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)

The action of copper (CuSO4, 5 mg/kg, oral) on selected neuropharmacological actions of cannabis resin (CI, oral) was studied on albino rats and mice. Copper potentiated the barbiturate hypnosis-potentiating activity of CI in albino rats and mice and had no effect on hypothermic activity in albino rats. Single doses of copper partially inhibited tolerance to barbiturate hypnosis-potentiation activity and markedly delayed the development of tolerance to hypothermic activity of CI. Oral as well as i.c.v. copper (CuSO4, 0.1 microgram) in single dose antagonised the tolerance to hypothermic activity of cannabis or THC for one to two weeks. Copper-CI interaction could be antagonised by penicillamine. Zinc (ZnSO4, 5 mg/kg, oral) had an action similar to that of copper in antagonising the development of tolerance to the hypothermic activity of CI, but magnesium (MgSO4, 5 mg/kg, i.p.) was devoid of any such action. Studies indicate that, although copper has no significant neuropharmacological action, it interacts with CI activity, especially in tolerant rats, in effects on hypothermia. The site of action of copper is possibly the hypothalamus, where it inhibits the processes of tolerance development to CI on the noradrenergic neurone.
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PMID:Studies on the interactions of copper and cannabis. 41 40

The toxicity of Z-103 (catena-(S)-[mu-[N alpha-(3-aminopropionyl) histidinato(2-)-N1,N2,O:N tau]-zinc], CAS 107667-60-7) was evaluated in mice and rats after single administration. LD50 values in mice were 1269 mg/kg for males and 1331 mg/kg for females by the oral route, 220 mg/kg for males and 165 mg/kg for females by the intraperitoneal route, and 758 mg/kg for males and 874 mg/kg for females by the subcutaneous route. LD50 values in rats were 8441 mg/kg for males and 7375 mg/kg for females by the oral route, 405 mg/kg for males and 422 mg/kg for females by the intraperitoneal route and more than 5000 mg/kg for both sexes by the subcutaneous route. No sex differences were observed. A decrease in locomotor activity, ventral posture, crouching, hypothermia and respiratory depression were observed in both mice and rats as the main clinical signs. In addition to these changes, induration, swelling and crust formation were observed at the subcutaneous injection site.
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PMID:Single dose toxicity study on catena-(S)-[mu-[N alpha-(3-aminopropionyl) histidinato(2-)-N1,N2,O:N tau]-zinc] in mice and rats. 179 79

Tumor necrosis factor (TNF) is a peptide secreted by macrophages in response to endotoxin that can produce many of the changes seen in septic shock. After cecal ligation and puncture (CLP) rats gradually develop tachycardia, hypotension, tachypnea, and hypothermia. At 5 h post-CLP, rats have a peak in serum levels of endotoxin and 60% of rats have blood cultures that grow Gram-negative rods (Escherichia coli and Klebsiella pneumonia). At 20 h post-CLP all rats develop positive blood cultures. Serum levels of TNF are not reproducibly measurable in rats following CLP. Rats undergoing CLP have a 50-80% mortality with deaths usually occurring 24-72 h postinjury. Repetitive (twice daily x 6 d) i.p. injection of sublethal doses of recombinant human TNF-alpha (100 micrograms/kg) to rats undergoing CLP 1 d after the treatment period resulted in a significant reduction in mortality compared to control rats previously unexposed to rTNF (P less than 0.03). Animals treated with rTNF had no hypotension or hypothermia after CLP and regained normal food intake faster than control rats. 12 h after CLP the gene expression for manganous superoxide dismutase (MnSOD), an inducible mitochondrial metalloenzyme responsible for cellular resistance to injury from toxic reactive oxygen species, was higher in livers of rats treated with rTNF suggesting that the TNF treatment augmented expression of this protective enzyme. Unlike MnSOD, expression of the gene for copper-zinc SOD was not affected by CLP or rTNF treatment. The results suggest that prior treatment with recombinant TNF can ameliorate the lethality, hypotension, hypothermia, and anorexia of Gram-negative sepsis in rats and that the mechanism may be related to enhanced hepatic expression of the gene for MnSOD. Repeated administration of recombinant TNF may be a strategy to minimize mortality and morbidity of Gram-negative sepsis.
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PMID:Treatment with recombinant human tumor necrosis factor-alpha protects rats against the lethality, hypotension, and hypothermia of gram-negative sepsis. 205 27

The ability of intraoperative hypothermia to modify the metabolic response to cardiopulmonary bypass (CPB) was assessed by serial alterations in iron, zinc and copper, and in their molar binding ratios to their respective transport proteins, in 20 male patients under-going elective coronary artery surgery and randomised to an operative blood temperature of 28 degrees C or 20 degrees C. Decreases in serum iron and zinc concentrations, typical of the acute phase response, were preceded by early rises. Significant alterations in the metal: protein molar binding ratios preceded significant changes in the serum concentrations of the metals and occurred earliest in the zinc: albumin binding ratio, which was apparent by the time of skin incision. An intraoperative temperature of 20 degrees C modified iron and zinc concentrations and their protein binding ratios during surgery but not in the post-operative period. These early changes in trace metals and their protein binding ratios are a simple and inexpensive method of quantitating the response to surgical injury and may be useful in assessing new interventions in cardiopulmonary bypass. An awareness of the trace element response to surgical injury is essential to avoid misdiagnoses of iron deficiency anaemia or zinc deficiency.
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PMID:The effects of intraoperative hypothermia and cardiopulmonary bypass on trace metals and their protein binding ratios. 226 37

To investigate the practicality of hypothermia and hypometabolism as sensitive indices of toxicity in the mouse, oxygen consumption was monitored continuously and body temperature was measured at 30 min postinjection following the intraperitoneal administration of various metal salts. Eleven metal ions were tested: Al3+, Cd2+, Co2+, Cr2+, Cu2+, Hg2+, Mg2+, Mn2+, Ni2+, Pb2+, and Zn2+. All metals induced dose-dependent reductions in both oxygen consumption (hypometabolism) and deep body (colonic) temperature. Comparative toxicity of the metal ions was evaluated by calculating the dose of metal ion in dimensions of mmol/kg body mass needed to reduce colonic temperature to 35 degrees C. The order of toxicity from lowest to highest was as follows: Cr less than Al less than Pb less than Mn less than Mg less than Zn less than Cu less than Co less than Ni less than Hg less than Cd. The threshold doses for reducing body temperature were less than 5% of the LD50 in 6 of the metals studied. Metal salts with relatively low LD50 doses such as Hg, Cd, and Ni were most efficacious in inducing hypothermia and hypometabolism. Moreover, there was a direct linear relationship between dose for inducing hypothermia or hypometabolism and the reported LD50. Hence, the hypothermia and hypometabolism test may prove to be a sensitive and rapid test for the evaluation of toxicity of environmental contaminants.
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PMID:Hypothermia and hypometabolism: sensitive indices of whole-body toxicity following exposure to metallic salts in the mouse. 229 93

To examine how fat might influence the metabolic effects of tumour necrosis factor alpha (TNF alpha), human recombinant TNF alpha was given intravenously to rats that had been fed for 12 weeks on diets containing (g/kg) 200 maize oil or 190 coconut oil + 10 maize oil. Rectal temperature and tissue composition measurements were made 8 and 24 h after injection. Ambient temperatures of 20 degrees and 25 degrees were employed to accentuate rectal temperature changes. Doses of 30 and 300 micrograms TNF alpha/kg body-weight were given, and brought about depression of serum zinc and albumin and elevation of copper. Muscle protein content was decreased and liver protein and Zn content enhanced by TNF alpha. Serum Zn and liver Zn content were negatively correlated 8 h after injections. Hypothermia developed within 1 h of injection. All responses except the rise in serum Cu and gain in liver Zn were more intense at the higher than at the lower dose of TNF alpha. Hypothermia was exacerbated by an environmental temperature of 20 degrees. The coconut-oil diet blunted the hypothermia and likewise the changes in serum albumin and Cu content 8 h after injections and in muscle and liver protein after 24 h. Changes in eicosanoid metabolism may be involved in the modulatory effects of the coconut-oil-enriched diet.
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PMID:Dietary fat modifies some metabolic actions of human recombinant tumour necrosis factor alpha in rats. 238 39

Cultured Chinese hamster V79 fibroblast cells at the transition from logarithmic to stationary growth have been shown to undergo apoptosis (programmed cell death) after cold shock [B. L. Soloff, W. A. Nagle, A. J. Moss, Jr., K. J. Henle, and J. T. Crawford, Biochem. Biophys. Res. Commun. 145, 876-883 (1987)]. In this report, we show that about 95% of the cell population was susceptible to cold-induced apoptosis, and the amount of cell killing was dependent on the duration of hypothermia. Cells treated for 0-90 min at 0 degrees C exhibited an exponential survival curve with a D0 of 32 min; thus, even short exposures to the cold (e.g., 5 min) produced measurable cell killing. The cold-induced injury was not produced by freezing, because similar results were observed at 6 degrees C, and cell killing was not influenced by the cryoprotective agent dimethyl sulfoxide. Cold-induced apoptosis was inhibited by rewarming at 23 degrees C, compared to 37 degrees C, by inhibitors of macromolecular synthesis, such as cycloheximide, and by 0.8 mM zinc sulfate. The results suggest that apoptosis represents a new manifestation of cell injury after brief exposure to 0-6 degrees C hypothermia.
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PMID:Cultured Chinese hamster cells undergo apoptosis after exposure to cold but nonfreezing temperatures. 239 28

The effects of hypoglycemia on cerebrovascular permeability to the Evans blue-albumin complex were studied in rats injected with 50 IU/kg, i.v. crystalline zinc insulin. One group of hypoglycemic animals was warmed to keep their body temperatures close to 37 degrees C, and the rats in the other group were allowed to become hypothermic by hypoglycemia. The arterial blood pressures of the hypoglycemic rats were continuously monitored during the coma and a significant rise in pressure was observed in most animals at the end of the coma. When glucose was administered i.v. to five animals of each group, this elevated pressure returned to normal values within 0.5 min and the animals slowly recovered normal behavior. At termination of the coma, most brains in the hypothermic hypoglycemic group showed an intensive and extensive staining by Evans blue; whereas only two brains in the normothermic hypoglycemic group showed any noticeable extravasation of Evans blue-albumin. Arterial PO2, PCO2, and pH were determined and no significant difference was found between values from animals in hypoglycemic coma and the controls. Four animals were surface-cooled and were used to examine the effects of hypothermia on blood-brain barrier permeability. These brains did not show any macroscopically evident Evans blue-albumin extravasation. The results indicated that prolonged, severe hypoglycemia with hypothermia caused a profound blood-brain barrier dysfunction whereas normothermic hypoglycemia resulted in few cases of any noticeable increase in blood-brain barrier permeability.
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PMID:Effect of insulin-induced hypoglycemia on blood-brain barrier permeability. 298 97

We have previously shown that somatostatin (SS) immunoreactive (-i) neurons, located in the rat dentate hilus, are vulnerable to cerebral ischemia (Johansen et al., 1987). Within 40 h after ischemia, the cells show clear signs of cell death. At the same time, we observed that dying cells, located in the projection field of the mossy fibers (dentate hilus and CA3 mossy fiber layer), accumulate free zinc. We now demonstrate that the hilar cells, accumulating zinc after ischemia, are SS-i cells. Since it is known that hypothermia can ameliorate ischemic brain damage, we furthermore studied whether hypothermia (29 degrees C) protects the vulnerable SS-i neurons in hilus from zinc accumulation and ischemic cell death. We found that hypothermia both prevented ischemia-induced neuronal zinc accumulation and cell death. We speculate that hilar SS-i cells are highly vulnerable to ischemia, and develop rapid ischemic cell death, because they accumulate zinc shortly after ischemia.
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PMID:Hypothermia protects somatostatinergic neurons in rat dentate hilus from zinc accumulation and cell death after cerebral ischemia. 768 76

Oral exposure to chlorpyrifos (CHP) in the rat results in an initial hypothermic response followed by a delayed fever. Fever from infection is mediated by the release of cytokines, including interleukin-6 (IL-6) and tumor necrosis factor (TNF alpha). This study determined if the CHP-induced fever involves cytokine-mediated mechanisms similar to that of infectious fevers. Long-Evans rats were gavaged with the corn oil vehicle or CHP (10-50 mg/kg). The rats were euthanized and blood collected at various times that corresponded with the hypothermic and febrile effects of CHP. Plasma IL-6, TNF alpha, cholinesterase activity (ChE), total iron, unsaturated iron binding capacity (UIBC), and zinc were measured. ChE activity was reduced by approximately 50% 4 h after CHP. There was no effect of CHP on IL-6 when measured during the period of CHP-induced hypothermia or fever. TNF alpha levels nearly doubled in female rats 48 h after 25 mg/kg CHP. The changes in plasma cytokine levels following CHP were relatively small when compared to > 1000-fold increase in IL-6 and > 10-fold rise in TNF alpha following lipopolysaccharide (E. coli; 50 microg/kg; i.p.)-induced fever. This does not preclude a role of cytokines in CHP-induced fever. Nonetheless, the data suggest that the delayed fever from CHP is unique, involving mechanisms other than TNF alpha and IL-6 release into the circulation characteristic of infectious fevers.
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PMID:Are circulating cytokines interleukin-6 and tumor necrosis factor alpha involved in chlorpyrifos-induced fever? 1041 84


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