Changes in body temperature after administration of amino acids, peptides, dopamine, neuroleptics and related agents

Clark, William G.

doi:10.1016/0149-7634(79)90010-1

Cited by 153 publications

(32 citation statements)

References 343 publications

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“…Therefore, other possible explanations for the hypothermic effect of LVP administered peripherally should be considered. KRUK and BRITTAIN (1972) and CLARK (1979) jected intracerebroventricularly caused a fall in body temperature in the rats. Additionally, the antipyretic activity of vasopressin was consistently observed when the hormone was administered centrally in sheep (COOPER et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…The aim of this study was to elucidate whether the baroreflexive suppression of metabolism could be a dominant mechanism in producing a fall in body temperature after the intravenous injection of vasopressin in the unanesthetized rats. On the other hand, it was recently shown that central administration of vasopressin produced a fall in body temperature without any change in blood pressure in rats (KRUK and BRITTAIN, 1972;CLARK, 1979). Vasopressin introduced into the brain has an antipyretic effect in sheep (COOPER et al, 1979).…”

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confidence: 99%

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Baroreflexive suppression of heat production and fall in body temperature following peripheral administration of vasopressin in rats.

1984

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Intravenous injection of vasopressin LVP) in unanesthetized rats at an ambient temperature of 18°C caused a decrease in heat production (M) followed by a fall in colonic temperature (T01). These changes were preceded by an elevation of aortic blood pressure (BP) and bradycardia, and were related to the dosage of LVP administered. Temperature of the interscapular brown adipose tissue (BAT) significantly fell after LVP injections. Therefore, it can be said that the decrease in metabolism by the peripheral LVP is at least partly due to suppression of BAT thermogenesis. After bilateral sinoaortic deafferentation, however, the changes in these variables were greatly but not completely reduced except for the elevation of BP. LVP of 0.25 ,ug, more than sufficient to cause a significant elevation of BP when administered peripherally, had no effect on M and Tco1 when injected into the anterior hypothalamus. From these results, we conclude that the hypothermic effect of vasopressin administered peripherally is largely attributed to the baroreflexive suppression of nonshivering thermogenesis, and is not due to the action on the temperature regulatory centers. The slight but insignificant suppression of metabolism in the sinoaortic denervated rats following injection of LVP may be caused by a decreased blood flow to the thermogenic tissues.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Baroreflexive suppression of heat production and fall in body temperature following peripheral administration of vasopressin in rats.

1984

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“…In two very interesting and useful reviews (Clark, 1979;Clark & Lipton, 1985), the results of numerous studies concerning the thermoregulatory action of neuroleptics are quoted and indicate that the systemic injection of these dopamine antagonists generally elicits hypothermia in man and in animals exposed to normal room temperature. The phenothiazines are among the most widely used neuroleptics in the treatment of psychiatric disorders.…”

Section: Introductionmentioning

confidence: 99%

Neuroleptic‐induced hypothermia in mice: lack of evidence for a central mechanism

Boschi

Launay

Rips

1987

British J Pharmacology

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1 The present study investigated the ability of neuroleptic drugs to induce hypothermia in mice when they were administered intraperitoneally (i.p.) or intracerebroventricularly (i.c.v.). 2 Twelve neuroleptics belonging to five chemical classes including phenothiazines, butyrophenones, benzamides, thioxanthenes and diphenylbutylpiperidines were injected i.p. All of them, except benzamides, induced a dose-dependent decrease in rectal temperature. 3 Neuroleptics were administered i.c.v. via cannulae previously implanted in mice to determine whether this response might have a central origin. None of the drugs tested induced hypothermia at doses which did not produce toxic effects. These negative results suggest that neuroleptics act to elicit hypothermia via a peripheral, rather than a central mechanism. 4 Since some neuroleptics possess a-adrenolytic properties which could induce hypothermia by promoting vasodilatation, we attempted to antagonize the hypothermia produced by peripheral administration of two neuroleptics with phenylephrine, an a-adrenoceptor agonist that does not cross the blood-brain barrier. The hypothermia induced by both chlorpromazine and haloperidol was attenuated by phenylephrine, supporting the view that peripheral a-adrenoceptors may mediate neuroleptic-induced hypothermia.

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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 amino acids, peptides, dopamine, neuroleptics and related agents

Cited by 153 publications

References 343 publications

Baroreflexive suppression of heat production and fall in body temperature following peripheral administration of vasopressin in rats.

Baroreflexive suppression of heat production and fall in body temperature following peripheral administration of vasopressin in rats.

Neuroleptic‐induced hypothermia in mice: lack of evidence for a central mechanism

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

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