hyperalgesia/horúčka

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Development of hyperthermia and hyperalgesia following intracerebroventricular administration of endotoxin in the rat: effect of kinin B1 and B2 receptor antagonists.

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The present study investigated the development of hyperthermia and thermal and mechanical hyperalgesia following i.c.v. injections of E. coli lipopolysaccharide (LPS) in rats. LPS increased core temperature and this was prevented by i.c.v. administration of HOE 140, a kinin B2 receptor antagonist or

Dissociation of hyperalgesia from fever following intracerebroventricular administration of interleukin-1beta in the rat.

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Interleukin-1beta (IL-1beta) is a cytokine that contributes to the hyperalgesia, inactivity, and fever associated with illness. These three components of the illness response occur simultaneously following peripheral administration of IL-1beta. The objective of the present study was to determine

Opiates suppress carrageenan-induced edema and hyperthermia at doses that inhibit hyperalgesia.

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This study determined whether opiates alter vascular components of inflammation (hyperthermia, edema and plasma extravasation) in addition to the suppression of hyperalgesia. Rats were administered carrageenan into one hind paw and saline into the other hind paw, followed by i.p. injection of

Suppression of carrageenan-induced hyperalgesia, hyperthermia and edema by a bradykinin antagonist.

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Although bradykinin (BK) antagonists have antinociceptive effects, they have not been evaluated for anti-inflammatory activity. When administered with carrageenan into the rat hindpaw, NPC567 significantly blocked carrageenan-induced hyperalgesia, hyperthermia and edema. In addition, NPC567 did not

Polypeptide modulators of TRPV1 produce analgesia without hyperthermia.

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Transient receptor potential vanilloid 1 receptors (TRPV1) play a significant physiological role. The study of novel TRPV1 agonists and antagonists is essential. Here, we report on the characterization of polypeptide antagonists of TRPV1 based on in vitro and in vivo experiments. We evaluated the

Antihyperalgesic effects of (R,E)-N-(2-hydroxy-2,3-dihydro-1H-inden-4-yl)-3-(2-(piperidin-1-yl)-4-(trifluoromethyl)phenyl)-acrylamide (AMG8562), a novel transient receptor potential vanilloid type 1 modulator that does not cause hyperthermia in rats.

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Antagonists of the vanilloid receptor TRPV1 (transient receptor potential vanilloid type 1) have been reported to produce antihyperalgesic effects in animal models of pain. These antagonists, however, also caused concomitant hyperthermia in rodents, dogs, monkeys, and humans. Antagonist-induced

Prostaglandin E2 in the medial preoptic area produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla.

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Prostaglandin E2 (PGE2) produced in the medial preoptic region (MPO) in response to immune signals is generally accepted to play a major role in triggering the illness response, a complex of physiological and behavioral changes induced by infection or injury. Hyperalgesia is now thought to be an

Central pool of serotonin and tail-flick latency during two phases of biphasic fever in rats.

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In experiments on male Wistar rats, the acute phase reaction was induced by a bolus intravenous injection of Escherichia coli lipopolysaccharide (10 microg/kg) through a silicon catheter pre-implanted into the jugular vein. The colonic and skin temperature was measured with thermocouples. Changes in

A Novel Pregabalin Functionalized Salicylaldehyde Derivative Afforded Prospective Pain, Inflammation, and Pyrexia Alleviating Propensities.

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A novel pregabalin derivative named as pregsal ((S,E)-3-(((2-hydroxybenzylidene)amino)methyl)-5-methylhexanoic acid) was synthesized by a simple imination reaction between pregabalin and salicylaldehyde and was evaluated in the in vivo testing paradigms. The compound was characterized by UV, IR, 1

Prostanoids in the preoptic hypothalamus mediate systemic lipopolysaccharide-induced hyperalgesia in rats.

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The systemic administration of lipopolysaccharide (LPS), an experimental model of systemic bacterial infection is known to modulate nociception. It increases the prostaglandin E(2) (PGE(2)) levels in the preoptic area of the hypothalamus (POA) and the microinjection of PGE(2) into the POA and the

[Pain, fever and prostanoids].

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Although it has been known that prostanoids are involved in pain regulation and fever, the precise roles of their receptors and receptor subtypes are unclear. All prostanoid receptors have been cloned and mice deficient in each receptor have been developed. Recent studies using

Host biomarkers are associated with progression to dengue haemorrhagic fever: a nested case-control study.

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OBJECTIVE Dengue represents the most important arboviral infection worldwide. Onset of circulatory collapse can be unpredictable. Biomarkers that can identify individuals at risk of plasma leakage may facilitate better triage and clinical management. METHODS Using a nested case-control design, we

Prostaglandin E2 as a mediator of fever: the role of prostaglandin E (EP) receptors.

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Prostaglandin E2 (PGE2) is a principal fever mediator that induces hyperthermia when injected into the organum vasculosum lamina terminalis (OVLT) and the adjacent preoptic area of the hypothalamus (POA). PGE (EP) receptors have four subtypes, i.e. EP1, EP2, EP3, and EP4. In the rat OVLT/POA region,

A novel selective prostaglandin E2 synthesis inhibitor relieves pyrexia and arthritis in Guinea pigs inflammatory models.

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Prostaglandin E2 (PGE2), one of the terminal products in the cyclooxygenase pathway, plays an important role in various inflammatory responses. To determine whether selective inhibition of PGE2 may relieve these inflammatory symptoms, we synthesized a selective PGE2 synthesis inhibitor, compound A

Disrupting sensitization of transient receptor potential vanilloid subtype 1 inhibits inflammatory hyperalgesia.

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Transient receptor potential vanilloid subtype 1 (TRPV1) is a heat-sensitive ion channel that plays a key role in enhanced pain sensation after inflammation, but directly blocking TRPV1 causes hyperthermia and decreased sensitivity to painful levels of heat in animals and humans. Here we explore an

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