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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the early 1970's, calcium ions were implicated in the mechanism underlying the perturbation of the "set point" for body temperature produced by a thermolytic drug. Since Ca++ is thought to be involved in the incapacitating effects of ethanol on body temperature and motor coordination, this investigation sought to compare the differential central actions of a Ca++ chelating agent with those of a Ca++ channel antagonist on ethanol-induced poikilothermia and motor functions. A chronically indwelling cannula for intracerebroventricular (ICV) injection was implanted stereotaxically in each of 25 adult male Sprague-Dawley rats. Following postoperative recovery, each rat was given ethanol in a 20% v/v solution by the intraperitoneal route in a dose of 4.0 g/kg, which was selected to insure a clear-cut impairment of autonomic and motorial functions. Colonic temperature, behavioral sleep, righting reflex and degree of motor coordination on a rotorod were monitored at selected intervals for 5.0-7.0 hr after the injection of ethanol. Two experimental designs were used: First, either 12.5, 25 or 50 micrograms ethyleneglycol-bis-(beta-amino ethyl ether) N,N'-tetra-acetic acid (EGTA), or 25 or 50 micrograms verapamil, both dissolved in an artificial CSF vehicle, were infused ICV at the same time as ethanol's administration. In the second design, the compounds were infused at the nadir of the ethanol-induced temperature decline. EGTA infused ICV in the rat together with ethanol produced a dose-dependent inhibition of ethanol hypothermia and a more rapid recovery of the animal's righting reflex, arousal and motor coordination than that following ethanol alone. Although verapamil infused ICV in the 50 micrograms but not 25 micrograms dose minimized the poikilothermic response to ethanol, it was not as efficacious as that of EGTA. When infused ICV at the point of maximum fall in the rats' temperature. EGTA entirely reversed the hypothermia induced by ethanol and evoked a thermogenic response in the rat. In contrast, verapamil infused ICV in the same doses tended only to retard the further decline in the animal's body temperature. Similarly EGTA was far more effective than verapamil in ameliorating the other physiological actions of ethanol in terms of the reversal of areflexia, behavioral sleep and motor incoordination. These results suggest that the characteristic attributes of membrane Ca++ in terms of its binding and other neuronal properties play a significant functional role in the incapacitating action of ethanol on the diverse physiological processes mediated by the brain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alcohol-induced poikilothermia, sleep and motor impairment: actions on brain of EGTA and verapamil. 251 53

The management and evaluation of neurosurgical intracranial catastrophes require a multidisciplinary approach to optimize outcome. Intracranial pathology must be rapidly evaluated. Clinically, the patient's mental status, the degree and extent of focal neurologic deficits, and the dynamic nature of any changes in clinical status are assessed. The CT scan is invaluable for diagnosing and monitoring the progress and extent of intracranial pathology. Medical therapy for the control of intracranial hypertension must be undertaken simultaneously. This begins with provision of an adequate, protected airway and support of cardiopulmonary function. Specific measures to control intracranial hypertension include hyperventilation, osmotherapy, CSF removal, seizure control, autonomic control, sedation (primarily thiopental), muscle relaxation, mild hypothermia, and, if indicated, steroids. The goal of intraoperative management is physiologic support of systemic and cerebral hemodynamics. There should be a smooth transition from the discovery of the patient in extremis through the period of medical stabilization, operative intervention, and ultimate delivery of the patient to the intensive care facility for extended treatment.
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PMID:Perioperative management of intracranial catastrophes. 267 2

1. Hens received ICV injections of Ca2+ (1.98 g/100 ml) or Na+ (7.25 g/100 ml) at 28 degrees C and, following acclimation, at 37 or 20 degrees C, respectively. 2. At 28 degrees C (thermoneutrality), rectal temperature rose (P less than 0.05) following Na+ and fell (P less than 0.05) following Ca2+, similar to mammals and broiler chickens. 3. At 37 degrees C, Ca2+-induced hypothermia did not occur; nor did the Na+-associated hyperthermia at 20 degrees C. 4. Acclimation to a high or low temperature may produce an endogenous shift in CSF ion levels that make additional ion administration ineffective in affecting body temperature.
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PMID:Thermoregulatory responses of laying hens under cyclic environmental temperature to intraventricular calcium and sodium. 289 77

The effects of the novel veterinary sedative, medetomidine, were studied in rats. In addition to a dose-dependent sedation, which at high doses (greater than 100 micrograms/kg) included loss of the righting reflex and hypothermia, there was a concurrent decrease in the turnover rate of biogenic amines in the brain. Noradrenaline turnover was dose dependently decreased as judged by (i) the decrease in the brain concentration of its metabolite, MHPG-SO4, (ii) a decrease in the ability of alpha-methyl-p-tyrosine methyl ester to deplete brain noradrenaline stores and (iii) a dose-dependent decrease in the level of unconjugated MHPG in the CSF of freely moving rats. Brain dopamine turnover was also inhibited at higher doses as judged by the alpha-methyl-p-tyrosine method and by a decrease in the concentration of HVA in the rat brain 4 h after medetomidine. Serotonin turnover as estimated by the ratio of biogenic amine to its metabolite was also significantly depressed. These changes in brain biogenic amine turnover were inhibited by prior or simultaneous administration of alpha 2-adrenoceptor antagonists, either yohimbine or the more specific, novel alpha 2-antagonist, atipamezole.
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PMID:Behavioural and neurochemical effects of medetomidine, a novel veterinary sedative. 290 7

The purpose of this study was to characterize the alpha 1- and alpha 2-noradrenergic receptor sub-types which could mediate the hypothermic response produced by norepinephrine (NE) and other alpha-noradrenergic agonists applied to the thermosensitive zone of the hypothalamus. An array of four guide tubes was implanted stereotaxically so that their tips rested just above the anterior hypothalamic, preoptic area (AH/POA) of the cat. Following post-operative recovery, a micro-injection of an agonist or antagonist of NE receptors or control CSF vehicle was given in a volume of 1.0-2.0 microliter in the AH/POA in each of the unrestrained cats. The alpha 1-noradrenergic receptor agonist, phenylephrine, but not methoxamine, applied to the AH/POA produced a dose-dependent hypothermia of up to 2.0 degrees C. When applied similarly, the alpha 2-noradrenergic agonist clonidine, as well as norepinephrine, which acts on both alpha 1- and alpha 2-noradrenergic receptors, also induced a decline in the cat's core temperature of up to 1.5 degrees C. The hypothermic response of clonidine was inhibited by pre-treatment of the AH/POA with a micro-injection of the selective alpha 2-noradrenergic blocking agent, yohimbine. However, yohimbine given similarly in the cat's AH/POA potentiated significantly both the phenylephrine and norepinephrine-induced hypothermia. The combined alpha 1-, alpha 2-noradrenergic receptor antagonist, phentolamine, also injected into AH/POA inhibited the thermolytic response evoked by both phenylephrine and norepinephrine, whereas it was virtually ineffective against the clonidine-induced hypothermia. These results, therefore, strongly suggest that both alpha 1- and alpha 2-noradrenergic receptors subserve the coordinated thermoregulatory mechanisms in AH/POA which are required for the functional dissipation of body heat and the consequent evocation of hypothermia.
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PMID:Hypothermia: role of alpha 1- and alpha 2-noradrenergic receptors in the hypothalamus of the cat. 303 98

The circumscribed effect of ethyl alcohol on the local efflux of serotonin (5-HT) within the thermosensitive region of the anterior hypothalamic, pre-optic area (AH/POA) of the unrestrained rat was examined in relation to core temperature. A single guide cannula for push-pull perfusion was implanted stereotaxically in the AH/POA within coronal planes AP 7.0-8.2. Following 3-4 push-pull perfusions with control artificial CSF of a site identified as reactive to 5-HT, ethanol in a concentration of 2.75 (471 mM) or 5.5 (942 mM) percent was perfused at the same locus over a 5-10 min interval. Successive samples of perfusate were assayed for their content of 5-HT by high performance liquid chromatography using electrochemical detection (HPLC-EC). Within a circumscribed region of the AH/POA of the rat maintained at an ambient temperature of 22 degrees C, ethanol induced either an immediate or delayed hypothermia of short latency or a transient decline followed by an immediate increase in core temperature. In each case, the shift in temperature depended on the anatomical site of push-pull perfusion. Overall, the fall in core temperature was accompanied by an inhibition in the efflux of 5-HT. However, the consequent rise in the rat's core temperature was associated with an enhanced release of 5-HT in the samples of perfusate collected from the AH/POA. These results suggest that serotonergic synapses within the AH/POA are apparently involved in the thermolytic effects of ethanol as well as in the thermogenesis following the interval of heat loss.
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PMID:Temperature-related release of serotonin from unrestrained rats' pre-optic area perfused with ethanol. 341 63

Guide cannulae for microinjection and push-pull perfusion in the unrestrained cat were implanted bilaterally in the anterior hypothalamic, preoptic area (AH/POA) and posterior hypothalamus (PH). Postoperatively, the region was first identified in AH/POA which was reactive to norepinephrine or in PH to excess Ca++ ions; in both cases a hypothermic response was produced. Then either an artificial CSF control vehicle or the Ca++ ion channel blocking agent, verapamil, was perfused for 30 min by means of push-pull cannulae at a rate of 25.0 microliters/min. Verapamil 0.4, 2.0 and 4.0 micrograms/microliter) induced a concentration-dependent hypothermia when perfused within AH/POA sites but hyperthermia when perfused in the caudal hypothalamus. An anatomical analysis of the sites of perfusion revealed that verapamil's thermolytic effect was localized within the classical thermosensitive region of the cat's diencephalon, a region ventral to the anterior commissure and dorsal to the optic chiasm. On the other hand, the loci in which verapamil evoked thermogenesis were localized to a region dorsal to the mammillary bodies and caudal to the descending columns of the fornix. It is suggested that verapamil interferes with Ca++ ion channels in the PH to shift the cat's "set-point" temperature. Conversely, however, verapamil apparently could act on catecholaminergic terminals in AH/POA to enhance the presynaptic release of norepinephrine which, in turn, stimulates the heat loss pathway to yield hypothermia.
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PMID:Neuroanatomical mapping of hypothalamic regions mediating verapamil hyper- and hypothermia in the cat. 376 34

The activity of norepinephrine (NE) within the thermosensitive region of the anterior hypothalamic, pre-optic area (AH/POA) of the rat was examined in relation to changes in core temperature produced by ethyl alcohol. Following stereotaxic implantation of push-pull guide tubes, a specific site in the AH/POA, reactive or non-reactive to NE, was labeled with 1.0 microliter of [3H]-NE. Alcohol in a concentration of 2.75% or 5.5% was then perfused locally at the same site by push-pull cannulae or administered peripherally in a dose of 2.0 g/kg. In control experiments, artificial CSF was perfused alone. The perfusion of alcohol enhanced or delayed the release of [3H]-NE in AH/POA or failed to alter the efflux of the catecholamine, with the specific response dependent principally on the: (1) anatomical site of hypothalamic perfusion, (2) concentration of alcohol, and (3) interval of perfusion itself. During the perfusion of alcohol within a very circumscribed region in the AH/POA, vasodilatation, as reflected by an increase in skin temperature, and a hypothermia of short latency, occurred. The change in core temperature was usually accompanied by a delay in the efflux of [3H]-NE. After the peripheral administration of 2.0 g/kg alcohol, an alteration in NE efflux from the AH/POA was also induced during the course of a hypothermic response accompanied by vasodilatation. These results suggest that alcohol exerts a direct central effect on nerve cells comprising the thermoregulatory mechanism located within the hypothalamus. Further, the well-known thermolytic effect of alcohol could be mediated in part by noradrenergic synapses within AH/POA, by means of their phasic release of NE.
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PMID:Release of norepinephrine from the rat's hypothalamus perfused with alcohol: relation to body temperature. 406 63

In anaesthetized dogs at room temperatures of 28-33 degrees C, the cerebral ventricles were perfused with artificial CSF from the left lateral ventricular to the aqueductal cannulae. The animals' temperatures were recorded from the rectum. Addition of Ca(++) in excess to the artificial CSF perfusing the ventricles produced hyperthermia and addition of Na+ in excess produced hypothermia. Perfusion with medium deficient in Ca(++) and containing sodium edetate produced hypothermia. The temperature effects of Na(+) or Ca(++) in excess were mutually antagonistic.
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PMID:Effect on body temperature in dogs of perfusion of cerebral ventricles with artificiaL CSF deficient in calcium or containing excess of sodium or calcium. 478 40

To investigate the mechanisms responsible for the thermolytic action of neurotensin (NT), cannulae for intracerebroventricular (ICV) injection were implanted stereotaxically in Sprague-Dawley rats. Postoperatively, body temperature in the unrestrained rat was monitored continuously by a colonic thermistor probe. NT in a dose of 1.5-4.5 micrograms or CSF carrier vehicle was infused bilaterally in the cerebral ventricle (ICV) in a volume of 7.5 microliters. With the rats kept at an ambient temperature of 22 degrees C, NT given ICV produced a dose-dependent fall in core temperature of greater than 0.8 degree C. Pre-treatment of the animal's cerebral ventricle with amine receptor antagonists, phentolamine (20.0 micrograms), butaclamol (10.0 micrograms), methysergide (20.0 micrograms) or atropine (25.0 micrograms), all similarly infused ICV, failed to alter the hypothermia induced by NT. However, the calcium chelating agent, EGTA, given ICV in a dose of 4.0-8.0 micrograms blocked the thermolytic effect of NT on body temperature in a concentration-dependent manner. These results suggest that the central thermolytic action of NT is not mediated by catecholamine or other aminergic pathways which are implicated in the central mechanisms of thermoregulation. Rather, the peptide may act on a cellular process involving calcium activity in the hypothalamus, presumably to impair the maintenance of the animal's "set-point" for body temperature.
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PMID:Evaluation of neurotensin's thermolytic action by ICV infusion with receptor antagonists and a Ca++ chelator. 619 77


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