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

We examined the effects of acclimation temperature and two doses (2.5 and 25mgkg(-1)) of a pyrogen (lipopolysaccharide, LPS) on behavioral thermoregulation in juvenile green iguanas. Overall means of body temperatures for the three-day trial periods were compared among three groups of animals acclimated at 15, 25, and 34 degrees C. The responses of each group of animals to the two dosages of LPS and a control saline injection were examined. Within each treatment block, animals either chose high body temperatures characteristic of a fever response or chose low body temperatures characteristic of a hypothermic response. Thermoregulation was influenced by interaction effects between and among, and independent effects of, acclimation temperature, dose of LPS, and day. In some treatment blocks, individual lizard mass positively correlated with mean individual body temperature. Mean mass of lizards that chose higher body temperatures within a treatment block was higher than the mean mass of lizards that chose lower body temperatures. From these results, we concluded that LPS may induce two different behavioral thermoregulatory responses: fever or hypothermia. The actual amplitude and direction of body temperature change appears to be affected by acclimation temperature and possibly by mass or energy reserves of the animal. If the energy reserves are not sufficient to sustain the higher rate of metabolism associated with the higher body temperatures of a hyperthermic or feverish state, the animal may resort to hypothermia.
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PMID:Effects of lipopolysaccharide and acclimation temperature on induced behavioral fever in juvenile Iguana iguana. 1107 Mar 45

We have shown previously that febrile range temperatures modify cytokine production by adult macrophages. In this study, we compared the effects of moderate hyperthermia and hypothermia on the kinetics of lipopolysaccharide (LPS)-induced cytokine expression in monocytes and macrophages of newborns and adults. During culture at 40 degrees C, the initial rates of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) secretion were preserved, but the duration of secretion was shorter than the duration at 37 degrees C. TNF-alpha and IL1-beta concentrations in 24-h 40 degrees C culture supernatants were reduced 18%-50%. IL-6 concentration in 24-h 40 degrees C cultures was reduced 26%-29% in all cells except adult macrophages. At 32 degrees C, changes in early (2 h) and sustained (24 h) cytokine expression were reversed compared with those caused by hyperthermia. Culturing adult macrophages at 32 degrees C blunted early secretion of TNF-alpha and IL-6 by 69% and 65%, respectively, and increased TNF-alpha concentration at 24 h by 48% compared with levels at 37 degrees C. In adult monocytes cultured at 32 degrees C, early IL-6 and IL-1 beta secretion was decreased 64% and 51%, respectively. We speculate that the burst/suppression cytokine profile at febrile temperatures might enhance early activation of host defenses and prevent prolonged exposure to potentially cytotoxic cytokines. Hypothermia, on the other hand, may worsen outcome in infections by delaying and prolonging cytokine production.
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PMID:Effects of hypothermia and hyperthermia on cytokine production by cultured human mononuclear phagocytes from adults and newborns. 1115 70

The study was designed to test whether intact vagal innervation of the liver is required for the formation of tolerance to lipopolysaccharide (LPS). Wistar rats were subjected to either denervation of the liver (transection of the hepatic and both celiac branches of the abdominal vagus) or sham surgery. Two weeks later, each rat had an osmotic pump implanted subcutaneously. The pump was filled with either a suspension of Escherichia coli LPS (18 mg/ml) in saline or saline alone. Via a catheter, the pump delivered its content into the right jugular vein at a rate of approximately 0.72 microl/kg/h (approximately 13 microg/kg/h of LPS) over 28 d. On day 25 of the infusion, each animal had another catheter implanted into the left jugular vein. Three days later, each rat was injected with a lethal bolus dose of LPS (15 mg/kg) and had its colonic temperature recorded. The saline-infused sham-operated rats responded to the bolus injection of LPS with hypothermia followed by a fever (mean response magnitude 1.0+/-0.2 degrees C); 91% of the animals died within 24 h. The LPS-primed shams developed marked tolerance: When challenged with a lethal dose of LPS, they exhibited a significantly smaller thermal response (magnitude 0.5 +/- 0.2 degrees C) and none died. No group of the vagotomized animals, whether LPS- or saline-primed, became tolerant: Both groups exhibited similar hypothermic responses to the bolus LPS injection and a substantial mortality rate (40 and 100%, respectively). The study shows that prolonged infusion of low doses of LPS leads to the formation of tolerance and that vagal denervation of the liver by hepato-celiac vagotomy suppresses this process. The mechanisms of vagal control of the formation of LPS tolerance remain speculative.
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PMID:Does the formation of lipopolysaccharide tolerance require intact vagal innervation of the liver? 1118 17

The organophosphate pesticide (OP) chlorpyrifos leads to an acute period of hypothermia followed by a delayed fever in the rat. Methyl scopolamine, a peripheral muscarinic antagonist, is thought to have little effect on body temperature of the rat because it does not cross the blood brain barrier. However, administration of methyl scopolamine (1 mg/kg, i.p.) during the period of chlorpyrifos-induced fever results in a rapid recovery of core temperature. This indicates a peripheral cholinergic pathway is operative in the febrile response to chlorpyrifos and possibly other modes of fever. In this study, we evaluated the possible antipyretic role of methyl scopolamine (i.p.) to a variety of stimuli that lead to fever-like responses in the rat: stress-induced (handling and cage switch), chlorpyrifos-induced (15 mg/kg, p.o.), nocturnal-induced, and lipopolysaccharide (LPS)-induced fever (50 microg/kg, i.p.). Methyl scopolamine led to marked reversal in the elevated core temperature caused by handling, cage switch, and during the nocturnal phase. It is of interest to note that all these elevations of core body temperature are prostaglandin mediated and are blocked with the antipyretic drug, sodium salicylate. However, LPS-induced fever, also a prostaglandin dependent fever, was unaffected by methyl scopolamine. Methyl scopolamine also lowered baseline core temperature when administered during the afternoon, but not during the morning in unstressed animals. It is proposed that a peripheral cholinergic pathway, possibly mediated through afferent vagal pathways, is operative in controlling core temperature during fevers associated with stress, nocturnal phase, and a pesticide. During recovery from exposure to a LPS, the fever appears to be mediated independently of peripheral cholinergic activation.
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PMID:A peripheral mechanism of fever: differential sensitivity to the antipyretic action of methyl scopolamine. 1118 22

The multiple effects of vagotomy on the thermoregulatory response to systemic inflammation are reviewed (primarily, for the model of intravenous lipopolysaccharide administration in the rat). The following conclusions are drawn. (1) Vagotomy-associated thermoeffector insufficiency is likely to account for the attenuation of the fever response observed in some--but not all--studies; such an insufficiency is, however, preventable by postoperative care, including the use of a liquid diet. (2) The febrile response to low doses of lipopolysaccharide (monophasic fever) is mediated by the hepatic (but not gastric or celiac) vagal fibers, presumably afferent; the same fibers are likely to be involved in the development of tolerance to low doses of circulating endotoxins. (3) Phase 1 of the polyphasic febrile response to moderate doses of lipopolysaccharide involves capsaicin-sensitive afferents (either nonvagal only or both nonvagal and vagal), does not involve cholecystokinin A-receptors, and may involve peripheral prostaglandins. (4) Febrile phase 2 does not require the integrity of abdominal nerve fibers, either vagal or nonvagal, at least in the rat. (5) Phase 3 of the febrile response to intravenous lipopolysaccharide (and perhaps the response to intraperitoneal lipopolysaccharide) involves capsaicin-insensitive vagal fibers, presumably efferent; the involvement of these fibers in febrigenic mechanisms is strongly modulated by an unknown factor. (6) A hepatoceliac vagal, presumably efferent, mechanism ('an anti-inflammatory pathway') counteracts the development of lipopolysaccharide-induced hypothermia and shock.
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PMID:Thermoregulatory manifestations of systemic inflammation: lessons from vagotomy. 1118 25

Antidepressants produce various immunomodulatory effects, as well as an attenuation of the behavioral responses to immune challenges, such as lipopolysaccharide (LPS). To explore further the effects of antidepressants on neuroimmune interactions, rats were treated daily with either fluoxetine (Prozac) or saline for 5 weeks, and various behavioral, neuroendocrine, and immune functions were measured following administration of either LPS or saline. Chronic fluoxetine treatment significantly attenuated the anorexia and body weight loss, as well as the depletion of CRH-41 from the median eminence and the elevation in serum corticosterone levels induced by LPS. Chronic treatment with imipramine also attenuated LPS-induced adrenocortical activation. In rats and in mice, which normally display a biphasic body temperature response to LPS (initial hypothermia followed by hyperthermia), chronic treatment with fluoxetine completely abolished the hypothermic response and facilitated and strengthened the hyperthermic response. The effects of antidepressants on the responsiveness to LPS are probably not mediated by their effects on peripheral proinflammatory cytokine production, because LPS-induced expression of TNFalpha and IL-1beta mRNA in the spleen (assessed by semiquantitative in situ hybridization) was not altered following chronic treatment with either fluoxetine or imipramine. The effects of antidepressants on the acute phase response may have important clinical implications for the psychiatric and neuroendocrine disturbances that are commonly associated with various medical conditions.
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PMID:Effects of antidepressant drugs on the behavioral and physiological responses to lipopolysaccharide (LPS) in rodents. 1128 53

At standard laboratory ambient temperatures (T(a)) of 20-24 degrees C, peripheral injections of lipopolysaccharide (LPS) reliably produce fever in young rats. In contrast, old rats may show a blunted fever, no fever, or even hypothermia after LPS. In the present study we hypothesized that old rats might use behavioral thermoregulation to help them develop a fever. Young and old rats were implanted with temperature transmitters. At least 1 wk postoperatively they were placed in a thermally graded alleyway (T(a) 10-40 degrees C). On the third and sixth day they were taken out of the gradient, placed at an T(a) of 23 degrees C, injected intraperitoneally with LPS or saline, and left at 23 degrees C for 3 h. At the end of that time, all young rats had become febrile, whereas the old rats had not. When the rats were replaced in the thermal gradient, the young animals continued to develop a fever that was similar to fever in young rats left at 23 degrees C. The old animals chose significantly warmer positions in the thermal gradient than did the young animals and only then became febrile. Although there was a tendency for the young rats to prefer higher T(a) after LPS than after saline, these differences were not significant. However, the differences in the old rats were significant. These results suggest that the LPS had increased the thermal set point in the old rats, but they could develop febrile responses only at the warm T(a) they selected.
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PMID:Fever and behavioral thermoregulation in young and old rats. 1129 68

Interleukin (IL)-1 and tumor necrosis factor (TNF) promote slow-wave sleep (SWS), whereas IL-10 inhibits the synthesis of IL-1 and TNF and promotes waking. We evaluated the impact of endogenous IL-10 on sleep-wake behavior by studying mice that lack a functional IL-10 gene. Under baseline conditions, C57BL/6-IL-10 knockout (KO) mice spent more time in SWS during the dark phase of the light-dark cycle than did genetically intact C57BL/6 mice. The two strains of mice showed generally comparable responses to treatment with IL-1, IL-10, or influenza virus, but differed in their responses to lipopolysaccharide (LPS). In IL-10 KO mice, LPS induced an initial transient increase and a subsequent prolonged decrease in SWS, as well as profound hypothermia. These responses were not observed in LPS-treated C57BL/6 mice. These data demonstrate that in the absence of endogenous IL-10, spontaneous SWS is increased and the impact of LPS on vigilance states is altered. Collectively, these observations support a role for IL-10 in sleep regulation and provide further evidence for the involvement of cytokines in the regulation of sleep.
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PMID:Cytokine- and microbially induced sleep responses of interleukin-10 deficient mice. 1135 86

Tumour necrosis factor (TNF) is a major mediator in septic shock and several inflammatory diseases such as hepatitis. Galactosamine (GalN) sensitises experimental animals for TNF and the combination TNF/GalN leads to a lethal inflammatory hepatitis. We describe that a single injection of lipopolysaccharide (LPS), interleukin-1 (IL-1) or TNF can desensitise against the lethality induced by TNF/GalN, but also against changes in metabolic parameters such as hypothermia and transaminase release, in a dose responsive way. We also describe the desensitising capacity of a component present in Mouse Liver Extract (MLE). The MLE desensitises mice against the effects of TNF/GalN in a dose responsive way. The activity of the MLE is heat labile and does not involve LPS, TNF, IL-1 or TNF soluble receptors. We describe partial and complete purification of the factor. Partially pure material protects mice against all changes induced by TNF/GalN. The protection is dose dependent and heat labile and also possible in endotoxin-hyporesponsive C3H/HeJ mice. The pure material protects against lethality, hypothermia and AST release and it appears as a heat labile protein of relative molecular weight of 70 kDa probably with a break down product of 35 kDa.
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PMID:Detection, characterisation and purification of a murine liver factor capable of desensitising towards the lethal activity of tumour necrosis factor. 1150 80

The mediation of orexin-A-induced hypothermia was investigated. Different doses of orexin-A (140-560 pmol) were administered intracerebroventricularly (i.c.v.) to adult male rats, and the colon temperature was used as an index of the thermoregulatory action. Orexin-A decreased both the basal colon temperature and the lipopolysaccharide-induced fever and exhibited a bell-shaped dose-response curve. I.c.v. pretreatment with neuropeptide Y (NPY) antiserum 24 h before orexin administration significantly decreased the hypothermic effect of orexin-A. These data strengthen the hypothesis that this appetite-regulating peptide might also play a role in thermoregulation, and its hypothermic effect seems to be mediated at least partially by NPY.
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PMID:The role of NPY in the mediation of orexin-induced hypothermia. 1183 Feb 77


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