Body-core temperature decreases during hypoxic hypoxia in Long–Evans and Brattleboro rats

Clark, Deborah J.; Fewell, James E.

doi:10.1139/y94-219

Cited by 11 publications

(3 citation statements)

References 15 publications

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“…Similar results have been observed for vasopressin, which, like lactate, increases in plasma and in cerebrospinal fluid during hypoxia [13,26] and also reduces T c when administered to mammals [21,27,31]. However, studies on Brattleboro rats (that lack vasopressin-producing neurons in the central nervous system) and vasopressin antagonists in Wistar rats have shown that rats develop anapyrexia regularly in response to hypoxia in the absence of vasopressin [9] or when its receptors are blocked [32].…”

Section: Discussionsupporting

confidence: 74%

Is lactate a mediator of hypoxia-induced anapyrexia?

Bícego

Steiner

Gargaglioni

et al. 2002

Pfl�gers Archiv European Journal of Physiology

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Hypoxia causes a regulated decrease in body core temperature ( T(c)), termed anapyrexia, which seems to be a very effective way of preventing hypoxia-associated cell damage. Since during several pathological states the supply of O(2) is a limiting factor, the clinical importance of anapyrexia is evident. However, the mechanisms involved in this response remain unclear. We tested the hypothesis that lactate, a classic companion of hypoxia, is a mediator of hypoxia-induced anapyrexia, using the inhibitor of acid lactic production dichloroacetate (DCA). Each of 28 rats was placed in a chamber ventilated with humidified air at an ambient temperature of 24-26 degrees C. After a control period of 30 min the animals were given saline or 100 mg/kg DCA i.p. Then, 30 min later, the chamber was flushed with a 7% O(2) gas mixture for 2 h. At the end of the experiment, the animals were decapitated and blood samples collected for measurements of plasma lactate. T(c) was measured by biotelemetry. DCA did not affect the T(c) or basal lactate levels of normoxic rats. Hypoxia elicited a significant decrease in T(c) and an increase in plasma lactate levels. Although DCA decreased plasma lactate levels during hypoxia, it caused no change in the course of hypoxia-induced anapyrexia. Correspondingly, no correlation was found between the drop in T(c) and the rise in plasma lactate during hypoxic conditions. These results do not support the hypothesis that lactate is a mediator of hypoxia-induced anapyrexia in rats.

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Section: Discussionsupporting

confidence: 74%

Is lactate a mediator of hypoxia-induced anapyrexia?

Bícego

Steiner

Gargaglioni

et al. 2002

Pfl�gers Archiv European Journal of Physiology

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“…However, there is only one published study (7) that evaluated the participation of AVP in hypoxia-induced anapyrexia, in which AVP does not seem to mediate the reduction in T b . In that study, anapyrexia was similar in both Brattleboro rats (which lack AVP-containing cells in the central nervous system) and Long-Evans rats (used as a control) (7). However, thermoregulation may be aberrant in Brattleboro rats.…”

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confidence: 88%

Endogenous vasopressin does not mediate hypoxia-induced anapyrexia in rats

Steiner

Cárnio²,

Antunes‐Rodrigues

et al. 1999

Journal of Applied Physiology

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The present study was designed to test the hypothesis that arginine vasopressin (AVP) mediates hypoxia-induced anapyrexia. The rectal temperature of awake, unrestrained rats was measured before and after hypoxic hypoxia, AVP-blocker injection, or a combination of the two. Control animals received saline injections of the same volume. Basal body temperature was 36.52 +/- 0.29 degreesC. We observed a significant (P < 0.05) reduction in body temperature of 1. 45 +/- 0.33 degreesC after hypoxia (7% inspired O2), whereas systemic and central injections of AVP V1- and AVP V2-receptor blockers caused no change in body temperature. When intravenous injection of AVP blockers was combined with hypoxia, we observed a reduction in body temperature of 1.49 +/- 0.41 degreesC (V1-receptor blocker) and of 1.30 +/- 0.13 degreesC (V2-receptor blocker), similar to that obtained by application of hypoxia only. Similar results were observed when the blockers were injected intracerebroventricularly. The data indicate that endogenous AVP does not mediate hypoxia-induced anapyrexia in rats.

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“…The effects of the V1 antagonist on baseline core temperature suggests that V1 receptors could be involved in tonic thermoregulatory processes. It is also interesting to note that several studies have found that the V1 antagonist does not block hypoxic‐induced hypothermia in the rat ( Clark & Fewell 1994 ; Steiner et al , 1999 ). That cholinergic stimulation is critical in the chlorpyrifos‐induced but not hypoxic‐induced hypothermia suggests that cholingergic‐induced vasopressin release is operative in the former but not the latter.…”

Section: Discussionmentioning

confidence: 97%

Possible Role of Vasopressin in the Thermoregulatory Response to Chlorpyrifos in the Rat

Yang

Gordon

2002

Pharmacology & Toxicology

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Arginine vasopressin is a naturally occurring antipyretic which is released into the CNS to prevent excessive elevations in body temperature during fever. Circulating levels of arginine vasopressin may also have a role in the tonic control of body temperature. We have found that the organophosphate insecticide chlorpyrifos will raise blood pressure and lower body temperature in the rat. Because arginine vasopressin is a potent hypertensive agent and is capable of lowering core temperature, we suspected that arginine vasopressin may be involved in the thermoregulatory response to chlorpyrifos. To this end, core temperature and motor activity of male and female Sprague-Dawely rats were monitored before and after treatment with the corn oil vehicle or chlorpyrifos (15 mg/kg in females; 30 mg/kg in males; oral) concomitant with injection of a saline vehicle or a type 1 arginine vasopressin antagonist (20 mg/kg in females; 30 mg/kg in males; intraperitoneally). Rats dosed with chlorpyrifos and saline underwent a 2-3 ae reduction in core temperature Ͼ50% decrease in motor activity. The V1 antagonist attenuated the hypothermic effect of chlorpyrifos in both sexes. Chlorpyrifos-induced inhibition in motor activity was unaffected by the V1 antagonist. In another experiment, the V1 antagonist (30 mg/kg) was co-administered with saline or 0.2 mg/kg oxotremorine, a muscarinic agonist that stimulates a heat loss response and partially mimics the effects of chlorpyrifos. The V1 antagonist attenuated the hypothermic effect of oxotremorine in both sexes. Plasma arginine vasopressin levels were determined in male rats 3 hr after corn oil or 30 mg/kg chlorpyrifos. There was no significant effect of chlorpyrifos on plasma levels of arginine vasopressin. That the V1 antagonist blocked the hypothermic effect of chlorpyrifos suggests that the thermoregulatory response to chlorpyrifos is mediated by central and/or systemic vasopressin release. The lack of a significant increase in plasma vasopressin after chlorpyrifos suggests that localized release of vasopressin may be involved in the thermoregulatory response to chlorpyrifos.

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Body-core temperature decreases during hypoxic hypoxia in Long–Evans and Brattleboro rats

Cited by 11 publications

References 15 publications

Is lactate a mediator of hypoxia-induced anapyrexia?

Is lactate a mediator of hypoxia-induced anapyrexia?

Endogenous vasopressin does not mediate hypoxia-induced anapyrexia in rats

Possible Role of Vasopressin in the Thermoregulatory Response to Chlorpyrifos in the Rat

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