Thermoregulatory responses of dystrophic hamsters to changes in ambient temperatures

1985 ◽  
Vol 63 (9) ◽  
pp. 1145-1150 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos ◽  
J. A. Thornhill

The ability of dystrophic hamsters to maintain their body temperature despite abnormal muscle and brown adipose tissue, two organs involved in thermoregulation, was evaluated. Dystrophic hamsters (CHF 146) between the ages of 30 and 160 days kept at 21 °C had core (rectal) temperatures (TR) that were 0.5–1.5 °C lower than Golden Syrian controls. The reduced core temperatures of dystrophic hamsters were unlikely the result of an incapacity to generate heat since the dystrophic hamsters were able to maintain their TRs during 3 h of acute cold stress (4 °C) and to adapt to prolonged cold exposure. However, TRs of cold-acclimated dystrophic hamsters were still 1 °C below TRs of cold-acclimated control animals. By contrast, increasing the ambient temperature raised TRs of both normal and dystrophic hamsters. When kept at 32 °C overnight, the TRs of dystrophic hamsters remained significantly below those of control animals. When heat-exposed dystrophic hamsters were returned to 21 °C, their TRs returned to values significantly lower than those of control hamsters. Thus, dystrophic hamsters showed a capacity to thermoregulate, like control hamsters, but appeared to do so at a lower temperature. The reduced core temperatures of dystrophic hamsters kept at 21 °C cannot be explained by a reduction in metabolic activity since newborns and 30- and 140-day-old dystrophic hamsters had rates of oxygen consumption [Formula: see text] and carbon dioxide production [Formula: see text] that were similar to those of controls. These results suggest that the thermoregulatory set point may be altered in dystrophic hamsters.

1992 ◽  
Vol 70 (3) ◽  
pp. 408-411 ◽  
Author(s):  
Peter B. Frappell ◽  
Andrea Dotta ◽  
Jacopo P. Mortola

Aerobic metabolism (oxygen consumption, [Formula: see text], and carbon dioxide production, [Formula: see text]) has been measured in newborn rats at 2 days of age during normoxia, 30 min of hyperoxia (100% O2) and an additional 30 min of recovery in normoxia at ambient temperatures of 35 °C (thermoneutrality) or 30 °C. In normoxia, at 30 °C [Formula: see text] was higher than at 35 °C. With hyperoxia, [Formula: see text] increased in all cases, but more so at 30 °C (+20%) than at 35 °C (+9%). Upon return to normoxia, metabolism readily returned to the prehyperoxic value. The results support the concept that the normoxic metabolic rate of the newborn can be limited by the availability of oxygen. At temperatures below thermoneutrality the higher metabolic needs aggravate the limitation in oxygen availability, and the positive effects of hyperoxia on [Formula: see text] are therefore more apparent.Key words: neonatal respiration, oxygen consumption, thermoregulation.


1985 ◽  
Vol 249 (2) ◽  
pp. R262-R265 ◽  
Author(s):  
B. J. Moore ◽  
S. J. Armbruster ◽  
B. A. Horwitz ◽  
J. S. Stern

The rate of oxygen consumption was measured in 2-day Zucker preobese (fa/fa), homozygous (Fa/Fa) lean, and lean rats of unknown genotype (Fa/?) over the ambient temperature range of 26-35 degrees C. Significant differences in body mass were found among the three groups at this early age, the preobese pups having the greatest body mass. To account for body mass differences, the oxygen consumption data were expressed in terms of metabolic body size (ml O2 consumed X g body mass-2/3 X h-1). This mass-independent rate of oxygen consumption was significantly lower in the preobese pups than in the homozygous lean (Fa/Fa) pups at both thermoneutral (33-34 degrees C) and cold (26-27 degrees C) ambient temperatures at which, respectively, minimal and maximal rates of oxygen consumption were observed. This reduction in energy expenditure occurs before the establishment of hyperphagia or decreased levels of activity in the preobese pups. These data support the view that attenuated energy expenditure is a significant contributor to the early development of obesity in the Zucker fatty rat and point to the possibility of defective brown adipose tissue-mediated thermogenesis in the preobese pup.


Author(s):  
Родионова ◽  
Lyubov Rodionova ◽  
Сухов ◽  
Boris Sukhov ◽  
Самойлова ◽  
...  

The research was carried out on 9rabbits (males) of Chinchilla breed with modeling of standard perforating fracture of femoral bone. We performed intraosseous introduction of nanocomposite elemental selenium and heteropolysaccharide arabinogalactan 50mg Se/kg to individuals of experimental group (n=3) and NaCl 0,9% to individuals of control group (n=6). It was established that local intraosseous introduction of the nanocomposite with perforated fracture model did not affect basal metabolic indicators (body temperature, oxygen consumption, carbon dioxide production), but boosted the metabolic processes in the area of the surgical wound from the 9th to 21st days. It proves the bioavailability of the drug and the possibility of creating a local depot of selenium using a nanocomposite.


2008 ◽  
Vol 294 (6) ◽  
pp. R1968-R1979 ◽  
Author(s):  
Preeti H. Jethwa ◽  
Helen I'Anson ◽  
Amy Warner ◽  
Hayden M. Prosser ◽  
Michael H. Hastings ◽  
...  

The genes encoding prokineticin 2 polypeptide (Prok2) and its cognate receptor ( Prokr2/ Gpcr73l1) are widely expressed in both the suprachiasmatic nucleus and its hypothalamic targets, and this signaling pathway has been implicated in the circadian regulation of behavior and physiology. We have previously observed that the targeted null mutation of Prokr2 disrupts circadian coordination of cycles of locomotor activity and thermoregulation. We have now observed spontaneous but sporadic bouts of torpor in the majority of these transgenic mice lacking Prokr2 signaling. During these torpor bouts, which lasted for up to 8 h, body temperature and locomotor activity decreased markedly. Oxygen consumption and carbon dioxide production also decreased, and there was a decrease in respiratory quotient. These spontaneous torpor bouts generally began toward the end of the dark phase or in the early light phase when the mice were maintained on a 12:12-h light-dark cycle and persisted when mice were exposed to continuous darkness. Periods of food deprivation (16–24 h) induced a substantial decrease in body temperature in all mice, but the duration and depth of hypothermia was significantly greater in mice lacking Prokr2 signaling compared with heterozygous and wild-type littermates. Likewise, when tested in metabolic cages, food deprivation produced greater decreases in oxygen consumption and carbon dioxide production in the transgenic mice than controls. We conclude that Prokr2 signaling plays a role in hypothalamic regulation of energy balance, and loss of this pathway results in physiological and behavioral responses normally only detected when mice are in negative energy balance.


1980 ◽  
Vol 58 (7) ◽  
pp. 842-848 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock

Rats were maintained at 24 and 4 °C (WA, CA) and fed either a pelleted stock diet (WAS, CAS) or a varied and palatable cafeteria diet (WAC, CAC). Resting oxygen consumption ([Formula: see text], 29 °C) was significantly elevated by 15, 14, and 24% in WAC, CAS, and CAC rats, respectively, compared with WAS controls and these differences were completely abolished by injection of propranolol in all but CAC rats, where [Formula: see text] remained only slightly elevated. Experimental groups showed an increased capacity to respond to the thermogenic effects of norepinephrine (percentage increase in [Formula: see text]: WAS, 43 ± 5; WAC, 88 ± 6; CAS, 75 ± 6; CAC, 128 ± 5) and greather deposits of interscapular brown adipose tissue (IBAT) (WAC, 542 ± 27; CAS, 469 ± 27; CAC, 1111 ± 85 mg) compared with WAS controls (339 ± 22 mg).When exposed to 5 °C, WAS rats shivered continuously whereas in the WAC animals shivering had ceased by 5 h. Rectal temperature was maintained at a higher level in the WAC rats than in the WAS group (WAS, 34.7 ± 0.9 °C; WAC, 36.2 ± 0.5 °C; p < 0.01). Injection of propranolol lowered the core temperature of WAC rats and caused shivering to recommence but had no effect on WAS rats.The similarities between diet- and cold-induced thermogenesis suggest that both have a common metabolic origin residing in BAT and that dietary-induced thermogenesis may be important in the maintenance of body temperature as well as in energy balance regulation.


1995 ◽  
Vol 79 (3) ◽  
pp. 801-804 ◽  
Author(s):  
K. Hammarlund ◽  
T. Norsted ◽  
T. Riesenfeld ◽  
G. Sedin

To study the effect of intubation on respiratory water loss (RWL) during heat stress, 10 young nonsedated lambs were exposed to radiative heat stress both when intubated and when not. RWL, oxygen consumption (VO2), and carbon dioxide production were monitored continuously by using a flow-through system with a mass spectrometer for gas analysis. When the lambs were not intubated, heat stress caused RWL to increase by 218%, whereas VO2 and body temperature remained unchanged. When the lambs were intubated, heat stress caused RWL to increase by 131% and VO2 to increase by 36%. On extubation during heat stress, RWL increased by 117 +/- 48% (standard error of the estimate) of the preextubation value and body temperature started to fall. This study shows that intubation reduces the ability of the lamb to increase RWL and heat loss during heat stress in a warm environment, possibly as an effect of exclusion of the nose and a reduction in dead space. After extubation, RWL increases markedly, a finding that might also be valid for intubated infants.


1991 ◽  
Vol 69 (6) ◽  
pp. 761-766 ◽  
Author(s):  
Philip J. Scarpace ◽  
Bradley S. Bender ◽  
Stephen E. Borst

Fever is a complex and important nonspecific, host defense mechanism against infection. The generation of the heat necessary to increase body temperature may involve thermogenesis in brown adipose tissue. To investigate whether the febrile response to Escherichia coli peritonitis involves thermogenesis in brown adipose tissue, we assessed whole rat oxygen consumption and brown adipose tissue mitochondrial guanosine 5′-diphosphate binding. Non-lethal doses of E. coli, 1 × 106 to 1 × 108 colony forming units, induced a fever for greater than 8 h. In contrast, a dose of 1 × 109 colony forming units resulted in a progressive hypothermia culminating in death. A 48% increase in oxygen consumption (p < 0.05) in E. coli-infected rats occurred almost immediately, preceded the development of the fever, and was sustained throughout the fever. There was a highly significant correlation (r = 0.736, p < 0.01) between oxygen consumption and body temperature for both control and infected animals. Guanosine 5′-diphosphate binding assessed by multi-point Scatchard analysis of [3H]guanosine 5′-diphosphate binding to isolated mitochondria was increased by 45.4 ± 7.3% at 1.75 h and by 31.9 ± 9.0% at 3.5 h (p < 0.05). The greater increase was during the rising phase of the fever. Unexpectedly, a lethal dose of 5 × 109 colony forming units of E. coli also increased guanosine 5′-diphosphate binding sites by 54.4 ± 14.2% (p < 0.05) despite a hypothermia of −1.71 ± 0.29 °C. These data indicate that peritonitis induces a fever that is correlated with oxygen consumption and increased guanosine 5′-diphosphate binding sites, suggestive of brown adipose tissue thermogenesis activation. This thermogenesis appears to be contributing at least some of the heat necessary for the febrile response in rats.Key words: rat, guanosine 5′-diphosphate binding, oxygen consumption.


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