AMP does not induce torpor

2007 ◽  
Vol 293 (1) ◽  
pp. R468-R473 ◽  
Author(s):  
Steven J. Swoap ◽  
Meaghan Rathvon ◽  
Margaret Gutilla
Keyword(s):  
Heart Rate ◽  
Adenosine Receptor ◽  
Maximum Rate ◽  
Adenine Nucleotides ◽  
Induced Hypothermia ◽  
Animal Kingdom ◽  
Fasted State ◽  
Severe Hypothermia ◽  
Hypothermic Effect ◽  
Torpor Bouts

Torpor, a state characterized by a well-orchestrated reduction of metabolic rate and body temperature (Tb), is employed for energetic savings by organisms throughout the animal kingdom. The nucleotide AMP has recently been purported to be a primary regulator of torpor in mice, as circulating AMP is elevated in the fasted state, and administration of AMP causes severe hypothermia. However, we have found that the characteristics and parameters of the hypothermia induced by AMP were dissimilar to those of fasting-induced torpor bouts in mice. Although administration of AMP induced hypothermia (minimum Tb = 25.2 ± 0.6°C) similar to the depth of fasting-induced torpor (24.9 ± 1.5°C), ADP and ATP were equally effective in lowering Tb (minimum Tb: 24.8 ± 0.9°C and 24.0 ± 0.5°C, respectively). The maximum rate of Tb fall into hypothermia was significantly faster with injection of adenine nucleotides (AMP: −0.24 ± 0.03; ADP: −0.24 ± 0.02; ATP: −0.25 ± 0.03°C/min) than during fasting-induced torpor (−0.13 ± 0.02°C/min). Heart rate decreased from 755 ± 15 to 268 ± 17 beats per minute (bpm) within 1 min of AMP administration, unlike that observed during torpor (from 646 ± 21 to 294 ± 19 bpm over 35 min). Finally, the hypothermic effect of AMP was blunted with preadministration of an adenosine receptor blocker, suggesting that AMP action on Tb is mediated via the adenosine receptor. These data suggest that injection of adenine nucleotides into mice induces a reversible hypothermic state that is unrelated to fasting-induced torpor.

scholarly journals Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

2017 ◽  
Vol 122 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Anthony R. Bain ◽  
Michael M. Tymko ◽  
Mathew G. Rieger ◽  
Connor A. Howe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Adenosine Receptor ◽  
Hypobaric Hypoxia ◽  
End Tidal ◽  
Double Blinded

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text]. At high altitude, theophylline ( n = 6) had no effect on CBF compared with placebo ( n = 6) when end-tidal gases were comparable ( P > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.

The Effect of Swimming Activity and Section of the Vagus Nerves on Heart Rate in Rainbow Trout

1974 ◽  
Vol 60 (2) ◽  
pp. 305-319 ◽  
Author(s):  
IMANTS G. PRIEDE
Keyword(s):  
Heart Rate ◽  
Maximum Rate ◽  
Critical Speed ◽  
Swimming Activity ◽  
Vagus Nerves ◽  
Maximum Heart Rate ◽  
Heart Rates ◽  
Cardiac Responses ◽  
Different Temperatures ◽  
Speed Up

1. Heart rates associated with swimming activity were measured in intact and vagotomized fish at 6.5 and 15 °C. 2. Low swimming speeds had no effect on heart rate but above a threshold speed it increased logarithmically with swimming speed up to the critical speed and maximum heart rate. 3. Times for recovery after exercise increased rapidly above the critical speed. 4. Bilaterally vagotomized fish at 6.5 °C showed high resting heart rates and erratic cardiac responses to exercise. 5. In bilaterally vagotomized fish at 15 °C heart rates were normal except for a low maximum rate. 6. It is concluded that the vagus nerve can function differently at different temperatures.

Myocardial metabolism and performance in hypoxia: effect of epinephrine

1978 ◽  
Vol 45 (5) ◽  
pp. 791-796 ◽  
Author(s):  
J. Kypson ◽  
G. Hait
Keyword(s):  
Fatty Acids ◽  
Heart Rate ◽  
Free Fatty Acids ◽  
Glucose Utilization ◽  
Myocardial Metabolism ◽  
Mechanical Performance ◽  
Adenine Nucleotides ◽  
Metabolic Changes ◽  
And Performance ◽  
Energetic Reserves

Effects of epinephrine (10(-5) M) on mechanical performance, glycolysis, glycogenolysis, lipolysis, and metabolism of adenine nucleotides were studied in isolated hypoxic rabbit hearts. The exposure of hearts to hypoxia decreased their mechanical performance and heart rate, but increased their utilization of glucose by 50% and the release of lactate by 139%. Myocardial stores of glycogen and ATP declined by 53 and 84%, respectively, but their breakdown products such as lactate, pyruvate, AMP, and inosine accumulated in these hearts. Myocardial content of free fatty acids decreased, and the amount of glycerol increased in hypoxic hearts. Epinephrine stimulated mechanical performance and heart rate of hypoxic hearts, but decreased myocardial glycogen and ATP even more by 62 and 33%, respectively. Though glucose utilization remained unchanged, the release of lactate increased by 66% from hypoxic hearts treated with epinephrine. However, epinephrine failed to stimulate myocardial lipolysis in hypoxic hearts. These metabolic changes due to epinephrine would lead to accelerated depletion of energetic reserves in hypoxic heart and its earlier deterioration.

Role of adenosine in the hypoxia-induced hypothermia of toads

2000 ◽  
Vol 279 (1) ◽  
pp. R196-R201 ◽  
Author(s):  
Luiz G. S. Branco ◽  
Alexandre A. Steiner ◽  
Glenn J. Tattersall ◽  
Stephen C. Wood
Keyword(s):  
Body Temperature ◽  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
Thermal Gradient ◽  
Induced Hypothermia ◽  
Intracerebroventricular Injection ◽  
Exposure Control ◽  
Adenosine Receptor Antagonist ◽  
Thermoregulatory Function

The concept that hypoxia elicits a drop in body temperature (Tb) in a wide variety of animals is not new, but the mechanisms remain unclear. We tested the hypothesis that adenosine mediates hypoxia-induced hypothermia in toads. Measurements of selected Tb were performed using a thermal gradient. Animals were injected (into the lymph sac or intracerebroventricularly) with aminophylline (an adenosine receptor antagonist) followed by an 11-h period of hypoxia (7% O2) or normoxia exposure. Control animals received saline injections. Hypoxia elicited a drop in Tb from 24.8 ± 0.3 to 19.5 ± 1.1°C ( P < 0.05). Systemically applied aminophylline (25 mg/kg) did not change Tb during normoxia, indicating that adenosine does not alter normal thermoregulatory function. However, aminophylline (25 mg/kg) significantly blunted hypoxia-induced hypothermia ( P < 0.05). To assess the role of central thermoregulatory mechanisms, a smaller dose of aminophylline (0.25 mg/kg), which did not alter hypoxia-induced hypothermia systemically, was injected into the fourth cerebral ventricle. Intracerebroventricular injection of aminophylline (0.25 mg/kg) caused no significant change in Tb under normoxia, but it abolished hypoxia-induced hypothermia. The present data indicate that adenosine is a central and possibly peripheral mediator of hypoxia-induced hypothermia.

scholarly journals Superfast periodicities in distress vocalizations emitted by bats

2019 ◽  
Author(s):  
Julio C. Hechavarría ◽  
M. Jerome Beetz ◽  
Francisco Garcia-Rosales ◽  
Manfred Kössl
Keyword(s):  
Heart Rate ◽  
Low Frequency ◽  
Agonistic Interactions ◽  
Animal Kingdom ◽  
Carollia Perspicillata ◽  
Animal Group ◽  
Distress Calls ◽  
Distress Vocalizations

AbstractCommunication sounds are ubiquitous in the animal kingdom, where they play a role in advertising physiological states and/or socio-contextual scenarios. Distress sounds, for example, are typically uttered in distressful scenarios such as agonistic interactions. Here, we report on the occurrence of superfast temporal periodicities in distress calls emitted by bats (species Carollia perspicillata). Distress vocalizations uttered by this bat species are temporally modulated at frequencies close to 1.7 kHz, that is, ∼17 times faster than modulation rates observed in human screams. Fast temporal periodicities are represented in the bats’ brain by means of frequency following responses, and temporally periodic sounds are more effective in boosting the heart rate of awake bats than their demodulated versions. Altogether, our data suggest that bats, an animal group classically regarded as ultrasonic, can exploit the low frequency portion of the soundscape during distress calling to create spectro-temporally complex, arousing sounds.

Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts

1996 ◽  
Vol 80 (1) ◽  
pp. 291-297 ◽  
Author(s):  
T. Tveita ◽  
M. Skandfer ◽  
H. Refsum ◽  
K. Ytrehus
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Maximum Rate ◽  
Energy Charge ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Mechanical Function ◽  
Control Value

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.

Evidence supporting involvement of leukotrienes in LPS-induced hypothermia in mice

1999 ◽  
Vol 276 (1) ◽  
pp. R52-R58 ◽  
Author(s):  
Lada Paul ◽  
Vadim Fraifeld ◽  
Jacob Kaplanski
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ex Vivo ◽  
Induced Hypothermia ◽  
Significant Elevation ◽  
Hypothermic Effect ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

The aim of the present study was to examine a possible involvement of leukotrienes (LTs) in lipopolysaccharide (LPS)-induced body temperature (Tb) response. We examined the effect of MK-886, an inhibitor of LT synthesis, on changes in Tb, plasma tumor necrosis factor-α (TNF-α), hypothalamic LT, and PGE2 production. Intraperitoneal injection of LPS (50 μg/mouse) led to a decrease in Tb starting 1 h after the injection. The hypothermic effect of LPS was accompanied by a significant elevation in TNF-α level in plasma and in LT and PGE2 production by ex vivo-incubated hypothalamus. MK-886 (1 mg/kg ip) administered 4 h before LPS efficaciously prevented LPS-induced hypothermia in mice. Pretreatment of mice with MK-886 did not alter the LPS-stimulated increase in plasma TNF-α. MK-886 significantly inhibited LT and enhanced PGE2 production in hypothalamus compared with LPS alone. These results suggest that 1) LPS-induced hypothermia may be mediated by LTs and 2) the antihypothermic effect of MK-886 is not associated with TNF-α bioactivity.

Role of l-glutamate in systemic AVP-induced hypothermia

2003 ◽  
Vol 94 (1) ◽  
pp. 271-277 ◽  
Author(s):  
Flavia M. Paro ◽  
Maria C. Almeida ◽  
Evelin C. Carnio ◽  
Luiz G. S. Branco
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Loss ◽  
Kynurenic Acid ◽  
Body Core Temperature ◽  
Induced Hypothermia ◽  
Metabotropic Receptors ◽  
Systemic Injection ◽  
Ionotropic Receptors ◽  
Brown Adipose

It has been reported that systemic injection of arginine vasopressin (AVP) induces a drop in body core temperature (Tc), 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 ofl-glutamate ionotropic receptors, α-methyl-(4-carboxyphenyl)glycine (MCPG), an antagonist ofl-glutamate metabotropic receptors, or saline 15 min before intravenous injection of AVP (2 μg/kg) or saline. Tc, 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 Tc 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 Tc 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.

The thermoregulatory mechanism of melatonin-induced hypothermia in chicken

1998 ◽  
Vol 274 (1) ◽  
pp. R232-R236 ◽  
Author(s):  
I. Rozenboim ◽  
L. Miara ◽  
D. Wolfenson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Body Temperature ◽  
Heat Losses ◽  
Induced Hypothermia ◽  
White Leghorn ◽  
Evaporative Water ◽  
Dose Dependent ◽  
Respiratory Evaporation

The involvement of melatonin (Mel) in body temperature (Tb) regulation was studied in White Leghorn layers. In experiment 1, 35 hens were injected intraperitoneally with seven doses of Mel (0, 5, 10, 20, 40, 80, or 160 mg Mel/kg body wt) dissolved in ethanol. Within 1 h, Mel had caused a dose-dependent reduction in Tb. To eliminate a possible vehicle effect, 0, 80, and 160 mg/kg body wt Mel dissolved in N-methyl-2-pyrrolidone (NMP) was injected. NMP had no effect on Tb, with Mel again causing a dose-dependent hypothermia. In experiment 2 ( n= 30), Mel injected before exposure of layers to heat reduced Tb and prevented heat-induced hyperthermia. Injection after heat stress had begun did not prevent hyperthermia. Under cold stress, Mel induced hypothermia, which was not observed in controls. In experiment 3 ( n= 12), Mel injection reduced Tband increased metatarsal and comb temperatures (but not feathered-skin temperature), respiratory rate, and evaporative water loss. Heart rate rose and then declined, and blood pressure increased 1 h after Mel injection. Heat production rose slightly during the first hour, then decreased in parallel to the Tbdecline. We conclude that pharmacological doses of Mel induce hypothermia in hens by increasing nonevaporative skin heat losses and slightly increasing respiratory evaporation.

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