The effects of cholinesterase inhibitors on the body temperature of the rat

Meeter, E.; Wolthuis, Otto L.

doi:10.1016/0014-2999(68)90004-6

Cited by 70 publications

(16 citation statements)

References 8 publications

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“…However, chlorpromazine hypothermia appears to be brought about by a less selective action, being accompanied by large increases in tail blood flow and a loss of piloerection (Kollias & Bullard, 1964). The mechanism of DEF-induced hypothermia would appear to be quite distinct from that produced by cholinomimetics such as oxytremorine or anticholinesterases such as soman since these are both blocked by atropine (Maikel, 1970;Meeter & Walthius, 1968). The finding that the falls in body temperature could be largely prevented by large intraperitoneal injections of noradrenaline, and that DEFtreated animals could increase their oxygen consumption normally in response to such injections, clearly suggested that the inhibition of thermogenesis was not due to lack of metabolic capacity.…”

Section: Discussionmentioning

confidence: 99%

SELECTIVE INHIBITION OF THERMOGENESIS BY TRIBUTYL S,S,S,‐PHOSPHOROTRITHIOATE (DEF)

Ray

1980

British J Pharmacology

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1 Rats and mice given tributyl S,S,S,-phosphorotrithioate (DEF) showed large dose-related falls in body temperature which lasted from several hours to several days at environmental temperatures below thermoneutrality (30 to 31°C).2 DEF produced only mild sedation and a remarkable degree of motor control was retained even when body temperatures fell below 30°C. At the dose producing maximal hypothermia only 2% of rats died within the first 24 h, although prolonged hypothermia was usually lethal. 3 Hypothermia was associated with a complete block of cold-induced thermogenesis, with relatively little effect on basal metabolism at thermoneutrality. 4 Heat conservation mechanisms (peripheral vasoconstriction and piloerection) appeared to be unaffected by DEF and retained their usual temperature thresholds. 5 Adrenal catecholamine secretion in response to handling or acute cold exposure was normal in DEF-treated rats but the fall in body temperature could be markedly reduced by large intraperitoneal injections of noradrenaline, although not atropine. The increase in oxygen consumption produced by injected catecholamines was also unaffected by DEF treatment. 6 It is concluded that the block of cold-induced thermogenesis probably results from a lack of catecholamine release at the tissue level. That this is likely to be mediated at a peripheral site is suggested by the lack of effect of intracerebroventricular DEF.

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Section: Discussionmentioning

confidence: 99%

SELECTIVE INHIBITION OF THERMOGENESIS BY TRIBUTYL S,S,S,‐PHOSPHOROTRITHIOATE (DEF)

Ray

1980

British J Pharmacology

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“…There are several data to support the latter hypothesis, although the mechanisms by which this occurs in the POAH have not been clearly delineated. It was demonstrated as early as the 1960s by Meeter (1969) that increased tail skin blood flow is an important avenue of heat loss for the development of hypothermia in OP-poisoned rats. Following i.v.…”

Section: Hypothermiamentioning

confidence: 99%

“…injection of soman, rats displayed a rapid increase in tail skin temperature that preceded a drop in T c to ∼ 32°C -when the tail was wrapped in pre-heated cotton wool to reduce heat loss through this organ the rate of hypothermia development was reduced, indicating that this was an important organ for heat exchange (Meeter, 1969). To determine the regulated nature of this response, the rats were externally heated with a 60 W light bulb and reflexive adjustments in tail skin blood flow were recorded -once T c was raised from 32 to ∼ 33°C, rat tail skin temperature increased abruptly as a reflexive mechanism to return it to its previous hypothermic level (Meeter, 1969). These studies are similar to those conducted by Liebermeister (see previous section on thermoregulatory control) on fever and suggest that OP-induced hypothermia represents a regulated reduction in response to a decrease in the thermal setpoint.…”

Section: Hypothermiamentioning

confidence: 99%

Thermoregulatory responses to environmental toxicants: The interaction of thermal stress and toxicant exposure

Leon

2008

Toxicology and Applied Pharmacology

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“…Since then abundant evidence has been obtained in support of this suggestion in a number of mammals by studying the effects of cholinomimetic substances on body temperature following their injection into the cerebral ventricles or into different regions of the hypothalamus. Experiments of this kind were done in mice (Friedman & Jaffe, 1969), rats (Hulst & de Wied, 1967;Meeter & Wolthuis, 1968;Myers & Yaksh, 1968;Lomax, Foster & Kirkpatrick, 1969;Meeter, 1969Meeter, , 1971Avery, 1972;Baird & Lang, 1973), sheep, goats and rabbits (Bligh, Cottle & Maskrey, 1971), cats (Baird & Lang, 1973) and monkeys (Myers & Yaksh, 1969). The nature of the thermoregulatory response to cholinomimetic substances was found to differ in different species and to be dependent on the dose of the substance injected, the ambient temperature, and when injected into the hypothalamus on the actual site of injection.…”

Section: Introductionmentioning

confidence: 99%

Cholinergic Mechanisms in Central Thermoregulation in Pigeons

Chawla

Johri

Saxena

et al. 1975

British J Pharmacology

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1In unanaesthetized pigeons the effect on cloacal temperature was studied of acetylcholine (ACh), carbachol, atropine and (+)-tubocurarine injected into a cannulated lateral cerebral ventricle. The experiments were carried out at an ambient temperature of 19-25 C. 2 ACh or carbachol injected intraventricularly produced hyperthermia, and in larger doses hyperthermia followed by hypothermia. These were central effects because they were not obtained when these drugs were injected in the same doses intravenously. 3 Atropine injected intraventricularly produced hypothermia which was greater and longer lasting than the hypothermia produced with the same dose of atropine injected intravenously. After the intraventricular injection of atropine the hyperthermic effects of ACh and of carbachol were abolished. 4 (+)-Tubocurarine injected intraventricularly produced a long-lasting hyperthermia in doses which had no effect on temperature when injected intravenously. After the intraventricular injection of tubocurarine the hypothermic effects of ACh and of carbachol were abolished. 5 It is concluded that the effects of ACh and carbachol imitate the effects of ACh released from cholinergic neurones in the central pathway involved in temperature regulation. The hypothermic effect of atropine is attributed to unmasking the activity of continuously released ACh acting on nicotinic receptors, and the hyperthermic effect of tubocurarine to unmasking the activity of continuously released ACh acting on muscarinic receptors.

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The effects of cholinesterase inhibitors on the body temperature of the rat

Cited by 70 publications

References 8 publications

SELECTIVE INHIBITION OF THERMOGENESIS BY TRIBUTYL S,S,S,‐PHOSPHOROTRITHIOATE (DEF)

SELECTIVE INHIBITION OF THERMOGENESIS BY TRIBUTYL S,S,S,‐PHOSPHOROTRITHIOATE (DEF)

Thermoregulatory responses to environmental toxicants: The interaction of thermal stress and toxicant exposure

Cholinergic Mechanisms in Central Thermoregulation in Pigeons

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