Inhibition of shivering as a cause of metabolic suppression with norepinephrine in warm- and cold-acclimated rats.

Shibata, Hiroyuki; Nunomura, Tadahiro; Nagasaka, Tetsuo

doi:10.2170/jjphysiol.32.519

Cited by 9 publications

(5 citation statements)

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“…It has been reported that administration of vasopressor substances such as norephinephrine and phenylephrine suppresses heat production through the sinoaortic baroreceptor reflex in unanesthethized animals (12,29,30,36). In 1984, Shido et al (31) demonstrated that the fall in T c after peripheral injection of AVP is greatly reduced after bilateral sinoaortic deafferentation.…”

Section: Discussionmentioning

confidence: 99%

“…The authors concluded that the effect of systemic AVP on T c could be attributed, at least in part, to the baroreflexive suppression of nonshivering thermogenesis. Because BAT is under sympathetic nervous system control (11,28), the lowered metabolism after vasopressin may be due to reduced sympathetic nervous activity in the tissue (30). On the other hand, Morrison (20) suggested that sympathetic activity to BAT is under weak baroreflex control.…”

Section: Discussionmentioning

confidence: 99%

“…Shido et al (31) attributed this effect to the baroreflex-ive suppression of nonshivering termogenesis, i.e., a reduction of interscapular brown adipose tissue (BAT) thermogenesis; however, heat loss through the tail was not assessed. Modulation of BAT thermogenesis had already been reported for other vasopressor substances like norepinephrine, phenylephrine (12,30), and angiotensin II (10), which indicates that the effect of AVP, at least the hypothermic one, may not be selective. In the present study, we have chosen AVP as an experimental model to induce hypothermia because a number of previous studies used AVP (15,23,31,33), which allows one to easily reconcile the available data.…”

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Role of l-glutamate in systemic AVP-induced hypothermia

Paro

Almeida

Cárnio³

et al. 2003

Journal of Applied Physiology

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It has been reported that systemic injection of arginine vasopressin (AVP) induces a drop in body core temperature (T(c)), but little is known about the mechanisms involved. Because glutamate is an important excitatory neurotransmitter involved in a number of thermoregulatory actions, in the present study, we tested the hypothesis that glutamate plays a role in systemic AVP-induced hypothermia. Wistar rats were pretreated intracerebroventricularly (icv) with kynurenic acid, an antagonist of l-glutamate ionotropic receptors, alpha-methyl-(4-carboxyphenyl)glycine (MCPG), an antagonist of l-glutamate metabotropic receptors, or saline 15 min before intravenous injection of AVP (2 microg/kg) or saline. T(c), brown adipose tissue (BAT) temperature, blood pressure, heart rate, and tail skin temperature were measured continuously. Administration of saline icv followed by intravenous AVP caused a significant drop in T(c) brought about by a reduction in BAT thermogenesis and an increase in heat loss through the tail. MCPG treatment (icv) did not affect the fall in T(c) induced by AVP. Treatment with kynurenic acid (icv) abolished AVP-induced hypothermia but did not affect the AVP-evoked rise in blood pressure or drop in heart rate and BAT temperature. Heat loss through the tail was significantly reduced in animals injected with AVP and pretrated with kynurenic acid. These data indicate that ionotropic receptors of l-glutamate in the central nervous system participate in peripheral AVP-induced hypothermia by affecting heat loss through the tail.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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confidence: 90%

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Role of l-glutamate in systemic AVP-induced hypothermia

Paro

Almeida

Cárnio³

et al. 2003

Journal of Applied Physiology

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“…However, little is known about the mechanisms of suppression in peripheral tissues by this vasopressor hormone. It was reported that administrations of vasopressor substances such as norepinephrine and phenylephrine suppressed heat production through the sinoaortic baroreflex in the unanesthetized animals (WASSERSTRUM and HERD, 1977;HOHTOLA et al, 1980;SHIBATA, 1982;SHIBATA et al, 1982). 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.…”

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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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“…It has been shown that the T cor of animals can be lowered by changes in arterial blood pressure [23,24]. Romanovsky et al [25] have shown that in rats with endotoxin shock, a fall in T cor and a downward shift of threshold T cor for heat production were accompanied by moderate hypotension.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Cryogens Existing in the Blood of a Hypothermic Patient

Shido

Sugimoto

Imoto

et al. 2004

JJP

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tions except hypothermia-associated symptoms such as bradycardia, hypotension and slow body movement. In the laboratory data, however, there were some abnormal findings, e.g., slight increases in plasma levels of the BUN, electrolytes (Na and Cl), and energy substrates (total cholesterol, triglyceride, and blood sugar). The hematological changes were judged to be induced by hemoconcentration or hypometabolism associated with hypothermia. The plasma levels of TSH and some liver enzymes (GOT, GPT, and LDH) were slightly increased, indicating the possibility of hypothyroidism. However, plasma concentrations of free thyroxin and free triiodothyronine were within normal ranges; furthermore, l-thyroxin replacement therapy did not improve hypothermia. There were no other abnormal findings, e.g., in pituitary function tests or in magnetic resonance imaging studies of the head, especially in the hypothalamo-pituitary region. So even though we performed various physical, psy- Abstract:We treated a young female patient who suffered from severe hypothermia. The etiology of the hypothermia was not identified, though various medical examinations were performed. Intraperitoneal (i.p.) injections of the patient's serum produced a significant and profound hypothermia in rats that was not associated with circulatory shock. The patient's serum was separated into 4 fractions by the use of various types of centrifugal filtration units according to molecular weights (MW), i.e., below 10 kDa, 10-30 kDa, 30-100 kDa, and beyond 100 kDa. The first two fractions never induced hypothermia in rats, but the i.p. injections of the fraction with MW from 30 to 100 kDa consistently produced hypothermia. The fraction with MW beyond 100 kDa caused marked hypothermia in one out of 3 rats tested. The results suggest that the patient was excessively producing endogenous cryogenic substances of which MW may be greater than 30 kDa.

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Inhibition of shivering as a cause of metabolic suppression with norepinephrine in warm- and cold-acclimated rats.

Abstract: The metabolic response of warm-acclimated (25•Ž for 4 weeks) and cold-acclimated (5•Ž for 4 weeks) rats to infused norepinephrine (NE)

Cited by 9 publications

References 11 publications

Role of l-glutamate in systemic AVP-induced hypothermia

Role of l-glutamate in systemic AVP-induced hypothermia

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

Endogenous Cryogens Existing in the Blood of a Hypothermic Patient

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