Role of neuronal nitric oxide synthase in hypoxia-induced anapyrexia in rats

Steiner, Alexandre A.; Cárnio, Evelin Capellari; Branco, Luiz Guilherme de Siqueira

doi:10.1152/jappl.2000.89.3.1131

Cited by 18 publications

(10 citation statements)

References 42 publications

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“…1). When inspired O 2 was reduced from 21 (room air) to 7%, T c dropped quickly during the first 30 min and continued to drop more slowly up to 90 min and then practically plateaued, a response similar to that observed in previous studies subjecting rats to 7% inspired O 2 [33]. DCA did not affect the magnitude or the shape of the curve of hypoxia-induced anapyrexia.…”

Section: Resultssupporting

confidence: 84%

“…Beginning 30 min later, the chamber was ventilated for 2 h with a humidified hypoxic gas mixture of 7% inspired O 2 (AGA, Brazil) and T c was recorded every 2 min. The severity of hypoxia and the time of exposure to hypoxia were chosen on the basis of previous studies from our laboratory [33]. At the end of the experiments the rats were immediately decapitated for blood collection.…”

Section: Effect Of Dca On T C and Plasma Lactate Levels Of Hypoxic Ratsmentioning

confidence: 99%

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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: Resultssupporting

confidence: 84%

Section: Effect Of Dca On T C and Plasma Lactate Levels Of Hypoxic Ratsmentioning

confidence: 99%

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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“…As to the neurochemistry of the anapyrexic response, several mediators have been described to participate, including the gaseous neuromodulators NO (336) and CO (257). The role of the CBS-H 2 S pathway has been more recently assessed (186) based on the following rationale: (i) in the brain, H 2 S effects have been credited to increases in cAMP (233), and particularly in the hypothalamus the gas has been shown to modulate autonomic function (76); and hypoxia-induced anapyrexia is at least partially mediated by cAMP accumulation in the AVPO [cf.…”

Section: Effects Of Exogenous and Endogenous H 2 S On Thermoregulationmentioning

confidence: 99%

Gaseous Mediators in Temperature Regulation

Branco

Soriano

Steiner

2014

Comprehensive Physiology

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Deep body temperature (Tb) is kept relatively constant despite a wide range of ambient temperature variation. Nevertheless, in particular situations it is beneficial to decrease or to increase Tb in a regulated manner. Under hypoxia for instance a regulated drop in Tb (anapyrexia) is key to reduce oxygen demand of tissues when oxygen availability is diminished, leading to an increased survival rate in a number of species when experiencing low levels of inspired oxygen. On the other hand, a regulated rise in Tb (fever) assists the healing process. These regulated changes in Tb are mediated by the brain, where afferent signals converge and the most important regions for the control of Tb are found. The brain (particularly some hypothalamic structures located in the preoptic area) modulates efferent activities that cause changes in heat production (modulating brown adipose tissue activity and perfusion, for instance) and heat loss (modulating tail skin vasculature blood flow, for instance). This review highlights key advances about the role of the gaseous neuromodulators nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) in thermoregulation, acting both on the brain and the periphery.

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“…Inhibition of nitric oxide synthesis causes a fall in body temperature in rats exposed to environmental temperatures below the lower critical temperature of their thermoneutral zone (Almeida et al 1999a;Branco et al 1997;Kamerman et al 2002;Steiner et al 1998Steiner et al , 2000. Although decreased thermogenesis apparently is responsible, at least partially, for the hypothermia induced by inhibitors of nitric oxide synthase (Barros and Branco 1998;Gautier and Murariu 1999;Nakano et al 2001), it is unclear whether the hypothermia reflects a regulated or unregulated drop in body temperature.…”

Section: Introductionmentioning

confidence: 99%

Inhibitors of nitric oxide synthesis block cold-induced thermogenesis in rats

Kamerman

Laburn²,

Mitchell³

2003

Can. J. Physiol. Pharmacol.

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N-nitro-arginine methyl ester (L-NAME), an unspecific nitric oxide synthase inhibitor, was administered to individually caged Sprague-Dawley rats exposed to cold (18 degrees C) and thermoneutral (30 degrees C) environmental temperatures during the active phase of the animals' circadian cycle. Unrestrained rats were administered intraperitoneal injections of 100 mg x kg-1 L-NAME or 1 mL x kg-1 saline. Telemetry was used to measure abdominal temperature. On a separate occasion, metabolic rate and evaporative water loss were measured using indirect calorimetery, before and after the injection of 100 mg x kg-1 L-NAME, in rats exposed to the two environments. Injection of L-NAME had no significant effect on body temperature, metabolic rate, or evaporative water loss in rats exposed to the 30 degrees C environment. In the 18 degrees C environment, L-NAME injection caused a prolonged fall in body temperature ( F(1,12) = 17.43, P = 0.001) and a significant decrease in metabolic rate (Student's t test, P = 0.001) and evaporative water loss (one-sample t test, P = 0.04). Therefore, the effects that systemic injection of L-NAME has on body temperature are dependent on environmental temperature, with nitric oxide synthase inhibition seemingly preventing the metabolic component of cold defence.

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Role of neuronal nitric oxide synthase in hypoxia-induced anapyrexia in rats

Cited by 18 publications

References 42 publications

Is lactate a mediator of hypoxia-induced anapyrexia?

Is lactate a mediator of hypoxia-induced anapyrexia?

Gaseous Mediators in Temperature Regulation

Inhibitors of nitric oxide synthesis block cold-induced thermogenesis in rats

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