Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In previous studies we documented an increase in the levels of the serotonin metabolite, 5-hydroxyindoleacetic acid, in the congenitally hyperammonemic sparse fur mouse. To extend these findings, brain serotonin receptors were studied in these animals. Radioligand binding assays were performed using [3H]ketanserin to label serotonin2 sites and 8-[3H]hydroxy(di-n-propylamino)tetralin to label serotonin1A sites in cortical membrane homogenates. The capacity (Bmax) for [3H]ketanserin binding was significantly lower (-21%; p less than 0.05) in sparse fur animals than in control animals; there was no change in affinity (KD). In contrast, the capacity for 8-[3H]hydroxy(di-n-propylamino)tetralin binding was significantly greater (26%; p less than 0.05) in sparse fur compared with control animals. No difference in affinity was observed. Using two behavioral assays, the functional responsiveness of these serotonin receptors was compared in sparse fur and control animals. Head twitch activity elicited by administration of the serotonin agonist quipazine was studied as a behavior mediated by serotonin2 receptors. Compared with controls, sparse fur mice demonstrated a significantly decreased head twitch response (p less than 0.005). Hypothermia elicited by administration of 8-hydroxy(di-n-propylamino)tetralin was studied as a physiologic response mediated by serotonin1A receptors. Although there were not overall group differences in the dose-response data, there was a significant increase in the hypothermia induced by 8-hydroxy(di-n-propylamino)tetralin in sparse fur compared with control mice (p less than 0.02) at the highest dose. These data provide further support for a link between hyperammonemia and alterations in the serotonin system.
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PMID:Brain serotonin2 and serotonin1A receptors are altered in the congenitally hyperammonemic sparse fur mouse. 153 55

Rabbit pups are completely dependent on a maternal pheromone for the release of suckling behavior. However, if the mother is perfumed prior to nursing, pups will learn to respond to the novel odor with the characteristic nipple-search behavior in just one 3-4 min nursing episode. In a first investigation of the processes underlying this recently developed learning paradigm, time-dependent effects of hypothermia on retention of the task could be demonstrated. Thus pups whose whole body was cooled to a mouth temperature of 7 degrees C immediately after conditioning (n = 10) and tested 24 h later for 3 min on a perfumed fur did not differ significantly in their search response from naive, untreated controls (n = 10). In contrast, pups cooled 4 h after conditioning (n = 10) demonstrated clear retention of the learned response and searched as vigorously as conditioned but uncooled animals (n = 10). As pups of all groups demonstrated normal nipple-search behavior when tested on a lactating doe, the deficits associated with immediate cooling appear to have been specific to the learning task and time of treatment.
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PMID:Rapid odor conditioning in newborn rabbits: amnesic effect of hypothermia. 174 94

Previous studies of rats subjected to total sleep deprivation by the disk-over-water method had shown a large increase in energy expenditure (EE) and an initial increase followed by a later decrease in body temperature (Tb). It had been proposed that the increase in Tb resulted from regulation toward a higher temperature or setpoint, that the later decline in Tb resulted from excessive heat loss, and that the increase in EE supported both of these thermoregulatory changes. To evaluate this proposed role of the increase in EE, we examined whether blunting the EE rise in sleep-deprived rats by making them hypothyroid attenuated and/or shortened the initial increase in Tb and accelerated the later decline in Tb. Rats made hypothyroid by propylthiouracil administration (TxD rats) were totally sleep deprived and compared to hypothyroid yoked control (TxC) rats and to previously studied, untreated, totally sleep-deprived (TSD) rats. Neither TxD nor TxC rats showed large increases in EE like those of TSD rats. TxD rats did not initially increase Tb, as TSD rats had. Presumably, TSD rats had been able to support an initially elevated Tb, in spite of excessive heat loss, by large increases in EE, although even these increases were eventually insufficient. TxD rats showed much earlier and greater declines in Tb than TxC and TSD rats, eventually becoming severely hypothermic. These results support the interpretation that the large increase in EE previously seen in TSD rats had been compensatory for deprivation-induced thermoregulatory deficits. TxD rats survived an average of 17.1 days, which was not significantly different from survival time in TSD rats. However, there were differences in mortal processes between the two groups. TxD rats died or were sacrificed after chronic, severe hypothermia without observable signs of other morbid pathology. TSD rats had not shown similarly low Tb until just prior to death, but had shown signs of severe pathology, including severely debilitated appearance, disheveled fur, and severe lesions on their tails and on the plantar surfaces of their paws. These signs were diminished or absent in TxD rats, possibly due to blunted EE, lower Tb, or other effects of hypothyroidism. Because the skin changes seen in TSD rats were minimal in TxD rats, they could not have been responsible for the excessive heat loss.
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PMID:Sleep deprivation in the rat: XIII. The effect of hypothyroidism on sleep deprivation symptoms. 189 21

An adult mouse (18-20 g) model was developed for studying the pathogenesis of Campylobacter isolates. Iron-loaded BALB/c mice given 10(8)-10(9) Campylobacter colony forming units by intraperitoneal injection developed a severe mucoid diarrhea within 4 h. Severe diarrhea, consisting of unformed stools containing blood, mucus, and fecal leukocytes, persisted for 24 h. Diarrheal symptoms in surviving mice resolved gradually; no diarrhea was observed 5 days after inoculation. Mice not pretreated with iron developed no diarrheal symptoms, and no severe diarrhea was produced in mice inoculated orally. A transient (less than 24 h) bacteremia occurred in mice inoculated either orally or intraperitoneally. Liver, spleen, and kidney were positive for Campylobacter for 48 h; intestinal contents were positive for 5-7 days. Mice given greater than or equal to 10(10) colony forming units showed symptoms of endotoxemia (ruffled fur, inactivity, shaking, tearing, and hypothermia) and died without diarrheal symptoms. Mice given nonpathogenic Escherichia coli strain HB101, heat-killed C. jejuni cells (greater than 10(10)), C. jejuni lipopolysaccharide extract, or purified lipopolysaccharide from either Vibrio cholerae 569B or Salmonella typhimurium showed no diarrheal symptoms.
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PMID:Campylobacter diarrhea in an adult mouse model. 350 19

Antitumor effects of i.v. injected human recombinant tumor necrosis factor (rTNF) against solid Meth A tumors in mice appeared to be critically dependent on the dose and were limited by its toxicity. Extensive necrosis and complete cures were only induced by doses having untoward effects, such as diarrhea, hypothermia, ruffled fur, and lethargy. Murine tumor necrosis serum (TNS, 0.5 ml) had about the same antitumor potential and induced all side effects except diarrhea. More extensive necrosis and approximate doubling of the incidence of complete regression in the absence of gross side effects were observed upon administration of a low dose of rTNF combined with detoxified endotoxin, nontoxic poly A:U, or submicrogram doses of toxic endotoxin. The separate constituents had little antitumor effects, if any at all. Increasing the dose of toxic endotoxin resulted in a further potentiation of necrosis, overt toxicity, but no cures. Muramyl dipeptide and interferon alpha/beta did not potentiate effects of rTNF. In vitro growth of Meth A cells was not inhibited by toxic endotoxin, rTNF or the combination, although TNS was highly inhibitory. Data show that therapeutic effects of rTNF and its synergy with endotoxin are not due to direct effects on the tumor cells and that the extent of prompt in vivo tumor necrosis does not predict the course of tumor growth. Therapeutic effects of both TNS and toxic endotoxin probably involve a synergy between low levels of TNF and other factors/effects induced by endotoxin. Detoxified endotoxin and poly A:U probably induce the latter effects and little or no TNF, so explaining the absence of side effects, their weak antitumor potential, and their powerful synergistic action with rTNF. A role for interferon alpha/beta as an induced synergistic factor is not likely. Muramyl dipeptide and TNF might share properties needed for synergy with endotoxins.
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PMID:Synergistic action of human recombinant tumor necrosis factor with endotoxins or nontoxic poly A:U against solid Meth A tumors in mice. 382 51

This experiment was designed to study the effect of ambient temperature (Ta) on the thermoregulatory response after the injection of the acetylcholinesterase blocking agent, physostigmine, into the preoptic/anterior hypothalamic area (POAH) of the rat. Three doses of physostigmine (3.0, 30.0 and 60.0 micrograms) were injected in a volume of 1.0 microliter in the preoptic/anterior hypothalamic area of unrestrained rats at three different ambient temperatures (15, 25 and 35 degrees C). Brain temperature (Tbr) and gross changes in behavior were monitored continuously throughout the duration of each experiment. Physostigmine induced hypothermia at ambient temperatures of 15 and 25 degrees C but not at 35 degrees C. Immediately prior to and during the hypothermic response the animals displayed behavioral reflexes such as fur licking and a sprawled posture which presumably enhanced heat loss. Generally, soon after the peak of the hypothermic response (approximately 30 min), the rats displayed heat-conserving behavior (huddled position, piloerection of the fur). These data indicate that the activity of cholinergic synapses within the preoptic/anterior hypothalamic area increases with decreasing ambient temperature. The behavioral observations suggest some role for the cholinergic system in the activation of heat-dissipating responses in the rat.
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PMID:Effect of ambient temperature on thermoregulation in rats following preoptic/anterior hypothalamic injection of physostigmine. 406 23

The muskoxen (Ovibos moschatus), a native of Greenland and the Canadian North West Territories, give birth in late April, and the newborn calves are known to tolerate an ambient temperature (Ta) of -35 degrees C. At birth the calves weigh about 8 kg, increasing in weight with 0.6 kg . day-1 for the first 30 days. With a deep body temperature (DBT) of 39.5 degrees C (range 37.7-41.3 degrees C) the newborn calves are consequently able to maintain a thermogradient of at least 70 degrees C between body core and the environment. The calves use primarily two modes of thermal protection: High metabolic heat production and prime fur insulation. Metabolic rate was about 3.5 W . kg-1 at thermoneutrality in calves aged from 8 h to 7 days. Lower critical temperature at this age was about -7 degrees C and a drop in Ta to -30 degrees C increased metabolism to about 5.3 W . kg-1. Upper critical temperature at age 4-7 days is as low as 20 degrees C, while it in calves aged only 18-24 h appears to be even lower. The calves possess great amounts of brown adipose tissue (BAT) at birth. Mitochondria from the BAT deposits were isolated and found to be in an extremely loose-coupled state with a great capacity for thermogenesis. Skeletal muscle contained very few mitochondria and is hardly employed in aerobic non-shivering thermogenesis. Calves shiver visibly while drying just after birth, but are normally not seen shivering thereafter. The conductance value for the dry pelt of newborn calves averaged 3.2 W . m-2 . 0 degrees C-1 (n = 4). Wetting of the pelt with ice-water at a Ta of 3 degrees C increased conductance to 8.8 W . m-2 . 0 degrees C-1. The conductance of the pelt was also influenced by wind, being 10 W . m-2 . C-1 at a wind-speed of 10 m . sec-1. The legs of the newborn calves are heavily furred and countercurrent circulation is not present, subcutaneous temperature just above the hooves being +29.8 degrees C at Ta of -24 degrees C as compared to 37.5 degrees C on the back. The newborn calves could cope with a Ta of -30 degrees C without apparent problems under experimental conditions, but they suffered hypothermia when exposed to a Ta of -33 degrees C in combination with wind of 10 m . sec-1.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modes of thermal protection in newborn muskoxen (Ovibos moschatus). 652 90

Blind male hamsters were maintained in running-wheel cages in a LD 12:12 light-dark cycle. After regular running patterns were established hypothermia was induced by ether anesthesia, wetting of the fur with ethanol, and cooling with ice. The hamsters were kept hypothermic for 3-24 h at colonic temperatures from 10 to 20 degrees C. Following hypothermia the animals were rewarmed and replaced in their home cages. Examination of the locomotor activity records showed phase shifts (delays) in activity onset that were correlated with the temperature and duration of the hypothermia but not with the circadian time at which the hypothermia was administered. The data were interpreted to mean that the circadian pacemaker was running at a reduced rate during the hypothermic bout. Calculation of the Q10 for the rate of the clock during hypothermia produced a range from 1.08 to 1.34 depending on the method of calculation. When compared with earlier data gathered from rats under similar conditions, the hamsters circadian pacemaker appears to be better temperature compensated.
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PMID:Temperature dependence of the hamster circadian pacemaker. 684 68

Blind female rats were maintained in running-wheel cages in a 12-h light-dark cycle. Hypothermia was induced by ether anesthesia, wetting of the fur by ethanol, and covering with ice. Rats were put in restraining cages and colonic temperatures were maintained between 20 and 32 degrees C for 3-16 h by cooling with ice and water. On recovery from hypothermia, the rats were replaced in their home wheels. Examination of the activity records showed significant phase delays associated with temperatures lower than 28 degrees C. At 20 degrees C, the phase delays indicated that the clock was running at about 64% normal speed giving a mean Q10 of 1.33, which is quite a bit higher than previously reported. It is speculated that, because the rat maintains its body temperature within narrow limits after the neonatal stage, it has lost the precise temperature compensation for the period of its biological clock that has been so well documented in other organisms.
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PMID:Temperature dependence of rat circadian pacemaker. 724 97

Chronic total sleep deprivation (TSD) in the rat produces an initial elevation and then declining body temperatures, increasing metabolic rate and eventual death. Because TSD rats will engage in warming behavior, one hypothesis is that the metabolic increase is an unsuccessful attempt at warming to combat a lethal hypothermia. However, TSD rats also undergo weight loss and progressive deterioration of skin and fur, suggesting TSD-induced pathological catabolic activity, possibly secondary to increased metabolic rate, that could be lethal. To evaluate these alternatives, the metabolic rate of rats was increased by thyroxine (T4) treatment while subjecting them to TSD. Compared to TSD rats not given T4, they had higher metabolic rates, higher body temperatures and reduced warming behavior, but their survival period was 37% shorter. Thus, it is unlikely that hypothermia is the cause of death in TSD rats. Weight and appearance declined more rapidly in T4-treated rats, but at the same proportions of survival time, skin pathology and decline in appearance were less evident in T4-treated rats than in TSD rats not given T4. Thus, there is some doubt whether a general pathological catabolic process is the cause of death. It is also possible that a specific morbid process normally reversed by sleep was accelerated by T4 administration.
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PMID:Sleep deprivation in the rat: XIX. Effects of thyroxine administration. 767 63


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