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

To determine the effect of hypothermia on superoxide injury after cerebral contusion, the induction of Cu,Zn-superoxide dismutase was examined 6 h after contusion in rats using Northern blotting. Cu,Zn-superoxide dismutase gene expression increased at the periphery of the contusion, which may indicate the severity of the superoxide stimulus. This increase was preserved after contusion under hypothermia, which may show that superoxide injury is still severe although brain edema is decreased.
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PMID:Induction of Cu,Zn-superoxide dismutase after cortical contusion injury during hypothermia. 782 Jun 38

This review describes recently recognized pathophysiologic mechanisms responsible for brain damage during ischemia and reperfusion and new therapeutic concepts developed on a rational basis. Mediators of secondary damage include excitotoxins such as glutamate, acidosis, free radicals, and the disturbance of the microcirculation seen in the early phase of recirculation. Glutamate is an excitatory neurotransmitter, which may turn neurotoxic when the energy supply is limited. Tissue acidosis down to pH 6.0 develops regularly in cerebral ischemia and disturbs a variety of neuronal functions, causing glial swelling and neuronal death. Free radicals attack brain lipids, the cell membrane and myelin in particular, and are produced during reperfusion. Disturbance of the microcirculation aggravates ischemic damage. Suggested therapeutic approaches include glutamate antagonists, normalization of tissue acidosis, and use of new diuretics to reduce glial swelling, protection of the brain by free radical scavengers such as 21-aminosteroids, tocopherol, allopurinol or superoxide dismutase, and hypothermia. Ways of ensuring fast reperfusion, including hypervolemic hemodilution and blood pressure stabilization, are suggested for resuscitation or early stroke. All data available indicate that the combination of several successful therapeutic principles will significantly improve outcome.
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PMID:[Neuroprotection. Models and basic principles]. 784 Apr 11

The metabolic effects of combined antegrade/retrograde and antegrade cardioplegia on myocardial protection were evaluated and compared in 30 patients who underwent myocardial revascularization. All patients had three-vessel coronary artery disease, and the revascularization was done with exclusive use of arterial grafts (internal mammary artery, gastroepiploic artery). Myocardial protection consisted of oxygenated crystalloid cardioplegia, topical slushed ice, and moderate systemic hypothermia (34 degrees C). The patients were randomly separated into two groups: group A (n = 15), who received antegrade cardioplegia, and group A/R (n = 15), who received combined antegrade/retrograde cardioplegia. There was no significant difference between the two groups concerning preoperative and intraoperative data. After the first dose of cardioplegia, right ventricular temperature was significantly lower in group A/R (15 +/- 2 degrees versus 19 +/- 5 degrees C; p < 0.05), and there was no significant difference between the two groups in left ventricular temperature. Coronary sinus blood samples were obtained before bypass and 5, 10, and 15 minutes after reperfusion; there was no difference between the two groups concerning lactates, superoxide dismutase, and glutathione peroxidase. After reperfusion, malondialdehyde levels increased significantly in group A and there was no change in group A/R, with a significant difference between the two groups (at 10 minutes after reperfusion, 0.80 +/- 0.20 versus 0.53 +/- 0.16 mumol/L; p < 0.05). Right and left ventricular myocardial biopsies were performed before bypass and 15 minutes after reperfusion; there was no significant difference between the two groups concerning adenosine triphosphate and creatine phosphate myocardial concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antegrade/retrograde cardioplegia in arterial bypass grafting: metabolic randomized clinical trial. 784 66

The effects of disulfiram (DS) and its major metabolite, diethyldithiocarbamate (DEDC), on the survival time under normobaric and hypobaric hypoxia were examined in mice. At an ambient temperature of 24 degrees C, DS at 0.5-3.0 mmol/kg (i.p.) caused a marked dose-dependent prolongation of the survival time in mice subjected to both types of hypoxia. DEDC also prolonged the survival time, but the effect was less at its higher doses with decreased brain superoxide dismutase. The maximum effects of DS and DEDC were found at 3 hr and 1 hr after injection, respectively. Of the metabolites of DEDC, the copper complex with DEDC caused a significant effect, whereas neither diethylamine nor carbon disulfide did. Furthermore, DS, DEDC and copper complex caused marked hypothermia, and the time course changes of hypothermia by DS and DEDC closely paralleled those of the degree of anti-hypoxic effects, respectively. At an ambient temperature of 36 degrees C, in which the body temperature was maintained near the normal level, both DS and DEDC still exhibited a weak anti-hypoxic effect. These results suggest that DEDC itself, formed as a metabolite of DS, and partly the copper complex produced the anti-hypoxic effect, which could not be explained by concomitant hypothermia alone.
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PMID:Protection by disulfiram and diethyldithiocarbamate against hypoxia-induced lethality in mice. 810 22

After prolonged ischemia, reperfusion of the myocardium with oxygenated blood results in high levels of superoxide anions. Several mechanisms for superoxide anion generation have been proposed, including increased xanthine oxidase activity, neutrophil activation, and arachidonate cascade activation. Superoxide anion accumulation may cause enzyme inactivation and lipid peroxidation in the sarcolemma with resultant intracellular calcium accumulation and excitation-contraction uncoupling. A review of a number of animal studies has shown that free radical scavengers such as superoxide dismutase and catalase can preserve myocardial function and metabolism during transplantation. In addition, other data indicate a role for inhibitors of free radical generation (i.e., allopurinol or oxypurinol), iron chelators (i.e., deferoxamine), or metabolic substrates such as L-glutamate in the inhibition of free radical myocardial injury. In addition, glutathione has been demonstrated to produce faster recovery of ventricular function in hypothermia preserved and reperfused rat hearts, presumably by inhibiting free radical production. Confirmatory data for human cardiac transplantation is not yet available.
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PMID:Oxygen free radicals in cardiac transplantation. 838

Total antioxidative activity, activity of water soluble fraction of antioxidative system, superoxide dismutase and catalase activities in brain, liver, myocard, skeletal muscle, kidney and serum at hypothermia 30 degrees C, 20 degrees C and self-warming from 20 degrees C to 37 degrees C were studied. Activity of antioxidative system is sustained at high level, except superoxide dismutase. The latter is activated significantly at 30 degrees C hypothermia prolonged up to 3 h. Dalargin injection 30 min before onset of cooling stabilizes the erythrocyte membrane without enhancement of antioxidative activity in majority of investigated tissues.
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PMID:[Antioxidant system in rat tissues in hypothermia and dalargin introduction]. 1218 26

This experiment was carried out to determine the effect of short-term hypothermia on blood malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glucose-6-phosphate dehydrogenase (G-6-PD) concentrations in rats. Twenty Sprague-Dawley rats were used weighing 180-200 g and on average 3.5 months old. They were randomly divided into two experimental groups: control (without cooling) and hypothermic (with cooling). The rats of the hypothermic group were cooled by immersion into cold water (10-12 degrees C), and the control rats were immersed into water of body temperature (37 degrees C) up to the neck without using any anaesthetic or tranquilizer for 3 min Rectal body temperatures of both groups were measured and blood samples to analyse MDA, GSH, SOD, GSH, GSH-Px and G-6-PD were collected immediately after the treatment. It was found that the MDA level was higher and the GSH and G-6-PD levels were lower in the hypothermic group than those in the controls. There was no difference between the control or hypothermic group regarding SOD or GSH-Px levels. It is concluded that acute hypothermia increased the lipid peroxidation and decreased the GSH and G-6-PD levels in rats.
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PMID:Effect of short-term hypothermia on lipid peroxidation and antioxidant enzyme activity in rats. 1222 69

Following a transient ischemic insult there is a marked increase in free radical (FR) production within the first 10-15 min of reperfusion and again at the peak of the inflammatory process. Hypothermia decreases lipid peroxidation following global ischemia, raising the possibility that it may act by reducing FR production early on and by maintaining or increasing endogenous antioxidant systems. By means of FR fluorescence, Western blot, immunohistochemistry, and enzymatic assay, we studied the effects of mild hypothermia on superoxide (O(-*)(2)) anion production, superoxide dismutase SOD expression, and activity following focal cerebral ischemia in rats. Mild hypothermia significantly reduced O(-*)(2) generation in the ischemic penumbra and corresponding contralateral region, but did not alter the bilateral SOD expression. SOD enzymatic activity in the ischemic core was slightly reduced in hypothermia-treated animals compared with normothermic controls. Our results suggest that the neuroprotective effect of mild hypothermia may be due, in part, to a reduction in neuronal and endothelial O(-*)(2) production during early reperfusion.
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PMID:Effects of mild hypothermia on superoxide anion production, superoxide dismutase expression, and activity following transient focal cerebral ischemia. 1246 May 44

This study was designed to investigate the influence of intraischemic liver temperature on oxidative stress during postischemic normothermic reperfusion. In C57BL/6 mice, partial hepatic ischemia was induced for 90 min and intraischemic organ temperature adjusted to 4 degrees C, 15 degrees C, 26 degrees C, 32 degrees C, and 37 degrees C. As detected by electron spin-resonance spectroscopy, plasma/blood concentrations of hydroxyl and ascorbyl radicals were significantly increased in all groups after ischemia/reperfusion independent of the intraischemic temperature. In tissue, however, postischemic lipid peroxidation was attenuated after organ cooling down to 32 degrees C-26 degrees C and not detectable after ischemia at 15 degrees C-4 degrees C. mRNA expression of superoxide dismutase-1 and heme oxygenase-1, measured during reperfusion, was significantly elevated in the group at 37 degrees C as compared to the hypothermic groups at 4 degrees C-32 degrees C. The reduction of radical generation was associated with a prevention of adenosine monophosphate hydrolysis during ischemia in the hypothermic groups. In conclusion, ischemia-reperfusion-induced oxidative stress in the liver tissue is non-linearly-dependent on intraischemic temperature, whereas the plasma/blood concentration of radicals is not affected by organ cooling. Oxidative stress is reduced through mild hypothermia at 32 degrees C-26 degrees C and inhibited completely at 15 degrees C. Reduction of initial intracellular radical generation and prevention of secondary oxidant-induced tissue injury are possible mechanisms of this protection.
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PMID:Impact of intraischemic temperature on oxidative stress during hepatic reperfusion. 1455 54

Hypothermic perfusion of the heart decreases oxidative phosphorylation and increases NADH. Because O(2) and substrates remain available and respiration (electron transport system, ETS) may become impaired, we examined whether reactive oxygen species (ROS) exist in excess during hypothermic perfusion. A fiberoptic probe was placed on the left ventricular free wall of isolated guinea pig hearts to record intracellular ROS, principally superoxide (O(2)(-).), and an extracellular reactive nitrogen reactant, principally peroxynitrite (ONOO(-)), a product of nitric oxide (NO.) + O(2)(-). Hearts were loaded with dihydroethidium (DHE), which is oxidized by O(2)(-). to ethidium, or were perfused with l-tyrosine, which is oxidized by ONOO(-) to dityrosine (diTyr). Shifts in fluorescence were measured online; diTyr fluorescence was also measured in the coronary effluent. To validate our methods and to examine the source and identity of ROS during cold perfusion, we examined the effects of a superoxide dismutase mimetic Mn(III) tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME), and several agents that impair electron flux through the ETS: menadione, sodium azide (NaN(3)), and 2,3-butanedione monoxime (BDM). Drugs were given before or during cold perfusion. ROS measured by DHE was inversely proportional to the temperature between 37 degrees C and 3 degrees C. We found that perfusion at 17 degrees C increased DHE threefold versus perfusion at 37 degrees C; this was reversed by MnTBAP, but not by l-NAME or BDM, and was markedly augmented by menadione and NaN(3). Perfusion at 17 degrees C also increased myocardial and effluent diTyr (ONOO(-)) by twofold. l-NAME, MnTBAP, or BDM perfused at 37 degrees C before cooling or during 17 degrees C perfusion abrogated, whereas menadione and NaN(3) again enhanced the cold-induced increase in ROS. Our results suggest that hypothermia moderately enhances O(2)(-). generation by mitochondria, whereas O(2)(-). dismutation is markedly slowed. Also, the increase in O(2)(-). during hypothermia reacts with available NO. to produce ONOO(-), and drug-induced O(2)(-). dismutation eliminates the hypothermia-induced increase in O(2)(-).
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PMID:Hypothermia augments reactive oxygen species detected in the guinea pig isolated perfused heart. 1464 63


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