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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothermia induces injury in its own right, but the mechanisms involved in the cell damage are still unclear. The aim of this study was to test the effects that glutathione (GSH) depletion induces on cell death in isolated rat hepatocytes, kept at 4 degrees C for 20 h, by modulating intracellular GSH concentration with diethylmaleate and buthionine sulfoximine (DEM and BSO). Untreated hepatocytes showed Annexin V stained cells (AnxV(+)), scarce propidium iodide stained cells (PI(+)) and presented a low level of lactate dehydrogenase (LDH) leakage after 20 h at 4 degrees C and rewarming at 37 degrees C. When DEM and BSO were added before cold storage, we observed a few AnXV(+) cells and an increase in PI(+) cells associated with LDH release in the incubation medium. Conversely, the addition of DEM and BSO only during rewarming caused a marked increase in cell death by apoptosis. Production of reactive oxygen species (ROS) and thiobarbituric acid species (TBARS), associated with a decrease in GSH concentrations, was higher when DEM and BSO were added before cold storage. Cells treated with DEM and BSO before cold storage showed lower ATP energy stores than hepatocytes treated with DEM and BSO only during rewarming. Pretreatment of hepatocytes with deferoxamine protected against apoptotic and necrotic morphology in conditions of GSH depletion. These results suggest that pretreatment of hepatocytes with DEM and BSO before cold storage induces necrosis, while the treatment of hepatocytes only during rewarming increases apoptosis. In both conditions, iron represents a crucial mediator of cell death.
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PMID:Apoptosis vs. necrosis: glutathione-mediated cell death during rewarming of rat hepatocytes. 1594 4

Methodic approaches for the purposeful changes of glutathione concentration in the brain and liver by administration of glutathione depletors and prodrugs have been modified. Two different depletors (diethylmaleate and buthionine sulfoximine) cause considerable increase of tolerance to the complete global cerebral ischemia and hypothermia development which correlate closely with the decrease of GSH concentration. Five GSH prodrugs (GSH esters and oxothiazolidine carboxilate) and GSH itself usually decrease slightly body temperature but do not influence tolerance to ischemia in the most of series. The increase of tolerance to the complete global cerebral ischemia is connected not with GSH accumulation, but with its decrease. Evidently one of the two opposite GSH effects, sensitizing or protecting one, can predominate in different forms of cerebral ischemia.
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PMID:[The correlation of tolerance to cerebral ischemia and body temperature with glutathione concentration]. 1611 94

Effects of oral vitamin E supplementation on blood malondialdehyde (MDA), glutathione (GSH) and vitamin E levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities in acute hypothermia of guinea-pigs were investigated. Thirty male guinea pigs, weighing 500-800 g were randomly divided into one of three experimental groups: A (control, without cooling), B (hypothermic) and C (hypothermic with vitamin E supplementation). The guinea-pigs of group C received daily oral supplementation of 460 mg kg(-1) bw vitamin E for 4 days before inducing hypothermia. Twenty-four hours after the last vitamin E supplementation, the guinea-pigs of the B and C groups were cooled by immersion into cold water (10-12 degrees C), and the control guinea-pigs were immersed into water of body temperature (37 degrees C) up to the neck for 5 min without using any anaesthetic or tranquilizer. Rectal body temperatures of groups were measured and blood samples for biochemical analysis were collected immediately after the cooling. The body temperature, GSH and vitamin E levels and GSH-Px enzyme activity of hypothermic guinea-pigs were lower (p < 0.05), but SOD enzyme activity was not different (p > 0.05) from those of control animals. Although, the body temperature of hypothermic with vitamin E supplementation group was lower (p < 0.05), all other parameters of this group were not different (p > 0.05) from the controls. It was concluded that oral supplementation of vitamin E can alleviate the lipid peroxidation-induced disturbances associated with hypothermia by increasing the serum vitamin E level to normal. However, more studies are needed to prove whether this vitamin can improve quality of life during the cold seasons.
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PMID:Effect of oral vitamin E supplementation on oxidative stress in guinea-pigs with short-term hypothermia. 1720 Sep 85

This study was carried out to examine the antioxidative potential, if any, of seabuckthorn leaf aqueous extract, administered orally in rats at a dose of 100 mg kg(-1) both in single and five doses, 30 min before cold (5 degrees C)-hypoxia (428 mm Hg)-restraint (C-H-R) exposure. The effect of the extract was studied on lipid peroxidation and antioxidant parameters in liver and gastrocnemius muscle of rats on attaining the rectal temperature (T(rec)) of 23 degrees C during C-H-R exposure and after recovery (T(rec)37 degrees C) from C-H-R-induced hypothermia. In untreated rats exposed to C-H-R, there was a significant increase in malondialdehyde (MDA) levels in liver and muscle along with decreased activity of catalase (CAT) and glutathione-S-transferase (GST) in liver and muscle. Single- and five-dose extract treatment restricted the increase in liver and muscle MDA levels and five doses of extract treatment further improved the levels of liver antioxidants, viz. reduced glutathione (GSH), on recovery of T(rec)37 degrees C, increased superoxide dismutase (SOD) during exposure and recovery, normalized CAT activity in liver during C-H-R exposure and an increase on recovery of T(rec)37 degrees C. The decreasing pattern of liver and muscle GST levels both in single-dose and five-dose extract treated rats was similar to that in untreated rats. Results suggested that supplementation with seabuckthorn extract helps to reduce oxidative stress in liver and muscle of rats during C-H-R exposure and post-stress recovery.
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PMID:Modulatory effect of seabuckthorn leaf extract on oxidative stress parameters in rats during exposure to cold, hypoxia and restraint (C-H-R) stress and post stress recovery. 1805 38

The present study was carried out to study mechanism of adaptogenic activity of seabuckthorn leaf extract, administered orally in rats both in single and five doses at a dose of 100mg/kg body weight 30min prior to C-H-R exposure. The efficacy of the extract was studied on circulating energy fuels, lipid peroxidation and anti-oxidant parameters in rats on attaining the T(rec) 23 degrees C during C-H-R exposure and after recovery (T(rec) 37 degrees C) from C-H-R induced hypothermia. Single dose treatment in rats restricted rise in blood malondialdehyde (MDA) levels and decrease in glutathione (GSH) and catalase (CAT) levels. Both single and five doses also restricted the rise in serum free fatty acids (FFA) and lactate dehydrogenase (LDH) levels on attaining T(rec) 23 degrees C during C-H-R exposure, suggesting more efficient utilization of FFA for energy production and better maintained cell membrane permeability. This suggested that the adaptogenic activity of the extract might be due to its anti-oxidative activity, maintained blood glucose levels, better utilization of FFA and improved cell membrane permeability.
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PMID:Effect of seabuckthorn leaf extracts on circulating energy fuels, lipid peroxidation and antioxidant parameters in rats during exposure to cold, hypoxia and restraint (C-H-R) stress and post stress recovery. 1816 86

We compared the effects of early and late stage hypothermia treatment after spinal cord injury. Five groups each consisting of seven rats were included in this study. In Group 1a (Clip applied-non-treatment group) and Group 1b (Clip applied-treated group) the spinal cords were harvested 1 h after the injury. In Group 2a (clip applied, non-treated group) and Group 2b (clip applied-treated group) the injured segments were harvested 24 h after injury. Group 3 was designed as the sham-operated group. The significantly lower levels of TBARS and GSH-Px in Group 2a, as compared with Group 1b suggests that the hypothermia was effective in the early stage of treatment (P < 0.05). In contrast, TBARS and GSH-Px levels were significantly increased at the 24 h timepoint following treatment (P < 0.05). Short-term systemic hypothermia reduces lipid peroxidation in the early stages after spinal cord injury. This beneficial effect disappears 24 h following systemic hypothermic treatment.
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PMID:Does hypothermic treatment provide an advantage after spinal cord injury until surgery? An experimental study. 1863 2

Although clinical hypothermia is used for reducing postischemic damage, injurious effects have also been reported. To determine whether hypoxia and oxidative stress are induced by systemic deep hypothermia, we used an in vivo rat model keeping the arterial Pco2 constant. Animals were divided into 4 groups: sham, 2 h deep hypothermia (21 degrees C), 1 h posthypothermia (rewarmed to 37 degrees C after 2 h deep hypothermia), and 3 h normothermia. Blood gases, portal vein blood flow, arterial pressure, and heart rate were monitored throughout the experiment. Liver enzyme antioxidant activity was also examined. The hemodynamic parameters decreased drastically during hypothermia, but were fully restored after rewarming. No changes in hepatic antioxidant activity (catalase, glutathione peroxidase, and superoxide dismutase) were observed. The redox level in liver (GSH/GSSG ratio) was preserved in hypothermia but decreased when animals were rewarmed. ALT did not increase and no evidence of tissue hypoxia was detected in liver regarding the restricted flow during hypothermia. With the described protocol, deep hypothermia is regarded as an experimental safe model.
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PMID:Deep hypothermia impact on acid-base parameters and liver antioxidant status in an in vivo rat model. 1952 42

Anti-oxidative potential of Rhodiola imbricata root aqueous extract was examined in rats, administered orally at a dose of 100 mg/kg both in single and multiple doses, 30 min prior to cold (5 degrees C)-hypoxia (428 mmHg)-restraint (C-H-R) exposure. Lipid per-oxidation, anti-oxidant parameters and lactate dehydrogenase (LDH), were studied in blood, liver and muscle of rats on attaining T(rec)23 degrees C during C-H-R exposure and after recovery (T(rec)37 degrees C) from C-H-R induced hypothermia. The results of untreated control rats on attaining T(rec)23 degrees C showed a significant increase in blood, liver and muscle malondialdehyde (MDA) and LDH levels. Hepatic catalase (CAT) and muscle glutathione S-transferase (GST) also increased significantly. Administration of single dose of Rhodiola imbricata root aqueous extract significantly restricted rise in blood MDA, increased blood reduced glutathione (GSH) and superoxide dismutase (SOD) activity with restricted rise in blood, liver and muscle LDH; improved liver and muscle SOD on attaining T(rec)23 degrees C and T(rec)37 degrees C; liver CAT on attaining T(rec)23 degrees C and liver GST during recovery. Multiple doses treatment of the extract further increased blood, liver and muscle GSH and GST levels; restricted increase in LDH on attaining T(rec)23 degrees C and recovery; increased CAT during recovery. Results suggested the anti-oxidant potential of Rhodiola root extract during C-H-R exposure and post-stress recovery and it also maintained cell membrane permeability.
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PMID:Anti-oxidative effect of Rhodiola imbricata root extract in rats during cold, hypoxia and restraint (C-H-R) exposure and post-stress recovery. 2007 93

Previous studies have demonstrated protective effects of mild hypothermia following acetaminophen (APAP)-induced acute liver failure (ALF). However, effects of this treatment in ALF due to other toxins have not yet been fully investigated. In the present study, the effects of mild hypothermia in relation to liver pathology, hepatic and cerebral glutathione, plasma ammonia concentrations, progression of encephalopathy, cerebral edema, and plasma proinflammatory cytokines were assessed in mice with ALF resulting from azoxymethane (AOM) hepatotoxicity, a well characterized model of toxic liver injury. Male C57BL/6 mice were treated with AOM (100 microg/g; i.p.) or saline and sacrificed at coma stages of encephalopathy in parallel with AOM mice maintained mildly hypothermic (35 degrees C). AOM treatment led to hepatic damage, significant increase in plasma transaminase activity, decreased hepatic glutathione levels, and brain GSH/GSSG ratios as well as selective increases in expression of plasma proinflammatory cytokines. Mild hypothermia resulted in reduced hepatic damage, improvement in neurological function, normalization of glutathione levels, and selective attenuation in expression of circulating proinflammatory cytokines. These findings demonstrate that the beneficial effects of mild hypothermia in experimental AOM-induced ALF involve both antioxidant and anti-inflammatory mechanisms.
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PMID:Antioxidant and anti-inflammatory effects of mild hypothermia in the attenuation of liver injury due to azoxymethane toxicity in the mouse. 2019 38

Endothelin antagonists are being investigated to prevent neuronal loss after cerebral ischemia. Acetaminophen has been tried in stroke patients to produce hypothermia so that injury following cerebral ischemia can be reduced. The aim of this study was to assess the effect of BQ123, an endothelin-A receptor antagonist, alone and in combination with acetaminophen on neurological outcome, oxidative stress and infarct volume in rats subjected to focal ischemia by occlusion of the middle cerebral artery. In normal rats, acetaminophen decreased, while BQ123 did not produce any change in body temperature, but rats treated with BQ123 and acetaminophen produced a significantly greater (41%) hypothermic response compared to acetaminophen group. In rats subjected to middle cerebral artery occlusion, neurologic deficit was observed; acetaminophen alone did not improve, but BQ123 alone and in combination with acetaminophen produced a significant improvement in neurological deficit. The level of malondialdehyde (MDA) increased and reduced glutathione (GSH) decreased in the brain following ischemia; acetaminophen did not but BQ123 alone and in combination with acetaminophen decreased MDA and increased GSH levels in ischemic rats. Cerebral ischemia produced significant infarction, the infarct volume decreased in response to BQ123 and its combination with acetaminophen. The infarct volume, MDA level and neurological deficit in ischemic rats significantly improved in rats treated with both BQ123 and acetaminophen compared to BQ123 alone. The results demonstrate that a combination of acetaminophen and BQ123 is more effective in reducing the neuronal damage following cerebral ischemia, and this combination may be worth investigating in stroke patients.
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PMID:Endothelin-A receptor antagonist BQ123 potentiates acetaminophen induced hypothermia and reduces infarction following focal cerebral ischemia in rats. 2063 81


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