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)

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Pentazocine and tripelennamine, which have been abused in combination by humans, were evaluated for pharmacologic interactions on autonomic, behavioral, and antinociceptive measures in chronic spinal dogs. Pentazocine (0.31-5 mg/kg, IV) produced miosis, hypothermia and antinociception which was mediated by spinal and supraspinal reflexes; these effects were antagonized by naltrexone. Tripelennamine (0.63-2.5 mg/kg, IV) elicited mydriasis, hyperthermia and antinociception; these effects were not blocked by naltrexone. Tripelennamine produced antinociception only on the supraspinally-mediated skin twitch reflex. Interactions between pentazocine and tripelennamine varied depending on the response measured. Effects of both drugs on pupils were additive. Temperature effects were infra-additive, with the hyperthermic effects of tripelennamine predominating over the pentazocine hypothermia, resulting in a complete physiologic antagonism of pentazocine hypothermia. Antinociception, measured by flexor reflex depression, represented only the effect of pentazocine, whereas skin twitch reflex antinociception reflected either infra-additive or additive properties. The coadministration of nonconvulsive doses of pentazocine and tripelennamine produced seizures indicating a potentiated adverse interaction. In summary, the patterns of the pentazocine-triplennamine interactions were complex and the effects of tripelennamine could not be attributed to opioid activity.
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PMID:Interactions between pentazocine and tripelennamine on autonomic and nociceptive measures in the dog. 278 Jul 81

Surgical intervention is generally accepted for acute type A dissection, but little is published regarding therapy for acute dissection of the transverse portion of the aortic arch, though involved in approximately 15% of cases. Often, surgical treatment is withheld if aortography suggests a primary tear in the aortic arch. Similarly, resection is limited to the ascending aorta despite intimal tears within the transverse portion of the arch. This work reports a 9-year experience with a policy of emergency resection for all acute aortic dissections involving the aortic arch. Intensive "antiimpulse" therapy is instituted and aortic angiograms are obtained. Type A dissections are resected under moderate hypothermia and, if the primary tear extends into the arch or is not found in the ascending aorta, the arch is explored during a brief period of deep hypothermia and circulatory arrest. If necessary, the arch is replaced during circulatory arrest, the patient's head is packed in ice, steroids are administered, and a barbiturate coma is induced. If arch replacement is anticipated preoperatively, surface cooling is also employed. Sixteen acute (up to 14 days) and three subacute (15 to 28 days) transverse arch dissections were treated in this manner between May 1979 and May 1988, with four (21%) hospital deaths (25%, acute; 0%, subacute). Mortality was related to left main coronary dissection with extensive myocardial infarction in two of our four cases, a third death was related to persistent seizures in a renal transplant patient requiring hemodialysis who had lupus cerebritis, and the fourth resulted from rupture of the descending aorta 15 days after arch replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urgent operation for acute transverse aortic arch dissection. 291 32

Dietary deprivation of thiamine combined with pyrithiamine administration in rats was used for pathophysiological and morphological investigations. The animals passed through three different symptomatic stages, ranging from slight neurological abnormalities to generalized seizures from day 8 up to day 11. Hypothermia was a consistent finding during the second week. Histological examination revealed two types of neuropathological lesions in the rats. Those in the colliculi inferiores and the vestibular nuclei were characterized by a bullous spongiform appearance of the neuropil with severely damaged, pale and oedematous nerve cells. Alterations in the thalamus and inferior olives, however, showed eosinophilic nerve cell necrosis of the ischemic type which resembles the thalamic pathology found in human cases of Wernicke's encephalopathy.
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PMID:Differentiation between brain lesions in experimental thiamine deficiency. 314 4

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system. 319 80

I retrospectively describe 20 episodes of water intoxication in 19 infants, with hypothermia, seizures, and hyponatremia. Overdilution of formula or aggressive supplementation with water or clear juices were documented in 16 of the 20 episodes. Seizures and respiratory distress were severe enough in six cases to require intubation and ventilatory support. Marked diaphoresis was noted as a premonitory symptom to seizures in eight children. The children were an average of 5.1 +/- 4.3 months of age; serum sodium values averaged 118 +/- 4.3 mmol/L. No evidence of excess production of antidiuretic hormone was found. Water intoxication in infants is common, and I discuss its possible relationship to demyelinating disease of the central nervous system.
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PMID:Seizures and hypothermia due to dietary water intoxication in infants. 356 73

The paroxysmal (px) chick is a mutant White Leghorn (Gallus domesticus) which appears normal at hatching and during the subsequent week. By ca. 8 days posthatching, various symptoms develop, of which the most obvious are depressed food intake (anorexia) and audiogenic seizures. Histological evidence suggests that central auditory and vestibular nuclei and fiber tracts begin to degenerate prior to seizure onset. This degeneration, which affects central and peripheral components of both systems, becomes increasingly severe over time although auditory stimulation continues to elicit seizures. Characterization and analysis of peripheral and brainstem auditory response to auditory stimuli indicated that major response differences between px and normal chicks exist in peaks reflecting brainstem activity (P3A, P3B, P4A, P5A). In 5 of 8 px chicks, these later response peaks were either grossly abnormal in terms of amplitude and latency (including amplitude input/output functions) or often entirely absent. Early peaks (P1A and P2A), however, in px waveforms were normal in morphology and amplitude, indicating normal function of peripheral auditory structures. Although lower body temperature of px chicks may account for some of the longer latencies observed, other abnormalities (e.g. absence of peaks) could not be produced in normal birds by induced hypothermia.
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PMID:Peripheral and brainstem auditory function in paroxysmal (px) White Leghorn chicks. 356 41

In West Germany, the antihistaminic diphenhydramine is marketed as a non-prescription hypnotic. Results of toxicological screening in cases of drug overdose indicate that poisoning with diphenhydramine represents a substantial part (4.5%) of the total number of intoxications. A total of 136 cases of diphenhydramine poisoning in 1982-1985 were evaluated with respect to age, ingested dose, plasma level, and clinical symptomatology. All patients had taken diphenhydramine with suicidal intent. Two-thirds of the patients were aged 14-30 years. In about 50% of the cases, between 6 and 40 times a therapeutic dose was ingested. Diphenhydramine plasma levels showed a wide range (0.1-4.7/micrograms/ml) due to differences in ingested dose and time between ingestion and admission to hospital. Impaired consciousness was the most common symptom. Psychotic behavior similar to catatonic stupor--often combined with anxiety--was highly specific for diphenhydramine poisoning. Further symptoms included hallucinations, mydriasis, tachycardia, and less frequently diplopia, respiratory insufficiency, and seizures. Primary treatment included gastric lavage, administration of activated charcoal and sodium sulfate. In one case, hemodialysis and ultrafiltration were performed which had only limited effect on diphenhydramine plasma elimination kinetics. This patient died of diphenhydramine overdose and extreme hypothermia. All intoxications except the one mentioned before had an uncomplicated clinical course. In vitro experiments indicate that diphenhydramine may be almost completely removed from the plasma compartment by hemoperfusion. Routine analysis of urine samples in diphenhydramine overdose led to the identification of 4 previously unknown metabolites and artifacts of diphenhydramine.
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PMID:Clinical symptomatology of diphenhydramine overdose: an evaluation of 136 cases in 1982 to 1985. 358 86

Functional development of the brain of rats exposed to methylazoxymethanol (MAM) at a dose of 1, 5 or 20 mg/kg, i.p., on day 15 of fetal life was assessed using pharmacological responses to several CNS acting drugs. In the rats treated with 20 mg/kg of MAM, the following results were observed: A marked decrease in the rearing activity in an openfield, failure of the development of supersensitivity in cataleptic response to haloperidol administered weekly, an increase in the head down sniffing frequency after apomorphine administration, prolongation of pentobarbital-induced sleeping time, a decrease in the seizure threshold to picrotoxin and kainic acid, and a significant decrease in the growth rate. In addition, the rats administered 1 mg/kg of MAM, which have been reported to detect no biochemical changes in the brain, exhibited different responses to the drugs used: A marked decrease in the rearing activity, nearly normal threshold to picrotoxin and kainic acid, a pronounced hypothermia after chlorpromazine administration, and no significant change in the brain weights. The results suggest that rats exposed to MAM in varying doses would be useful for evaluating the developmental process of neurons and its unification.
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PMID:[Pharmacological assessment of functional alterations in the brain of rats exposed prenatally to methylazoxymethanol]. 360 68

Monosodium glutamate (MSG) administration to neonatal rodents produces convulsions and results in numerous biochemical and behavioral deficits. These studies were undertaken to determine if neonatal administration of MSG produced permanent alterations in seizure susceptibility, since previous investigations were inconclusive. A flurothyl ether seizure screening technique was used to evaluate seizure susceptibility in adult mice that received neonatal injections of MSG (4 mg/g and 1 mg/g). MSG treatment resulted in significant reductions in whole brain weight but did not alter seizure threshold. A naloxone (5 mg/kg) challenge was also ineffective in altering the seizure thresholds of either control of MSG-treated mice. Flurothyl ether produced hypothermia which was correlated with the duration of flurothyl exposure; however, the relationship of hypothermia to seizure induction was unclear. Flurothyl seizure testing proved to be a rapid and reliable technique with which to evaluate seizure susceptibility.
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PMID:Flurothyl seizure thresholds in mice treated neonatally with a single injection of monosodium glutamate (MSG): evaluation of experimental parameters in flurothyl seizure testing. 368 52


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