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 study was carried out in order to observe the protective effects of electroacupuncture (EA) and hypothermia on myocardial ischemic and reperfusion injury in pigs. Blood superoxide dismutase (SOD), malondialdehyde (MDA), creatine phosphokinase (CPK) and its isoenzyme (CK-MB), coronary artery flow (CAF) and myocardial heat-shock protein (HSP) mRNA expression were detected. It was observed that the MDA content increased and SOD activities decreased more significantly in control group compared with EA and EA+ hypothermia groups. CPK and CK-MB were found significantly increased in all three groups, but more remarkable in control group than in EA and EA+ hypothermia groups. HSP70 mRNA expression was found to be more in EA and EA+ hypothermia groups than that in control group 60 min after reperfusion. The results indicated that EA enhance the myocardial protection of hypothermia on ischemia/reperfusion injury. The mechanism may be related to the improvement of antioxidation and increased expression of HSP70 gene.
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PMID:Myocardial protective effects of electroacupuncture and hypothermia on porcine heart after ischemia/reperfusion. 1499 57

This study was undertaken to explore the myocardioprotective effects of the combination of ischemic preconditioning (IP) with hypothermia and St.II Thomas crystalloid cardioplegic solution (CCS) on immature hearts in the rabbit. Isolated immature rabbit hearts were perfused with Krebs-Henseleit bicarbonate buffer on Langendorff apparatus. In experiment 1, 24 hearts were divided into 4 groups (n=6 in each group): Con, IP1, IP2 and IP3 group. Hearts of the four groups underwent 0, 1, 2 or 3 cycles of IP respectively. Then all the hearts were subjected to a sustained ischemia period of 2 h at 20 degrees C and a postischemic reperfusion period of 30 min at 37 degrees C. In experiment 2, 48 hearts were divided into 6 groups (n=8 in each group): SCon1, SIP1, SCon2, SIP2, SCon3 and SIP3 group, according to hypothermia and the duration of sustained ischemia (30 min at 32 degrees C; 90 min at 25 degrees C, 2 h at 20 degrees C). The SIP1, SIP2 and SIP3 groups were preconditioned twice before the sustained hypothermic ischemia, while the SCon1, SCon2 and SCon3 groups were not preconditioned. CCS was applied during sustained ischemia, all the hearts were reperfused for 30 min at 37 degrees C. Heart rate (HR), left ventricular developed pressure (LVDP) and peak rate of increase or decrease of left ventricular pressure (+/-dp/dt(max)) were recorded. Tissue concentration of adenosine triphosphate (ATP), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were measured. At the end of reperfusion, values of product of LVDP and HR, +/-dp/dt(max) in IP2 group were 96%+/-21%, 101%+/-19% and 84% +/-15% of the baseline values respectively, which were significantly higher than those of Con group and IP3 group (P<0.01, P<0.05); also, the ATP content of IP2 group was higher than that of the Con group (P<0.01). When CCS was applied during sustained period of hypothermic ischemia at 32 degrees C or 25 degrees C, recovery rates of RPP (rate product, =LVDPxHR) and +dp/dt(max) in SIP1 group were 87% +/-14% or 99% +/-26% of the baseline values respectively (P<0.05, vs SCon1 group), the values in SIP2 group changed to 87% +/-16% or 102% +/-20% respectively (P<0.05, vs SCon2 group). Contents of ATP in SIP1 and SIP2 groups were significantly higher than those of SCon1 or SCon2 groups respectively (P<0.05), but MDA content of the two groups were significantly lower than those of SCon1 or SCon2 groups (P<0.05) respectively. The study indicates that IP attenuates hypothermic ischemia/reperfusion injury to immature rabbit hearts under 20 degrees C ischemia, two cycles of IP showing better myocardioprotective effects than 1 or 3 cycles of IP. When IP was combined with CCS which were applied during hypothermic ischemia period, the beneficial effects of IP were weakened as the temperature during the hypothermic period was elevated.
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PMID:Myocardioprotective effects of the combination of ischemic preconditioning with hypothermia and crystalloid cardioplegia in immature rabbits. 1522 56

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

We prospectively investigated non-invasive selective brain cooling (SBC) in patients with severe traumatic brain injury. Sixty-six in-patients were randomized into three groups. In one group, brain temperature was maintained at 33 - 35 degrees C by cooling the head and neck (SBC); in a second group, mild systemic hypothermia (MSH; rectal temperature 33 - 35 degrees C) was produced with a cooling blanket; and a control group was not exposed to hypothermia. Natural rewarming began after 3 days. Mean intracranial pressure 24, 48 or 72 h after injury was significantly lower in the SBC group than in the control group. Mean serum superoxide dismutase levels on Days 3 and 7 after injury in the SBC and MSH groups were significantly higher than in the control group. The percentage of patients with a good neurological outcome 2 years after injury was 72.7%, 57.1% and 34.8% in the SBC, MSH and control groups, respectively. Complications were managed without severe sequelae. Non-invasive SBC was safe and effective.
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PMID:Effects of selective brain cooling in patients with severe traumatic brain injury: a preliminary study. 1660 24

Hypometabolic state following hypothermia is known to protect tissues from ischemic injury. Hypothyroidism produces a hypometabolic state. The present study was undertaken to investigate the protective effects of hypothyroidism following cerebral ischemia and to ascertain the underlying mechanism. Euthyroid (E) and hypothyroid (H) animals were exposed to a 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion (I/R). Specific enzymatic methods and flowcytometry were used to assess the quantitative changes of molecules involved in neuronal damage as well as in protection. As compared to euthyroid ischemic reperfused (E + I/R) rats, H + I/R rats had insignificant neurological deficit, and smaller area of infarct. H + I/R rats had significantly lower markers of oxidative stress, and lactate dehydrogenase (LDH) activity (a marker for necrosis). Natural antioxidant activity (particularly superoxide dismutase) and integrity of mitochondria (membrane potential) were maintained in H + I/R group but not in E + I/R group. The number of neurons undergoing apoptosis significantly lower in hypothyroid ischemic rats as compared to euthyroid ones. These results suggest that hypothyroid animals face ischemia and reperfusion much better compared to euthyroid animals. A possible explanation could be the decreased oxidative stress and maintained antioxidant activity that finally leads to a decrease in necrosis and apoptosis. These observations may suggest strategies to induce brain-specific downregulation of metabolism that may have implications in the management of strokes in human beings.
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PMID:Reduction in oxidative stress and cell death explains hypothyroidism induced neuroprotection subsequent to ischemia/reperfusion insult. 1661 21

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

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 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


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