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)

On the basis of the above discussion, a number of useful guidelines appear for the anesthetic management of alcohol and drug abusers. 1. Because of the decreased ability of intoxicated patients to withstand hemorrhage, blood replacement therapy should probably be instituted earlier than in the nonintoxicated patient. 2. Because the chronic alcoholic may actually be iso-osmotically overhydrated, fluid therapy must be planned with care. 3. Because of the tendency to hypoglycemia, glucose should be added to the fluid management regimen. 4. Because of the enzyme induction effect of chronic ETOH ingestion, anesthetic agents that are in part metabolized (methoxyflurane, halothane, fluroxene) are perhaps best avoided. Increased ability to metabolize anesthetic agents appears to be associated with toxicity. 5. Because ETOH is a CNS depressant and has been shown to have amnesia-inducing properties, supplementation of nitrous oxide-relaxant technique with narcotics or other depressant drugs should be reduced, if not eliminated. 6. Because acutely intoxicated individuals are more prone to hypothermia, their core temperature should be monitored intraoperatively. All intravenous fluids should be warmed and a warming blanket should be employed, if necessary, to maintain body temperature. 7. Because of the sympathomimetic effect of many of the drugs, pulse and blood pressure can be misleading in the assessment of blood loss.
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PMID:Preanesthetic care. Intoxication and trauma. 96 73

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

Restraint stress for ten days (two times two hours daily) induces a hypersensitivity of the central cholinergic system, reflected by antagonism to amnesia induced by scopolamine at 0.1 mg/kg in a passive avoidance test and by hypersensitivity to the hypothermic effect of oxotremorine at 1 mg/kg. A restraint stress for 30 days, on the other hand, diminishes animal retention in the passive avoidance test and causes a hyposensitivity to oxotremorine-induced hypothermia, reflecting a hypoactivity of the central cholinergic system. An acute 24-hour stress causes no change. The relationship between chronic stress and associated memory deficits is discussed.
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PMID:Chronic stress and memory: implication of the central cholinergic system. 221 20

Effects of FKS-508 (AF102B; cis-2-methylspiro (1,3-oxathiolane-5,3')-quinuclidine), a novel M1-selective agonist, on central muscarinic responses in mice were examined in comparison with oxotremorine. FKS-508 was slightly less potent (6 times) in reversal of scopolamine-induced amnesia (passive avoidance failure), but far less potent (260 and 55 times) in producing hypothermia and tremor than oxotremorine. These results show that the selective M1 agonist FKS-508 differentiates highly between the central muscarinic effects.
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PMID:Central muscarinic activities of an M1-selective agonist: preferential effect on reversal of amnesia. 230 75

Alpha-MSH has a wide variety of putative biological activities in addition to its classical melanocyte dispersing activity. Since each of these activities appears to be mediated by a discrete receptor, this peptide is an excellent candidate for exploring conformational restrictions which determine the chemical-physical basis for hormone action on specific activities. Experiments One and Two evaluated several cyclic and linear analogs of alpha-MSH on retrieval of memory during the reactivation of memory for a passive avoidance response following hypothermia-induced amnesia. Three of the cyclic analogs appear to have enhanced the peptide's ability to serve as a reactivation agent. One of the linear Nle4,D-Phe7 analogs antagonized whereas three others enhanced reactivation. The D-Phe7 substitution in cyclic analogs did not affect reactivation. Another group of animals were trained on a step-through passive avoidance task and tested 25 days later. The cyclic analog enhanced memory whereas the D-Phe7 analog and alpha-MSH had no effect. Finally, two analogs were tested on a black-white discrimination. Although the cyclic analog had no effect on either acquisition or reversal of this learning, the Nle4,D-Phe7 analog significantly impaired reversal learning. The results from these preliminary studies suggest that structural modifications of alpha-MSH do alter its potency and pattern of actions in learning and memory situations.
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PMID:The effects of structure-conformation modifications of melanotropin analogs on learning and memory: D-amino acid substituted linear and cyclic analogs. 254 4

Reminder (Experiment 1) and familiarization (Experiment 2) treatments were found to have similar effects on the 24-hr retention performance of 24- to 26- and 90- to 100-day-old rats that either did or did not undergo an amnesic treatment (hypothermia) immediately after training. Similar degrees of retrograde amnesia and normal forgetting were evident in both trained age groups that were not subjected to familiarization or reminder treatments. These results suggest that memory processes in weanling and adult rats are similar in susceptibility to disruption by an established amnesic treatment (hypothermia) and in the ease of prevention of and recovery from amnesia by recognized preventive (familiarization) and alleviation (reminder) measures. The similarity of the effects of these preventive and alleviation treatments on normal forgetting and induced amnesia suggests that experimentally induced amnesia may be a fruitful approach to studying the ontogeny of memory processes and, more specifically, to studying factors that influence infantile amnesia.
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PMID:Preventing and alleviating hypothermia-induced amnesia in weanling and young adult rats. 261 Sep 12

Young rats (16-30 days), trained on a one-trial passive avoidance task, were subsequently submitted to the amnesic agent hypothermia 0, 5, 10, 20 or 30 min later, and tested for retention 6 h after training. While hypothermia administered 10 min after training was no longer effective in 30-day rats, it still induced a significant retrograde amnesia in younger animals. In 16- and 18-day rats, administration of hypothermia 20 min after training could still produce a slight but statistically non-significant amnesia. Additionally, exposition to a reinstatement treatment was found to alleviate the amnesic effects of hypothermia in 20- and 30-day-old animals, while it seemed ineffective in 16- and 18-day rats. These findings suggest that the more immature the animal, the longer the consolidation period, the more vulnerable the mnemonic trace, and the less effective a reinstatement treatment for alleviation of retrograde amnesia.
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PMID:Passive avoidance memory consolidation and reinstatement in the young rat. 339 38

Previous studies have demonstrated anterograde amnesia (AA) and its reversal in rats trained on passive avoidance tasks. The present investigation was conducted to determine whether induction and/or reversal of AA is limited to inhibitory learning tasks or whether these phenomena can be illustrated in behavioral situations involving choice. Accordingly, in Experiment 1, rats were trained on a T-maze escape task as either hypothermic (28 degrees C) or normothermic. Twenty-four hours later half of each acquisition group was tested as either hypothermic or normothermic. Results indicated a stern retention decrement for animals trained at a lower body temperature and tested as normothermic. However, this prograde memory deficit was attenuated when animals were recooled shortly prior to testing. In an attempt to extend the phenomenon of memory recovery observed in Experiment 1, Experiment 2 examined whether pretest injections of d-amphetamine (0.5 mg/kg), a purported amnesia-attenuating agent, could lessen the AA induced by hypothermia. Amphetamine, at least at the dose used, did not reduce the memory impairment. Results are interpreted in terms of the state dependent nature of memory.
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PMID:Hypothermia-induced anterograde amnesia and its reversal in rats trained on a T-maze escape task. 372 11

Cardiopulmonary arrest is a test of the brain's tolerance to global ischemia. 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. A wide spectrum of neurologic sequelae may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes of amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke. The distinctive features of these sequelae and their pathophysiologic aspects are discussed. Special attention is given to brain death and prognostication.
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PMID:Cardiopulmonary arrest. Pathophysiology and neurologic complications. 390 62

The effects of post-training and/or pretesting body cooling on retention of Pavlovian discriminated fear conditioning were examined in preweanling (16-day) and weanling (23-day) rats. Twenty-four retention was assessed in 16- and 23-day-old rats receiving hypothermia after training, after training and prior to testing, or at neither time. Amnesia was present in the preweanling but not weanling rats. Recovery from amnesia was not observed in the preweanling rats followed a second cooling treatment. Control groups indicated the differential amnesia was not the result of differences in 24 hr baseline retention, depth of hypothermia cooling, rate of recovery from hypothermia treatment, or body temperature immediately post-testing. The results are discussed with respect to current views of infantile amnesia and the growing evidence for similar nonmonotonic functions during ontogeny.
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PMID:Nonmonotonic age changes in susceptibility to hypothermia-induced retrograde amnesia in rats. 720 49


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