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)

A case of pseudocoarctation with dissecting aneurysm of the ascending aorta and arch is reported. A 49-year-old man was admitted with chest pain and loss of consciousness. Angiogram showed kinking of the aortic isthmus and dissecting aneurysm of the ascending aorta. There was no pressure gradient between arms and legs. Prosthetic graft replacement of the ascending aorta was successfully performed by the use of total cardiopulmonary bypass with moderate hypothermia. Etiology of the development of pseudocoarctation is unknown, however, hypothesis that embryological abnormality of the aortic arch is one of the contributing factors has been widely accepted. This case was accompanied by bicuspid aortic valve. It is suggested that the developmental etiology of this case seems to be similar to that of classical coarctation of the aorta. Development of the dissecting aneurysm is supposed to be due to hypertension of the upper body during exercise, even though there is no pressure gradient at rest.
Kyobu Geka 1992 Sep
PMID:[Pseudocoarctation associated with dissecting aneurysm of the aorta: a case report]. 151 14

In rats, kappa opioids decrease body temperature and the combination of a selective kappa agonist with chlorpromazine induces a profound hypothermia. Because of the greater density of kappa-opioid receptors and increased ratio of kappa to mu in the guinea pig, the actions of these drugs on body temperature were compared in this species. Groups of young adult, male Hartley guinea pigs were injected SC with trans-3,4-dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneace tamide methanesulfonate, hydrate (U50, 488H; 20-80 mg/kg) and chlorpromazine (2.5-5 mg/kg), either alone or in combination. Rectal temperatures were measured over a 5-h period. U50, 488H produced a dose-related decrease in temperature, with a mean maximum drop of approximately 7 degrees C. The maximum decrease with chlorpromazine was approximately 1.6 degrees C. When doses at the lower end of the range for each drug were given together, the combined effect was greater than that expected from the individual drugs. Both the peak effect and the duration of the hypothermia appeared to be potentiated. At the highest dose combination only an additive effect was seen. Compared to the rat, the hypothermic effect of the kappa agonist alone is much greater in the guinea pig. The potentiation between the two drugs, however, is greater in the rat.
Pharmacol Biochem Behav 1991 Sep
PMID:Production of hypothermia in the guinea pig by a kappa-agonist opioid alone and in combination with chlorpromazine. 166 7

The present study examined whether descending noradrenergic and serotonergic systems mediate the antinociceptive effect of the prototypical cannabinoid, delta-9-tetrahydrocannabinol (delta 9-THC). Rats were administered vehicle or delta 9-THC (10 mg/kg, i.v.) and subsequently given an intrathecal (i.t.) injection of either the alpha 2-noradrenergic antagonist yohimbine, or the non-specific serotonin (5-HT) antagonist, methysergide, through chronically implanted spinal catheters. Whereas yohimbine significantly reversed the cannabinoid-induced elevation of tail-flick latencies, methysergide had no effect. To examine whether yohimbine was indeed blocking the antinociceptive effects of delta 9-THC through a spinal mechanism, it was administered i.t. at either the lumbar or the upper thoracic level of the spinal cord. Antinociception was significantly reduced when yohimbine was administered in the lumbar region; however, administration in the upper thoracic region failed to have an effect. In addition, the effect of i.t. administered yohimbine and methysergide was assessed on two other indices sensitive to cannabinoids, hypothermia and ring immobility. As previously reported, i.v. administration of delta 9-THC led to hypothermia as well as immobility in the ring test which were not blocked by i.t. administration of either monoamine antagonist. To the contrary, methysergide potentiated the hypothermic effect of delta 9-THC. These findings indicate that cannabinoids activate descending noradrenergic neurons resulting in antinociception via the stimulation of spinal alpha 2-adrenoceptors.
Brain Res 1991 Sep 20
PMID:Cannabinoid-induced antinociception is mediated by a spinal alpha 2-noradrenergic mechanism. 166 84

We analyzed the role of adhesion molecules in the pathogenesis of experimental cerebral malaria (ECM), since tumor necrosis factor (TNF) plays a major role in this condition and has been shown to up-regulate in vitro expression of cell adhesion molecules (CAM), particularly intercellular CAM-1 (ICAM-1). We found increased expression of ICAM-1 on brain endothelial cells from mice with ECM. Treatment with monoclonal antibodies (mAb) directed against leukocyte function-antigen 1 (LFA-1, the ligand of ICAM-1) on days 6, 8 and 10 almost totally prevented ECM, while decreasing blood TNF levels. To exclude the possibility that the effects of anti-LFA-1 mAb resulted from an even partial inhibition of TNF overproduction, mice with signs of imminent death (hypothermia and neurologic defects) were treated with the anti-LFA-1 mAb, with dramatically protective effect. In contrast, injection of anti-ICAM-1 mAb on day 6 caused rapid death, while it was innocuous in normal mice. An mAb directed against complement receptor type 3 (CR3) was ineffective, as were injections of soluble human ICAM-1. These results suggest that adhesion of LFA-1+ cells to endothelial cells, stimulated by TNF to express high levels of ICAM-1, is critical in the pathogenesis of ECM. Emergency therapy at interfering with cytoadherence could be considered in the treatment of cerebral malaria in man, in which high blood TNF levels are also observed.
Eur J Immunol 1991 Sep
PMID:Late administration of monoclonal antibody to leukocyte function-antigen 1 abrogates incipient murine cerebral malaria. 167 17

Experimental studies on spinal cord (SC) injuries published from 1975 to 1989 in some of the most widely circulating neurosurgical journals were reviewed. The relatively large number of animal species utilized as well as the intensely variable dynamic or static methods employed to induce SC injury represent elements of confusion more than objective necessities in this field of research. In fact, the objective of SC injury research should be to solve the problem of severe SC injuries by either preventing and/or repairing SC damage, rather than looking for modalities to provoke a large spectrum of SC injuries with the result of establishing a correlation between for example, the clinical picture and trauma magnitude. It should be time to study all variables and treatments mainly in only one experimental model. The rat with a permanent paraplegia should represent such a model; the abdominal aorta occlusion for 45 minutes, distal to the renal arteries in rabbits should be the experimental model of choice for ischaemia. If a significant result, such as reversing permanent paraplegia, were obtained in rats, it would be logical to repeat the study in higher mammals and if successful, in humans. For the last decade of this century it is necessary to further study all the mechanisms implied in secondary SC damage as well as to attempt to repair definitive SC damage by using grafts and enhancing the potential regenerative ability of the SC with known and new growth factors. Presently, methylprednisolone, dexametasone, thiopental, naloxone, and hypothermia seem to have some clinical potentials that require studies in humans.
Neurol Res 1991 Sep
PMID:Experimental studies on spinal cord injuries in the last fifteen years. 168 22

The potency and efficacy of the selective dopamine D2 receptor agonist quinpirole, the mixed D1/D2 agonist apomorphine, and the selective D1 receptor agonist SKF 38393 in producing hypothermia and changes in locomotor activity were evaluated in four strains of mice: CBA/J, C57BL/6J, ICR Swiss and CF1. CBA/J mice previously have been shown to be deficient in dopamine cell and receptor number relative to other strains such as C57BL/6J mice, whereas ICR Swiss and CF1 are commonly used strains of mice. Quinpirole (0.125 to 1.0 mg/kg) was equiefficacious and equipotent in producing hypothermia in all 4 strains. Apomorphine (0.125 to 16 mg/kg) was equiefficacious in producing hypothermia in all 4 strains, but was approximately four-fold less potent in CBA/J mice than in the other strains. SKF 38393 had little effect on body temperature in any of the 4 strains. Basal motor activity was lowest in CBA/J mice, and tended to be highest in ICR Swiss mice. Quinpirole (0.125 to 32 mg/kg) had no effect on motor activity in CBA/J mice, but decreased motor activity in the other 3 strains. Apomorphine (1 to 16 mg/kg) produced modest increases in motor activity in all 4 strains. The magnitude of the changes produced by apomorphine was comparable in all strains when expressed as change from mean control values. SKF 38393 (8 to 64 mg/kg) also increased motor activity in all 4 strains, with comparable increases when expressed as change from mean control values. The present results are consistent with the interpretation that inherited deficiencies in dopamine cell and receptor number in CBA/J mice produce functional decrements in D2, but not D1, dopamine receptor function.
Pharmacol Biochem Behav 1991 Sep
PMID:Potency and efficacy of dopamine agonists in mouse strains differing in dopamine cell and receptor number. 168 81

The ability of neuroleptics to induce dopamine D2 receptor supersensitivity has been linked to the onset of tardive dyskinesia, the major side-effect of these drugs. Brain iron metabolism has been shown to be involved in the regulation of dopamine D2 receptors. We now examined the effect of chronic treatment with FeCl2 on chlorpromazine-induced D2 receptor supersensitivity. The results show that FeCl2 (5 mg/kg per day for 21 days) given to rats treated with chlorpromazine (10 mg/kg per day, for 21 days) prevented the onset of supersensitive biochemical and behavioral (apomorphine) expressions of DA D2 receptor. Inclusion of iron did not affect the chlorpromazine-induced sedation or hypothermia. Moreover, the combined chronic iron-chlorpromazine treatment produced the same net effects as chronic chlorpromazine on striatal amounts of dopamine, DOPAC (dihydroxyphenylacetic acid) and HVA (homovanillic acid). Chlorpromazine medication caused a decrease in liver non-haem iron levels (40%) but not in brain iron. The effect of the neuroleptic drug on iron stores and the involvement of iron in the neuroleptic-induced dopamine supersensitivity suggest that mobilization of iron from the periphery into the brain may play an important role in the mechanism of action of the neuroleptics.
Eur J Pharmacol 1991 Sep 17
PMID:Prevention of neuroleptic-induced dopamine D2 receptor supersensitivity by chronic iron salt treatment. 168 31

Extracellular 5-HT in the anterior hypothalamus/preoptic area (AH/POA) and caudate nucleus of the freely moving cat was measured using in vivo brain microdialysis. Administration of 8-OH-DPAT, a 5-HT1A receptor agonist that decreases 5-HT neuronal activity, decreased extracellular 5-HT in both brain areas. Extracellular 5-HT levels were also examined in relationship to the sleep-wake cycle, because previous data from our laboratory have indicated that behavioral state is the primary determinant of 5-HT neuronal discharge. As with 5-HT neuronal discharge, extracellular 5-HT was increased during active behavioral states and decreased during somnolent periods. These first two sets of findings confirm the ability of the microdialysis technique to measure physiological fluctuations in extracellular 5-HT levels and support the hypothesis that neuronal discharge is a major determinant of extracellular 5-HT levels. Levels of the 5-HT metabolite 5-hydroxyindole acetic acid (5-HIAA) in the AH/POA were also responsive to changes in behavioral state and administration of 8-OH-DPAT, though fluctuations in extracellular 5-HIAA were less robust and temporally delayed. Finally, extracellular 5-HT and 5-HIAA were examined in the AH/POA during fever induced by systemic injection of the synthetic pyrogen muramyl dipeptide. Previous data from our laboratory have indicated that 5-HT neuronal activity is unaffected by this manipulation, though 5-HT has been implicated specifically in thermoregulation. Pyrogen-induced hypothermia produced no specific change in 5-HT efflux, because any changes noted could be accounted for by behavioral state changes. These data are consistent with the hypothesis that the brain serotonergic system is closely linked to the sleep-wake-arousal cycle. However, extracellular 5-HT may be involved in thermoregulatory processes as part of a global role in modulating neuronal activity in coordination with the behavioral state of the animal.
J Neurosci 1991 Sep
PMID:Extracellular serotonin levels change with behavioral state but not with pyrogen-induced hyperthermia. 171 90

Acquisition of conditioned taste aversion (CTA) in rats is not prevented by functional decortication, anesthesia or hypothermia applied after intake of the flavored fluid and maintained throughout the action of the poison but is disrupted by bilateral application of 10 ng tetrodotoxin (TTX) into the parabrachial nuclei. The blockade is directly proportional to TTX dosage, indirectly proportional to distance of the injection site from parabrachial nuclei and equally affects CTAs using different CS (saccharin, NaCl) and different US (LiCl, carbachol, amphetamine, cycloheximide). CTA is disrupted by TTX applied up to 4 but not 8 days after a single CS-US pairing. TTX fails to disrupt overtrained CTA and elicits only a weak anterograde amnesia when applied 1 but 2 or more days before CTA acquisition. It is concluded that the parabrachial nuclei and the adjacent reticular formation probably represent the neural substrate of the permanent CTA engram the protracted consolidation of which is disrupted by prolonged cessation of impulse which is disrupted by prolonged cessation of impulse activity in the information storing network.
Arch Int Physiol Biochim Biophys 1991 Sep
PMID:Brain stem mechanisms of conditioned taste aversion learning in rats. 172 Jun 86

Two infants experienced subcutaneous fat necrosis (SCFN) at a relatively late age after cardiac surgery with induced hypothermia. The condition resolved in both patients over four weeks without treatment. The appearance of SCFN after the newborn period is very unusual, and in these patients was probably related to the hypothermia.
Pediatr Dermatol 1991 Sep
PMID:Subcutaneous fat necrosis in two infants after hypothermic cardiac surgery. 174 30


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