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prostaglandin/demam
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Nitric oxide mediates noradrenaline-induced hypothermic responses and opposes prostaglandin E2-induced fever in the rostromedial preoptic area.
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Noradrenaline (NA) microinjected into the rostromedial preoptic area (POA) elicits heat loss responses and opposes prostaglandin E(2)-induced fever. Here, I tested the hypothesis that local synthesis and release of nitric oxide (NO) mediates the NA-induced effects. The unilateral microinjection of
Administration of prostaglandin E2 into the striatum induces hyperthermia in rats.
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Changes in thermoregulatory function were assessed in unanesthetized rats after a unilateral injection of prostaglandin E2 (PGE2) into the striatum or the substantia nigra. Intrastriatal injection of PGE2, but not vehicle solution, induced a dose-dependent rise in rectal temperature. The
Hypothalamic prostaglandin E2 during lipopolysaccharide-induced fever in guinea pigs.
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Prostaglandin E2 (PGE2) is postulated to be a central mediator of fever. It is generally believed that it is produced in the preoptic area of the anterior hypothalamus (POA) because, among other evidence, its level increases both in the third ventricle and in the POA in response to pyrogens.
Stimulation of muscle protein degradation and prostaglandin E2 release by leukocytic pyrogen (interleukin-1). A mechanism for the increased degradation of muscle proteins during fever.
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To clarify the mechanisms underlying the loss of body protein during fever and sepsis, we incubated rat muscles with highly purified human leukocytic pyrogen. This polypeptide, which appears identical to interleukin-1, is released by leukocytes and signals the onset of fever in the hypothalamus. In
CCL3/macrophage inflammatory protein-1alpha induces fever and increases prostaglandin E2 in cerebrospinal fluid of rats: effect of antipyretic drugs.
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The aim of this study was to investigate whether the increase in body temperature caused by intracerebroventricular (i.c.v.) injection of recombinant mouse CCL3/MIP1alpha [C-C (two adjacent conserved cysteines) ligand 3/macrophage inflammatory protein-1alpha] constitutes solely a hyperthermic
The effect of central angiotensin II receptor blockade on interleukin-1beta- and prostaglandin E-induced fevers in rats: possible involvement of brain angiotensin II receptor in fever induction.
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We investigated the role of the brain angiotensin II (Ang II) receptor subtypes AT1 and AT2 in the development of fever induced in freely moving rats by administration of interleukin-1beta (IL-1beta) or prostaglandin E2 (PGE2). Intraperitoneal (i.p.) injection of IL-1beta (2 microg/kg) induced a
d-Amphetamine antagonizes prostaglandin E1-induced hyperthermia and suppression of fixed interval operant behavior in rats.
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The experiments reported herein were designed to study the effects of prostaglandin F2 alpha (PGF2 alpha) and PGE1 on operant behavior and rectal temperature of rats. A solution containing PGF2 alpha or PGE1 was infused intracerebroventricularly into rats trained to press a lever for food reward on
The effect of an inhibitor of adenylate cyclase on the development of pyrogen, prostaglandin and cyclic AMP fevers in the rabbit.
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An exotoxin of Bacillus thuringiensis known to inhibit adenylate cyclase in vitro has been used to investigate the role of cyclic AMP in the pathogenesis of fever in the rabbit. Intra-hypothalamic microinjections of the exotoxin are non-pyrogenic and significantly attenuate the hyperthermia caused
Effect of central cholinergic blockade on the hyperthermia evoked by prostaglandin E1 injected into the rostral hypothalamus of the rat.
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The possibility of a cholinergic involvement in the hyperthermic action produced by the injection of prostaglandin E1 (PGE1) into the anterior hypothalamic/preoptic region of the rat brain was examined. Intracerebral injection of either atropine or mecamylamine prior to the injection of PGE1 failed
Pattern differences in experimental fevers induced by endotoxin, endogenous pyrogen, and prostaglandins.
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To distinguish pattern differences in experimentally induced fevers, we investigated febrile responses induced by intravenous (IV), intracerebroventricular (ICV), and intra-preoptic/anterior hypothalamic (POA) administration of bacterial endotoxin (lipopolysaccharide, LPS), endogenous pyrogen (EP),
Endogenous opioids: role in prostaglandin-dependent and -independent fever.
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This study evaluated the participation of mu-opioid-receptor activation in body temperature (T(b)) during normal and febrile conditions (including activation of heat conservation mechanisms) and in different pathways of LPS-induced fever. The intracerebroventricular treatment of male Wistar rats
An extensive exploration of the rat brain for sites mediating prostaglandin-induced hyperthermia.
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Experiments designed to ascertain the site or sites within the brain where prostaglandins act to evoke hyperthermia were carried out. At an ambient temperature of 20 degrees C, microinjections of PGE1 (50-100 ng) or saline vehicle were made in restrained rats. The 272 sites tested formed a matrix
Prostaglandin E1 hyperthermia in water or food deprived rats.
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The effect of 48 hours of water deprivation on the colonic temperature response to intrahypothalamic injection of prostaglandin E1 (PGE1) was investigated in adult male rats. Water deprivation did not alter colonic temperature of rats at a neutral ambient temperature. Administration of PGE1 at doses
Restraint, but not frustration, induces prostaglandin-mediated hyperthermia in pigs.
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Three experiments were carried out to investigate stress hyperthermia in prepubertal pigs. Experiment 1 examined the effect of frustrative nonreward (psychological stress) on deep body temperature in animals (n = 7) trained to make operant responses for food following a 17.5-h period of deprivation.
Prostaglandin E2-induced fever in young and old Long-Evans rats.
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Aging is associated with a blunted or absent fever response to naturally occurring infections or to the peripheral administration of bacterial products and proinflammatory cytokines. We have recently shown that old Long-Evans rats are not defective in their capacity to develop a fever in response to
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