-1, IV), was shown to produce central and peripheral physiological signs characteristic of cholinergic agonists. It also induced hypothermia, elevated nociceptive thresholds, reduced locomotor activity and disrupted spontaneous alternation performance in rats. The centrally acting muscarinic antagonist, atropine (50 mu mole kg-1) prevented or reduced all the above effects of BM123 when given SC 40 min prior to the BM123 injection. In contrast, the peripherally acting muscarinic antagonist, N-methyl atropine, prevented only the peripheral effects and the elevated nociceptive thresholds. Habituation of activity during a 20 min session was observed in all groups despite different levels of general activity. These findings are consistent with a model in which atropine and N-methyl atropine compete with BM123 for reversible association with the muscarinic receptor. In the case of BM123 administered alone, the association results, first, in agonist effects and proceeds to form an irreversible complex. Our present results show that by competing with BM123 for mAChR sites during the initial, reversible state of the interaction, atropine blocks the cholinomimetic effects of the agonist during both this state and its otherwise subsequent irreversible state.
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PMID:Influence of atropine and N-methyl atropine pretreatments on behavioral and physiological effects of the irreversible muscarinic agonist, BM123. 357 64