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

In the unanesthetized rat, Ca++ ions in solutions ranging from 2.6 to 112.0 mM in excess of the normal level in CSF were applied at different sites in the brain and by three separate procedures, Colonic temperature was monitored and in certain experiments, the amount of food pellets and water consumed was measured simultaneously following the administration of excess Ca++ ions. An infusion into the lateral cerebral ventricle of excess calcium in a volume of 5.0 mul produced a concentration-dependent hypothermia, This fall in temperature was not attenuated by a prior intraventricular infusion of mecamylamine and often enhanced by atropine. Depending on the site, a microinjection of excess Ca++ ions in a volume of 0.5 to 1.0 mul directly into the hypothalamus produced hypothermia or feeding. The sites of maximum sensitivity at which excess calcium caused a decline in temperature were clustered in the caudal hypothalamus, whereas those at which calcium elicited feeding were distributed widely in caudo-lateral, medial and rostral hypothalamic areas. Push-pull perfusions at a rate of 20 to 25 mul per min for 10 to 20 min at homologous sites caused similar responses but the cation concentration required to evoke feeding or hypothermia was significantly less than that of either microinjection or intraventricular infusion. These findings demonstrate species continuity in the rat concerning anatomical localization of the postulated set-point mechanism for body temperature. Several different pathways in the feeding system are affected by an alteration in the hypothalamic level of calcium.
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PMID:Feeding and body temperature in the rat: diencephalic localization of changes produced by excess calcium ions. 18 84

The effects of 5,7-dihydroxytryptamine and L-tryptophan treatment on ethanol tolerance in the rat, as measured by the moving-belt test of motor impairment and by hypothermia, were examined in separate studies. A 2 x 2 design was used for all experiments. 5,7-Dihydroxytryptamine (200 microgram in 20 microliter CSF) or vehicle alone was administered once into both lateral ventricles of the rat. Desmethylimipramine was administered intraperitoneally prior to an intraventricular injection of 5,7-dihydroxytryptamine to prevent the destruction of norepinephrine. L-Tryptophan (75 mg/kg p.o. twice daily) or water was administered chronically. Ethanol (4--5 g/kg p.o.) or sucrose was given daily, and the development of tolerance was monitored at 5--7-day intervals. Chronic ethanol treatment produced tolerance to both the motor impairment and hypothermia effects of ethanol. 5,7-Dihydroxytryptamine and L-tryptophan treatment did not alter either the motor impairment or hypothermia produced by the initial dose of ethanol. 5,7-Dihydroxytryptamine produced a 75% depletion of brain 5-HT and slowed the development of tolerance to ethanol in both measurements. In contrast, elevation of 5-HT by L-tryptophan (39% increase by a single dose) facilitated the development of tolerance to ethanol, as seen in both measures. These findings support our hypothesis that brain 5-HT has a modulating role in the development of tolerance to ethanol.
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PMID:Effect of modification of brain serotonin (5-HT) on ethanol tolerance. 39 Oct 88

Total cerebral ischaemia in rats caused a marked increase in the cisternal CSF potassium concentration but little change in CSF sodium or chloride concentration. The anaesthetic techniques studied (pentobarbitone, halothane/oxygen and nitrous oxide/oxygen/relaxant) did not effect the potassium increase following cerebral ischaemia. We conclude that the mechanism of barbiturate protection following cerebral ischaemia is different from that of hypothermia.
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PMID:Effect of anaesthetic agents on the ionic composition of cerebrospinal fluid following total cerebral ischaemia. 62 2

After describing the various methods for measuring the intracranial pressure, the causes of the rise of pressure within the skull and the possibilities for compensation are discussed. The elasticity of the brain tissue, which can be determined by pressure/volume stress, plays a crucial role in compensating for pressure. A reciprocal influence exists between intracranial pressure, cerebral circulation and brain oedema, as well as between intracerebral pressure and peripheral circulation. The treament of raised intracranial pressure is possibly by CSF drainage, hyperventilation and hypothermia, as well as by drugs such as steroids and diuretics.
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PMID:[Increased intracranial pressure. Methods of measurement, pathophysiology and treatment (author's transl)]. 70 17

Within the rostral diencephalon of the cat, 113 sites were examined for their reactivity to 2.33--14.0 microgram dopamine (DA) or 2.33--14.0 microgram norepinephrine (NE) microinjected in a volume of 0.75 microliter. During each experiment, colonic temperature was monitored and additional physiological measures were recorded continuously. In contrast to CSF controls, an intrahypothalamic injection of either catecholamine at circumscribed sites evoked a dose-dependent fall in the cat's body temperature, with NE ordinarily evoking a more profound hypothermic response. The morphological sites of maximum sensitivity were localized in the anterior hypothalamic, preoptic region. At some but not all sites, a prior microinjection of 3.5--7.0 microgram phentolamine attenuated the magnitude of the DA-induced hypothermia and delayed its onset. Conversely, at all loci, the pretreatment by the injection of this alpha-adrenergic antagonist markedly reduced the absolute magnitude of the NE-induced fall in the cat's temperature. Similar pretreatment of a reactive hypothalamic locus with a beta-adrenergic receptor blocking agent, practolol (3.5 microgram), failed to alter the hypothermia following a microinjection of DA. Either of two DA receptor antagonists, haloperidol (0.04--7.0 microgram) or d-butaclamol (0.48--1.47 microgram), when given in a sufficient dose, effectively delayed the onset of the DA-hypothermia and reduced its absolute magnitude; however, the NE-induced decline in the cat's temperature was unaffected by DA receptor blockade. Endogenous stores of DA and/or NE in the cat's hypothalamus were radio-labeled with either 3H- or 14C-catecholamines or both, microinjected through the implanted guide tube into an identified amine-sensitive site. By using push-pull cannulae, the site was subsequently perfused for 5 min with artificial CSF at a rate of 25 microliter/min with samples collected at 15 min intervals. During either the third or fourth perfusion, the ambient temperature of the cat's chamber of 22--24 degrees C was elevated to 35--45 degrees C and maintained at this level for 15 or 30 min. This environmental warming evoked a release of either DA o; NE or both amines from certain circumscribed sites within the cat's rostral hypothalamus. Overall, these results provide pharmacological, physiological and anatomical evidence for a differential role of DA in the hypothalamic mechanism which mediates the heat loss processes.
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PMID:Dopamine in the hypothalamus of the cat: pharmacological characterization and push-pull perfusion analysis of sites mediating hypothermia. 70 54

Five methods of therapy for increased ICP were used in the treatment of 32 head-injured patients. The effects of steroids could not be evaluated. Withdrawal of CSF was always effective because intracranial volume was reduced and pressure must follow, but because of brain swelling and collapse of the ventricular system in this group of patients, it was not an effective permanent form of therapy. Hypertonic Mannitol reduced ICP in nearly every case irrespective of the degree of brain damage or the height of ICP. Hyperventilation was least effective in the most severely ill patients, presumably due to the non-responsiveness of the cerebral vessels to changes in PaCO2. The poorest response of ICP seemed to be with hypothermia.
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PMID:Analysis of the response to therapeutic measures to reduce intracranial pressure in head injured patients. 93 13

The effects of changes in ambient and central temperature, amines, PGEu and pyrogen were investigated with respect to the mechanism of Na+-Ca++ ratio in the posterior hypothalamus of the unrestrained cat. Guide tubes were implanted bilaterally above the posterior hypothalamic area of 23 cats so as to accommodate push-pull cannulae. After a Na+ or Ca++ sensitive site was identified by perfusion at 50 mul/min of an artificial CSF containing 10.4 mM excess Ca++ ions or 13.6 mM excess Na+ ions, several types of experiments were undertaken with the results summarized as follows: if the cat was exposed to a cold or warm environmental temperature as the posterior hypothalamus was perfused with excess cation, the typical hypothermia was produced by Ca++ and hyperthermia by Na+ ions. However, if the cat was exposed to peripheral cooling or warming 30 min prior to the perfusion, the fall or rise produced by Ca++ or Na+ was attenuated or prevented. In other experiments, 1.0 muCi 45Ca++ was injected in the ion sensitive site in the posterior hypothalamus to label stores of the cation. Raising of ambient temperature caused a retention of 45Ca++ in this hypothalmic area, whereas a cold environmental temperature enhanced the efflux of 45Ca++ at the same perfusion site. The magnitude of change in 45Ca++ efflux depended upon the intensity of the thermal challenge. Similarly, warming of the anterior hypothalmic, preoptic area by means of implanted thermodes caused an immediate diminution in 45Ca++ efflux in the posterior hypothalamus, whereas cooling of this anterior region augmented the extrusion of 45Ca++ ions from the posterior area. When substances which produce a temperature change were applied to the same thermosensitive zone, the direction of shift in 45Ca++ flux in the posterior area corresponded to the signal for heat production or heat loss. That is, the microinjection of 5-HT, PGE1 or Salmonella typhosa into the anterior hypothalamus enhanced the efflux of 45Ca++ in the posterior hypothalamus as hyperthermia developed, whereas a similar microinjection of norepinephrine reduced the 45Ca++ output from the same sites. Finally, locally anesthetizing the cells of the anterior hypothalamus by the nerve blocker, procaine, prevented the cold and heat-induced 45Ca++ eflux and retention, respectively. These results suggest that if the Na+-Ca++ ratio in the posterior hypothalamus establishes and maintains the set-point for body temperature of 37 degrees -38 degrees C, the mechanism of lability of Ca++ through changes in binding characteristics, transport, or metabolism of the cation serves two purposes: (1) the active defense of the set-point temperature through gradations in ion shifts; and (2) the upward or downward change in set-point value, pathological or normal, triggered by virtue of impulses relayed from the anterior hypothalamus.
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PMID:Hypothalamic Na+ and Ca++ ions and temperature set-point: new mechanisms of action of a central or peripheral thermal challenge and intrahypothalamic 5-HT, NE, PGEi and pyrogen. 97 10

Triggering of the CD3 molecule by in vivo injection of the hamster anti-murine CD3 monoclonal antibody 145-2C11 in adult BALB/c mice leads to massive although transient T cell activation. High levels of tumour necrosis factor (TNF), interferon-gamma (IFN-gamma), IL-2, IL-3 and IL-6 are released into the circulation 1 to 8 h after a single 10 micrograms 145-2C11 i.v. injection. This release induces an impressive self-limited physical reaction associating hypothermia, hypomotility (as assessed by actimetry), diarrhoea, piloerection and even death when high doses (a single dose of greater than 100 micrograms/mouse injection) are administered. In vivo injection of 145-2C11 to other selected mouse strains, namely NZW, CBA/J and C3H/HeJ, induced both different cytokine release patterns and sickness. 145-2C11 induced significant release of TNF and IL-2 in all four strains. At variance, IFN-gamma was only detected in BALB/c mice sera which, in terms of physical reaction (hypothermia and hypomotility) were the most affected. Higher and long-lasting circulating IL-3/GM-CSF levels were present in CBA/J sera, correlating with a later recovery. These results underline heterogeneity in the in vivo cell activation pattern among different mouse strains, when triggering T lymphocytes via the CD3/Ti molecule as compared to exclusive targeting of monocyte/macrophages by means of lipopolysaccharide.
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PMID:Inter-mouse strain differences in the in vivo anti-CD3 induced cytokine release. 172 Oct 15

Changes in the body temperature (Tbo) of the unrestrained rat as well as the hyperphagic-like ingestion of food were simultaneously determined during the sustained elevation of neuropeptide Y1-36 (NPY) within the anterior hypothalamic preoptic area (AH/POA). A single guide tube was implanted stereotaxically in each rat for repeated perfusions by means of push-pull cannulae of either the CSF solvent vehicle or NPY. Following postoperative recovery, each site in the AH/POA was perfused for 6.0 min at a rate of 20 microliters/min over four successive intervals at a concentration of 100 ng/1.0 microliters or 250 ng/1.0 microliters, with an interval of 6.0 min intervening between perfusions. During repeated perfusions of NPY in the fully sated and normothermic rat, concentration-dependent eating, or a hypothermia or both responses occurred simultaneously. Mean cumulative intakes of food over 3.0 h were 12.1 +/- 1.4 and 21.5 +/- 2.7 g following the 100 and 250 ng concentrations of NPY, respectively. The mean maximal declines in Tbo were -0.92 +/- 0.21 and -1.1 +/- 0.28 degrees C, respectively after the lower and higher concentrations of the peptide. Push-pull perfusions of artificial CSF control vehicle at homologous anatomical sites in the AH/POA were without effect on feeding or the Tbo of the rats. These results demonstrate that repeated and sustained elevation of NPY in the AH/POA can cause a perturbation of the neuronal mechanisms underlying the normal "set-point" for body temperature as well as satiety.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothermia and feeding induced simultaneously in rats by perfusion of neuropeptide Y in preoptic area. 176 96

During the last decade several studies of cerebral blood flow (CBF) and metabolism in the acute phase of head injury have been published. It is the aim of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO2), cerebral autoregulation (CA), and reactivity to PaCO2 and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to prolonged artificial hyperventilation, hypothermia, barbiturate sedation, and mannitol therapy. On the basis of present knowledge concerning cerebral circulation and its regulation, the author reviews the literature concerning methodology for experimental and clinical CBF measurements and regulation of CBF and cerebral oxygen uptake. Emphasis is placed on studies of the effect of body temperature (hypothermia) as a therapeutic tool in the control of cerebral metabolism, blood flow, and intracranial pressure. Although hypothermia significantly reduces cerebral metabolism and blood flow, the effect of hypothermia on cerebral blood flow, metabolism, ICP, and outcome after acute head injury has never been investigated in clinically controlled studies. Experimental and clinical studies concerning sensitivity of CBF for changes in PaCO2 are reviewed. The normal CO2 reactivity defined as absolute (delta CBF/delta PaCO2) and relative (% change CBF/delta PaCO2) or delta in CBF/PaCO2 mm Hg are mentioned. In awake normocapnic man the relative CO2 reactivity averages 4%/mm Hg and the absolute CO2 reactivity 2ml/mm Hg. Uncontrolled prospective studies show a therapeutic effect of artificially prolonged hyperventilation on outcome. Only one preliminary controlled study indicates that the outcome is poorer and recovery prolonged. Nevertheless, in the acute phase of HI, artificial hyperventilation is used routinely for control of intracranial hypertension and during the intensive care management of the patients. The steal and inverse steal phenomena are reviewed. Although of considerable theoretical interest these phenomena are without clinical significance in patients with head injury, unless clinical CBF measurements are performed. The frequency of the inverse steal phenomenon in studies of rCBF with a 16-channel Cerebrograph (intraarterial approach) is found to be about 10%. During prolonged hyperventilation experimental studies and clinical studies of apoplexy show an adaptation of CBF and CSF-pH and bicarbonate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy. 227 29


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