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

The pathological sequelae of traumatic brain injury (TBI) include increased oxidative stress due to the production of reactive oxygen species (ROS). Regulation of ROS levels following TBI is determined primarily by antioxidant enzyme activity that in turn can be influenced by nerve growth factor (NGF). Hypothermia is one of the current therapies designed to combat the deleterious effects of TBI. However, it has been shown to suppress post-trauma increases in NGF levels in rat brain. The present study sought to determine whether post-injury hypothermia also impairs the antioxidant response to injury, and if such an effect could be reversed by infusion of exogenous NGF. We employed a lateral controlled cortical impact injury model in rat, followed by moderate hypothermia treatment with supplemental intracerebroventricular infusion of NGF or vehicle. The time course of changes in post-injury/intervention levels of NGF and activity of three major enzymes responsible for ROS scavenging, catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), was determined in the hippocampus. Relative to levels in injured, normothermic animals, hypothermia treatment not only suppressed NGF levels, but also attenuated CAT and GPx activity, and increased SOD activity. Infusion of NGF in injured, hypothermia-treated animals was ineffective in restoring hippocampal antioxidant enzymes activity to levels produced after injury under normothermic conditions, although it was able to increase septal cholinergic (choline acetyltransferase) enzyme activity. These results have implications for clinical treatment of TBI, demonstrating that moderate hypothermia suppresses NGF and the antioxidant response after TBI; the latter cannot be countered by exogenous NGF administration.
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PMID:Effects of post-injury hypothermia and nerve growth factor infusion on antioxidant enzyme activity in the rat: implications for clinical therapies. 1528 6

In the present study, oral supplementation of l-arginine in rats was evaluated for its anti-stress and adaptogenic activity using the cold (5 degrees C)-hypoxia (428 mmHg)-restraint (C-H-R) animal model. A dose-dependent study of l-arginine was carried out at doses of 12.5, 25.0, 50.0, 100.0, 200.0 and 500.0 mg/kg body weight, administered orally 30 min prior to C-H-R exposure. The time taken by the rat to attain a rectal temperature of 23 degrees C (T(rec) 23 degrees C) during C-H-R exposure and its recovery to T(rec) 37 degrees C at normal atmospheric pressure and 32 +/- 1 degrees C were used as biomarkers of anti-stress and adaptogenic activity. Biochemical parameters related to lipid peroxidation, anti-oxidants, cell membrane permeability, nitric oxide and stress, with and without administration of the least effective l-arginine dose, were measured in rats on attaining T(rec) 23 degrees C and T(rec) 37 degrees C. The least effective adaptogenic dose of l-arginine was 100.0 mg/kg body weight. The C-H-R exposure of control rats, on attaining T(rec) 23 degrees C, resulted in a significant increase in plasma malondialdehyde (MDA), blood lactate dehydrogenase (LDH) and a decrease in blood catalase (CAT) and plasma testosterone levels. On recovery (T(rec) 37 degrees C) of control rats, there was a further decrease in CAT and plasma testosterone, and an increase in LDH. l-Arginine supplementation resulted in a significant decrease in plasma MDA, an increase in blood superoxide dismutase (SOD), CAT levels maintained at control values and a lower increase in LDH compared with controls (45.3 versus 58.5% and 21.5 versus 105.2%) on attaining T(rec) 23 degrees C during C-H-R exposure and on recovery to T(rec) 37 degrees C. The results suggested that l-arginine possesses potent anti-stress activity during C-H-R exposure and recovery from C-H-R-induced hypothermia.
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PMID:Anti-stress and Adaptogenic Activity of l-Arginine Supplementation. 1584 Dec 83

After an ischemic insult, a multi-faceted complex cascade of biochemical reactions occurs that ultimately causes neurons death. Above reactions exert an influence on: immunological changes (activation of the complement system and the generation of antibodies), increased inflammation (actions of proinflammatory cytokines and chemokines), the production of reactive oxygen species leading to oxidative stress, diminished mitochondrial function and activation of apoptotic pathways. There is also intensive release and wrong reversible escapement many of neurotransmitters. The last one throught oxidative desamination are one of the main sources most of free radicals. Central nervous system is particularly susceptible to ROS-induced damage due to the high oxygen demands of the brain and low concentration of endogenous antioxidants. lts refer both enzymatic antioxidants: catalase, glutathione peroxidase, glutathione reductase, superoxide dismutase and nonenzymatic antioxidants glutathione, vitamin a, c, e, coenzym Q, uric acid etc. Presently there are no neuroprotective treatments and prevention. One way of treatment testing in clinical trials is hypothermia inhibits above-mentioned processes.
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PMID:[Contribution and role of important biochemic factors in cerebral ischemia]. 1678 Feb 50

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

The release of reactive oxygen species has been described in hypothermic cells and tissues. Fructose 1,6-biphosphate (F1,6-BP) protects tissue stored at cold temperatures. We study the effect of F1,6-BP in vivo administration on anaesthetized rats exposed to cold stress (4 degrees C chamber for 30 min) and rewarming, to see if it alters cold-induced oxidative injury. Body temperatures show that the animals reached moderate hypothermia (26.80+/-0.62 degrees C) after 30 min of cold exposition. A decrease in mean arterial pressure was found. One group of animals was then rewarmed. Both hypothermia and rewarming increased the production of thiobarbituric acid-reactive substances, an index of lipid peroxidation, and reduced the antioxidant levels of plasmatic sulfhydryl groups, as well as decreasing the enzymatic activities of Cu,Zn-superoxide dismutase (Cu,Zn-SOD), catalase and GSH peroxidase in erythrocytes. Administration of F1,6-BP increased sulfhydryl groups and limited lipid peroxidation in plasma. It furthermore enhanced Cu,Zn-SOD and GSH peroxidase antioxidant activity in erythrocytes and preserved mean arterial pressure. Therefore, F1,6-BP has therapeutic potential based on its ability to reduce free-radical injury resulting from acute cold exposure and rewarming in vivo.
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PMID:Beneficial effects of fructose 1,6-biphosphate on hypothermia-induced reactive oxygen species injury in rats. 1860 97

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

Mild hypothermia and pharmacological postconditioning are widespread therapeutical treatment options that positively influence the clinical outcome after tissue hypoxia. In the study presented, a two-enzyme based in-vitro oxygen deficiency model in combination with cultured HT-1080 fibrosarcoma cells was employed to mimic the in-vivo situation of hypoxia and to evaluate the influence of mild hypothermia and postconditioning with catalase on hypoxia-mediated cell damage. Using the in-vitro oxygen deficiency model, partial pressure of oxygen was rapidly reduced to levels below 5mmHg in the culture media and cells responded with an increased expression of hypoxia inducible factor-1 on protein level. Hypoxia resulted in significant cell rounding and retraction of cytoplasmic cell extensions. Evaluation of cytotoxicity revealed a 3.5-fold increase in lactate dehydrogenase levels which was accompanied by 40-fold elevated levels of hydrogen peroxide. The hypoxia-induced increase of lactate dehydrogenase was 2.5-fold reduced in the hypothermia group, although morphological correlates of cytotoxicity were still visible. Hypothermia did not significantly influence hydrogen peroxide concentrations in the culture media. Pharmacological postconditioning with catalase however dose-dependently decreased hypoxia-induced lactate dehydrogenase release. This cytoprotective effect was accompanied by a dose-dependent, up to 50-fold reduction of hydrogen peroxide concentrations and retention of normal cell morphology. We suggest that the described in-vitro oxygen deficiency model is a convenient and simple culture system for the investigation of cellular and subcellular events associated with oxygen deficiency. Moreover, our in-vitro results imply that catalase postconditioning may be a promising approach to attenuate hypoxia-induced and hydrogen peroxide-mediated cell and tissue damage.
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PMID:Hypoxia-induced cell damage is reduced by mild hypothermia and postconditioning with catalase in-vitro: application of an enzyme based oxygen deficiency system. 1991 79

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

Septic shock is associated with life-threatening vasodilation and hypotension. To cause vasodilation, vascular endothelium may release nitric oxide (NO), prostacyclin (PGI2), and the elusive endothelium-derived hyperpolarizing factor (EDHF). Although NO is critical in controlling vascular tone, inhibiting NO in septic shock does not improve outcome, on the contrary, precipitating the search for alternative therapeutic targets. Using a hyperacute tumor necrosis factor (TNF)-induced shock model in mice, we found that shock can develop independently of the known vasodilators NO, cGMP, PGI2, or epoxyeicosatrienoic acids. However, the antioxidant tempol efficiently prevented hypotension, bradycardia, hypothermia, and mortality, indicating the decisive involvement of reactive oxygen species (ROS) in these phenomena. Also, in classical TNF or lipopolysaccharide-induced shock models, tempol protected significantly. Experiments with (cell-permeable) superoxide dismutase or catalase, N-acetylcysteine and apocynin suggest that the ROS-dependent shock depends on intracellular (*)OH radicals. Potassium channels activated by ATP (K(ATP)) or calcium (K(Ca)) are important mediators of vascular relaxation. While NO and PGI2-induced vasodilation involves K(ATP) and large-conductance BK(Ca) channels, small-conductance SK(Ca) channels mediate vasodilation induced by EDHF. Interestingly, also SK(Ca) inhibition completely prevented the ROS-dependent shock. Our data thus indicate that intracellular (*)OH and SK(Ca) channels represent interesting new therapeutic targets for inflammatory shock. Moreover, they may also explain why antioxidants other than tempol fail to provide survival benefit during shock.
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PMID:Reactive oxygen species and small-conductance calcium-dependent potassium channels are key mediators of inflammation-induced hypotension and shock. 2049 72


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