Changes in body temperature after administration of acetylcholine, histamine, morphine, prostaglandins and related agents

Clark, William G.

doi:10.1016/0149-7634(80)90015-9

Cited by 137 publications

(29 citation statements)

References 383 publications

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“…Fever, particularly PGE1 fever, has been abundantly reported in endotherms (see reviews in KLUGER, 1979;CLARK and CLARK, 1980;CLARK and LIPTON, 1985). Among ectotherms, a behavioral fever has also been observed in numerous vertebrate groups including reptiles (VAUGHN et al, 1974;LABURN et al, 1981), amphibians (MYHRE et al, 1977;CASTERLIN and REYNOLDS, 1977), and fishes (REYNOLDS et al, 1976;COVERT and REYNOLDS, 1977), and has been shown to be a protective against microbial infection (KLUGER, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…PGE1 fever has been described in a great number of mammals and birds, and in some species of reptiles, fish, and amphibians (see reviews in KLUGER, 1979;CLARK and CLARK 1980;CLARK and LIPTON, 1985). Even arthropods have developed fever after treatment with PGE1, as shown in crustaceans REYNOLDS, 1978, 1979), in arachnids (CABANAC and LE GUELTE,1980), and in insects (Louis et al, 1986).…”

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confidence: 99%

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Prostaglandin E1, prostaglandin E2, and endotoxin failure to produce fever in the Japanese freshwater snail Semisulcospira libertina.

Rossetti

Nagasaka

1988

Jpn.J.Physiol

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The thermopreferendum (preferred temperature) of the Japanese freshwater snail (Semisulcospira libertina) was determined in an aquatic temperature gradient after injection of prostaglandin E1, prostaglandin E2, and LPS. Injected doses of each pyrogen ranged from a toxic dose to less than 1/20th of the toxic dose. Toxic effect of the highest doses of pyrogen disappeared within 120 min. No fever occurred during the 150 min observation following the pyrogen injection. The present results support the hypothesis that fever was selected as a way of defending against infection only after the period of the emergence of the molluscus, i.e., the early Cambrian period.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Prostaglandin E1, prostaglandin E2, and endotoxin failure to produce fever in the Japanese freshwater snail Semisulcospira libertina.

Rossetti

Nagasaka

1988

Jpn.J.Physiol

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“…PGE2, apart from causing sedation and catalepsy, also produces hyperthermia in several species (Clark & Clark, 1980) and an E-type prostaglandin is released in the central nervous system during pyrogeninduced fever (Feldberg & Gupta, 1973). The site of the prostaglandin release and action is presumed to be the hypothalamic region of the brain (Ferreira, 1977).…”

Section: Methodsmentioning

confidence: 99%

ALTERATION IN THE LEVEL OF ENDOGENOUS HYPOTHALAMIC PROSTAGLANDINS INDUCED BY Δ⁹‐TETRAHYDROCANNABINOL IN THE RAT

Coupar¹,

Taylor²

1982

British J Pharmacology

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Whole brain and regional brain levels of prostaglandin E2 (PGE2)‐like material have been determined following administration of Δ9‐tetrahydrocannabinol (Δ9‐THC) in rats. Intravenous administration of Δ9‐THC 2 mg/kg, resulted in marked behavioural changes and hypothermia. The behavioural changes consisted mainly of catatonia (most apparent at 30 min after administration of Δ9‐THC), followed by sedation (most evident at 60 min). Hypothermia was marked from 30 min after administration of Δ9‐THC. Δ9‐THC did not alter the whole brain levels of PGE2‐like material 30, 60 or 120 min after administration. Δ9‐THC did not alter the levels of PGE2‐like material in the medulla oblongata/pons, midbrain, cortex and cerebellum, 30 min after administration. However, there was a significant reduction of PGE2‐like material in the hypothalamus, 30 min after Δ9‐THC. It is suggested that the Δ9‐THC‐induced decrease in hypothalamic PGE2‐like material may contribute to the hypothermia observed following Δ9‐THC administration.

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“…Change in Tb upon exposure to pharmacological agents. All presented data are derived from reviews published by Clark et al [29][30][31][32][33][34][35][36]. These reviews total 18,808 reports on changes in Tb (ΔTb) following exposure to a biochemical agent.…”

Section: Visualizing Drug-induced Changes In Body Temperaturementioning

confidence: 99%

“…Clark in Neuroscience and Biobehavioral Reviews [29][30][31][32][33][34][35][36]. According to the author, "this survey … intended to provide an immediate source of information on drug-induced changes in thermoregulation" [31].…”

Section: Visualizing Drug-induced Changes In Body Temperaturementioning

confidence: 99%

Survey and critical appraisal of pharmacological agents with potential thermo-modulatory properties in the context of artificially induced hypometabolism

Dirkes

Gulik

Heger

2015

JCTRes

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A reduction in body temperature can be achieved by a downward adjustment of the termoneutral zone, a process also described as anapyrexia. Pharmacological induction of anapyrexia could enable numerous applications in medicine. However, little is known about the potential of pharmacological agents to induce anapyrexic signaling. Therefore, a review of literature was performed and over a thousand pharmacologically active compounds were analyzed for their ability to induce anapyrexia in animals. Based on this analysis, eight agents (helium, dimethyl sulfoxide, reserpine, (oxo)tremorine, pentobarbital, (chlor) promazine, insulin, and acetaminophen) were identified as potential anapyrexia-inducing compounds and discussed in detail. The translational pitfalls were also addressed for each candidate compound. Of the agents that were discussed, reserpine, (oxo)tremorine, and (chlor) promazine may possess true anapyrexic properties based on their ability to either affect the thermoneutral zone or its effectors and facilitate hypothermic signaling. However, these properties are currently not unequivocal and warrant further examination in the context of artificially-induced hypometabolism. Keywords:thermoneutral zone hypothermia induction pharmacological agents animals body temperature

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Changes in body temperature after administration of acetylcholine, histamine, morphine, prostaglandins and related agents

Cited by 137 publications

References 383 publications

Prostaglandin E1, prostaglandin E2, and endotoxin failure to produce fever in the Japanese freshwater snail Semisulcospira libertina.

Prostaglandin E1, prostaglandin E2, and endotoxin failure to produce fever in the Japanese freshwater snail Semisulcospira libertina.

ALTERATION IN THE LEVEL OF ENDOGENOUS HYPOTHALAMIC PROSTAGLANDINS INDUCED BY Δ⁹‐TETRAHYDROCANNABINOL IN THE RAT

Survey and critical appraisal of pharmacological agents with potential thermo-modulatory properties in the context of artificially induced hypometabolism

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Changes in body temperature after administration of acetylcholine, histamine, morphine, prostaglandins and related agents

Cited by 137 publications

References 383 publications

Prostaglandin E1, prostaglandin E2, and endotoxin failure to produce fever in the Japanese freshwater snail Semisulcospira libertina.

Prostaglandin E1, prostaglandin E2, and endotoxin failure to produce fever in the Japanese freshwater snail Semisulcospira libertina.

ALTERATION IN THE LEVEL OF ENDOGENOUS HYPOTHALAMIC PROSTAGLANDINS INDUCED BY Δ9‐TETRAHYDROCANNABINOL IN THE RAT

Survey and critical appraisal of pharmacological agents with potential thermo-modulatory properties in the context of artificially induced hypometabolism

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Product

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ALTERATION IN THE LEVEL OF ENDOGENOUS HYPOTHALAMIC PROSTAGLANDINS INDUCED BY Δ⁹‐TETRAHYDROCANNABINOL IN THE RAT