Fever

Scholz, Holger

doi:10.1152/ajpregu.00774.2002

Cited by 6 publications

(3 citation statements)

References 23 publications

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“…Fever, a regulated increase in body temperature achieved by increasing the thermostatic setpoint, is a salient component of a host response to bacterial infection that in mammals includes immunologic, autonomic, endocrine, and behavioral adjustments (for reviews, see Refs. 73,102,115,176). In rats, sympathetic activation of BAT and cutaneous vasoconstriction play primary roles in the increases in temperature seen in experimental fever (65,92,166).…”

Section: Involvement Of Dmh In Physiological and Pathophysiological Tmentioning

confidence: 99%

The dorsomedial hypothalamus: a new player in thermoregulation

DiMicco

Zaretsky

2007

American Journal of Physiology-Regulatory, Integrative and Comp

259

218

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Neurons in the dorsomedial hypothalamus (DMH) play key roles in physiological responses to exteroceptive ("emotional") stress in rats, including tachycardia. Tachycardia evoked from the DMH or seen in experimental stress in rats is blocked by microinjection of the GABA(A) receptor agonist muscimol into the rostral raphe pallidus (rRP), an important thermoregulatory site in the brain stem, where disinhibition elicits sympathetically mediated activation of brown adipose tissue (BAT) and cutaneous vasoconstriction in the tail. Disinhibition of neurons in the DMH also elevates core temperature in conscious rats and sympathetic activity to least significant difference interscapular BAT (IBAT) and IBAT temperature in anesthetized preparations. The latter effects are blocked by microinjection of muscimol into the rRP, while microinjection of muscimol into either the rRP or DMH suppresses increases in sympathetic nerve activity to IBAT, IBAT temperature, and core body temperature elicited either by microinjection of PGE(2) into the preoptic area (an experimental model for fever), or central administration of fentanyl. Neurons concentrated in the dorsal region of the DMH project directly to the rRP, a location corresponding to that of neurons trans-synaptically labeled from IBAT. Thus these neurons control nonshivering thermogenesis in rats, and their activation signals its recruitment in diverse experimental paradigms. Evidence also points to a role for neurons in the DMH in thermoregulatory cutaneous vasoconstriction, shivering, and endocrine adjustments. These directions provide intriguing avenues for future exploration that may expand our understanding of the DMH as an important hypothalamic site for the integration of autonomic, endocrine, and behavioral responses to diverse challenges.

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Section: Involvement Of Dmh In Physiological and Pathophysiological Tmentioning

confidence: 99%

The dorsomedial hypothalamus: a new player in thermoregulation

DiMicco

Zaretsky

2007

American Journal of Physiology-Regulatory, Integrative and Comp

259

218

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“…[15,16]); this increase in body temperature is considered one of the cardinal features of inflammation and takes place in the same general time-frame in which NK cells are initiating their activation and functional activity, as both events are triggered by the same proinflammatory signals. However, despite the temporal linkage between cytokinedriven NK cell activation and the pyrogenicity of these same cytokines, a separate thermal component in the regulation of NK cell activation has not been fully characterized.…”

Section: Introductionmentioning

confidence: 99%

Enhancement of natural killer (NK) cell cytotoxicity by fever-range thermal stress is dependent on NKG2D function and is associated with plasma membrane NKG2D clustering and increased expression of MICA on target cells

Ostberg

Dayanç

Yuan

et al. 2007

Journal of Leukocyte Biology

109

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Circulating NK cells normally experience temperature gradients as they move about the body, but the onset of inflammation can expose them and their targets to febrile temperatures for several hours. We found that exposure of human peripheral blood NK cells and target cells to fever-range temperatures significantly enhances lysis of Colo205 target cells. A similar effect was not observed when NK cell lines or IL-2-activated peripheral blood NK cells were used as effectors, indicating that thermal sensitivity of effectors is maturation or activation state-dependent. Use of blocking antibodies revealed that this effect is also dependent on the function of the activating receptor NKG2D and its ligand MHC class I-related chain A (MICA). On NK cells, it was observed that thermal exposure does not affect the total level of NKG2D surface expression, but does result in its distinct clustering, identical to that which occurs following IL-2-induced activation. On tumor target cells, a similar, mild temperature elevation results in transcriptional up-regulation of MICA in a manner that correlates with increased sensitivity to cytolysis. Overall, these data reveal that NK cells possess thermally responsive regulatory elements, which facilitate their ability to capitalize on reciprocal, stress-induced changes simultaneously occurring on target cells during inflammation and fever.

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“…Since the publication of the "IL hypothesis," the effects of uremia and HD on the production of especially IL-1, TNF, and IL-6 by peripheral mononuclear cells have been studied extensively (36). An increase in cytokine generation might increase CT by stimulation of the anterior hypothalamic area (37). However, in this study, pre-and postdialysis values of TNF-␣, IL-1-ra, and IL-6 did not change during the different sessions and were not related to thermal variables.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ultrafiltration on Thermal Variables, Skin Temperature, Skin Blood Flow, and Energy Expenditure during Ultrapure Hemodialysis

Sande¹,

Rosales²,

Brener³

et al. 2005

Journal of the American Society of Nephrology

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The cause of the increase in core temperature (CT) during hemodialysis (HD) is still under debate. It has been suggested that peripheral vasoconstriction as a result of hypovolemia, leading to a reduced dissipation of heat from the skin, is the main cause of this increase in CT. If so, then it would be expected that extracorporeal heat flow (Jex) needed to maintain a stable CT (isothermic; T-control ‫؍‬ 0, no change in CT) is largely different between body temperature control HD combined with ultrafiltration (UF) and body temperature control HD without UF (isovolemic). Consequently, significant differences in ⌬CT would be expected between isovolemic HD and HD combined with UF at zero Jex (thermoneutral; E-control ‫؍‬ 0, no supply or removal of thermal energy to and from the extracorporeal circulation). During the latter treatment, the CT is expected to increase. In this study, changes in thermal variables (CT and Jex), skin blood flow, energy expenditure, and cytokines (TNF-␣, IL-1 receptor antagonist, and IL-6) were compared in 13 patients, each undergoing body temperature control (T-control ‫؍‬ 0) HD without and with UF and energy-neutral (E-control ‫؍‬ 0) HD without and with UF. CT increased equally during energy-neutral treatments, with (0.32 ؎ 0.16°C; P ‫؍‬ 0.000) and without (0.27 ؎ 0.29°C; P ‫؍‬ 0.006) UF. In body temperature control treatments, the relationship between Jex and UF tended to be significant (r ‫؍‬ ؊0.51; P ‫؍‬ 0.07); however, there was no significant difference in cooling requirements regardless of whether treatments were done without (؊17.9 ؎ 9.3W) or with UF (؊17.8 ؎ 13.27W). Changes in energy expenditure did not differ among the four treatment modes. There were no significant differences in pre-and postdialysis levels of cytokines within or between treatments. Although fluid removal has an effect on thermal variables, no single mechanism seems to be responsible for the increased heat accumulation during HD. A n inadequate vascular response to hypovolemia is an important contributory factor to intradialytic hypotension. Although various mechanisms have been implicated in the pathogenesis of impaired vascular response during hemodialysis (HD) (1-7), there are strong indications that this phenomenon is often related to changes in body temperature and extracorporeal blood temperature (8 -22).We and others have observed that the core temperature (CT) increased during standard-temperature (37 to 38°C) dialysis (16,18 -24) even with net energy loss from the patient to the extracorporeal system. This phenomenon strongly suggests that the dialysis procedure itself leads to internal heat accumulation. It has been observed that 4 h of standard dialysis leads to a positive internal heat balance of approximately 300 kJ, which represents approximately 30% of the energy expenditure (EEvmax) of the patient (25). The internal heat accumulation might very well be responsible for the impaired vascular response during HD, as the thermoregulatory response (leading to dilation of thermoregulatory vessels) wi...

show abstract

Fever

Cited by 6 publications

References 23 publications

The dorsomedial hypothalamus: a new player in thermoregulation

The dorsomedial hypothalamus: a new player in thermoregulation

Enhancement of natural killer (NK) cell cytotoxicity by fever-range thermal stress is dependent on NKG2D function and is associated with plasma membrane NKG2D clustering and increased expression of MICA on target cells

Effect of Ultrafiltration on Thermal Variables, Skin Temperature, Skin Blood Flow, and Energy Expenditure during Ultrapure Hemodialysis

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