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

The effect of pentobarbital and hypothermia on the development of ischemic brain edema was studied in 23 rhesus monkeys undergoing transorbital middle cerebral artery occlusion. Fifteen additional animals served as unclipped controls. Regional cortical cerebral blood flow (rCBF), arteriovenous oxygen content difference (AVDO2), and regional cortical metabolic rate of O2 (rCMRO2) were measured hourly until sacrifie 11 hours postocclusion, at which time ischemic cerebral edema was measured. In 8 animals no treatment followed the occlusion, and these developed edema. In 7 animals pentobarbial 14 mg/kg was administered intravenously 30 min after occlusion and 7 mg/kg every 2 hours thereafter. In this group ischemic brain edema was negligible. In 8 animals, hypothermia to 25.9 +/- 0.5 degrees C was started 30 min after occlusion and maintained until sacrifice; ischemic brain edema was not significantly altered from untreated-clipped animals. On the basis that both pentobarbital and hypothermia produced similar changes in rCBF, AVDO2, and rCMRO2, but only pentobarbital prevented edema, it is postulated that the mode of action of barbiturates in preventing ischemic brain edema is not entirely related to their known effect on blood flow and metabolism.
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PMID:Ischemic brain edema: comparative effects of barbiturates and hypothermia. 10 24

A total of 113 children with brain edema of infectious and toxic nature were studied. The main clinical syndrome in these conditions was an epileptical status. Among anticonvulsive drugs used seduxen appeared to be the most effective. The use of GABA, gas narcosis and myorelaxants is recommended as well. The rehydration by plasma, low molecular plasma substitutes and glucose-polyion solutions are discussed. The paper contains some information on contraindications for early dehydration and rehydration. Hypoxia is eliminated by providing adequate lung ventilation, oxygenotherapy or hyperbaric oxygenation, by using oxidative enzymes and drugs increasing the resistance of the brain to hypoxia and hypothermia. It is recommended that hormonal therapy should be used. The techniques of urgent measures and their sequence are given.
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PMID:[Principles for intensive therapy of status epilepticus in children]. 49 5

An imbalance of excitatory and inhibitory amino acid-ergic neurotransmission has been suggested to play a role in the pathogenesis of hepatic encephalopathy. For further evaluation of this hypothesis, several parameters of amino acid-ergic neurotransmission were studied in rats with acute liver failure induced by the administration of 300 mg per kg thioacetamide by gavage on two consecutive days. By appropriate supportive care, hypoglycemia, renal failure and hypothermia were avoided. Rats were monitored clinically and neurologically. Hepatic encephalopathy evolved in four distinct, easily recognizable stages. Light and electron microscopic examination of brains of rats with hepatic encephalopathy revealed only a slight swelling of nuclei of neurons and astrocytes without signs of neuronal degeneration or brain edema. In rats with hepatic encephalopathy, the concentrations of GABA, glutamate and taurine were decreased in the cerebral cortex, the hippocampus and the striatum, whereas those of aspartate and glycine were unchanged or increased. GABAA and benzodiazepine receptors were studied as parameters for the postsynaptic GABAA-benzodiazepine receptor complex, glutamic acid decarboxylase as parameter for presynaptic GABA-ergic neurons and stimulation of benzodiazepine binding by GABA as a parameter for a GABA-mediated postsynaptic event. None of these parameters was different in hepatic encephalopathy as compared to controls. Similarly, Ca++/Cl(-)-dependent and -independent glutamate receptors as parameters for glutamatergic neurons were unchanged in rats with hepatic encephalopathy. Thus, in rats with thioacetamide-induced liver failure and hepatic encephalopathy, changes of the concentrations of neurotransmitter amino acids occur in the brain. Other neurochemical parameters, however, failed to identify alterations of GABA-ergic or glutamatergic neurotransmission in hepatic encephalopathy.
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PMID:Hepatic encephalopathy in thioacetamide-induced acute liver failure in rats: characterization of an improved model and study of amino acid-ergic neurotransmission. 256 68

Two nearly drowned, 2 9/12 and 3 6/12 years old boys with profound hypothermia were admitted to our pediatric intensive care unit with all signs of clinical death. Both patients could be rewarmed and oxygenated by extracorporeal circulation. One of them died 36 hours after the accident with severe brain edema. The second one survived without any defect. Rewarming of cold-water nearly-drowned patients by extra-corporeal circulation seems to be a very effective way of treatment.
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PMID:[A drowning accident of long duration with deep hypothermia and rewarming with extracorporeal circulation. A report of 2 patients]. 279 11

Brain edema is a fatal complication of fulminant hepatic failure and its pathogenesis remains unclear. To determine its presence in a model of ischemic hepatic failure, rats were subjected to a portacaval anastomosis followed by hepatic artery ligation. Brain water was measured using the sensitive gravimetric method. Preliminary studies revealed marked hypothermia in devascularized animals kept at room temperature (26.9 degrees +/- 2.8 degrees C). An additional group of devascularized rats was kept in an incubator. As expected for hypothermia, such animals had a lower arterial pressure and heart rate; the duration of encephalopathy was markedly prolonged. Water content of the cortical gray matter was only increased in normothermic devascularized rats: 80.14% +/- 0.31%, normal; 80.06% +/- 0.22%, portacaval shunt only; 80.42% +/- 0.26%, devascularized at room temperature; 81.29% +/- 0.38%, devascularized at controlled temperature (p less than 0.001). Such differences could not be detected using the dry-weight technique in whole cerebral hemispheres. Astrocyte changes in the cortical gray matter were noted in both edematous and nonedematous devascularized groups, coupled with the presence of vesicles containing horseradish peroxidase in the endothelial capillary cell. This suggests that in this model, brain edema may be due to both a cytotoxic mechanism and changes in the permeability of the blood-brain barrier. Future studies with this widely used model will require strict control of temperature to allow interpretation of experimental results. A therapeutic role for hypothermia in the management of brain edema deserves further attention.
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PMID:Effect of body temperature on brain edema and encephalopathy in the rat after hepatic devascularization. 291 49

The resistance of the brain to ischemia depends not only on the duration and severity of flow reduction but also on a number of pre- and post-ischemic metabolic and hemodynamic factors which are able to improve or impair the post-ischemic recovery process. Among pre-ischemic protective factors, the suppression of metabolic rate by drugs or hypothermia, the increase of brain tissue energy reserves and the inhibition of membrane permeability of cations are of particular importance. In contrast, increase of metabolic rate and increase of tissue acidosis induced by hyperglycemia or residual blood flow, reduce the ischemic tolerance of the brain. As long as cell membranes do not depolarize during ischemia, restitution of blood flow results in spontaneous recovery. After depolarization of membranes, however, numerous post-ischemic complications evolve, such as the no-reflow phenomenon, post-ischemic hypoperfusion, post-ischemic brain edema, disturbances of the coupling between metabolic activity and blood flow, etc. These complications require therapeutic intervention in order to prevent irreversible injury. By optimizing this therapy in a model of 1 hour complete normothermic brain ischemia in cat and monkeys, post-ischemic recovery of energy metabolism, protein synthesis, spontaneous and evoked electrocortical activity and even integrative neurological performance were observed. The resistance of the brain to ischemia, in consequence, is much higher than previously assumed and can be substantially improved by adequate post-ischemic treatment.
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PMID:[Experimental principles of tolerance of the brain to ischemia]. 332 66

Retrograde cerebral perfusion has recently been the focus of interest as a simple new technique of brain protection during aortic arch operations. We undertook the experimental protocol of 120 minutes of retrograde cerebral perfusion followed by antegrade reperfusion. Eighteen mongrel dogs were used. Retrograde cerebral perfusion was maintained at a flow rate of 150 to 250 ml/min to keep the perfusion pressure from 15 to 25 mm Hg. Animals were divided into three groups as follows: in group I, no treatment was received during and after retrograde cerebral perfusion; in group II, mannitol (2 gm/kg) was administered before cardiopulmonary bypass was restarted; and in group III, antivasospastic substance (1,2-bis nicotinamido]-propane) was continuously injected during and after retrograde cerebral perfusion (1 mg/kg per minute). Cerebral blood flow decreased during retrograde cerebral perfusion in all three groups. Cerebrovascular resistance showed marked increases 30 and 60 minutes after cardiopulmonary bypass was restarted in group I compared with the values in groups II and III (group I: 3.35 +/- 0.73 and 5.00 +/- 1.57 mm Hg/ml per 100 gm per minute; group II: 1.30 +/- 0.33 and 1.03 +/- 0.17 mm Hg/ml per 100 gm per minute; group III: 1.24 +/- 0.41 and 0.98 +/- 0.24 mm Hg/ml per 100 gm per minute). The oxygen extraction level was reduced by cooling, but it rose to a higher level as a result of significant desaturation of returned blood even in deep hypothermia during retrograde cerebral perfusion. Both cerebral metabolic rate of oxygen and cerebral metabolic rate of glucose remained at low levels during retrograde cerebral perfusion. Ratios of cerebral blood flow to cerebral metabolic rate of oxygen and cerebral blood flow to cerebral metabolic rate of glucose were markedly reduced during retrograde cerebral perfusion. Intracranial pressure showed significant increases 30 and 60 minutes after cardiopulmonary bypass was restarted in group I compared with values in group II or group III (group I: 22.7 +/- 2.8 and 20.6 +/- 5.1 mm Hg; group II: 6.3 +/- 1.8 and 5.3 +/- 1.3 mm Hg; group III: 4.2 +/- 1.7 and 7.7 +/- 2.8 mm Hg). Water content of the brain tissue in group I (77.54% +/- 0.29%) was significantly higher than that in group II (74.71% +/- 0.76%) or group III (74.14% +/- 0.48%). These data suggest that the supply of oxygen or glucose by retrograde cerebral perfusion is not enough to maintain sufficient cerebral metabolism, which may cause brain edema during antegrade reperfusion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pharmacologic intervention for ischemic brain edema after retrograde cerebral perfusion. 858 29

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

Concerning hypothermia treatment, knowledge of time-temperature and of temperature distributions within tumor volumes is essential in order to obtain the maximal therapeutic effect. New techniques are being developed to overcome these difficulties. Two different heat sources, a contact Nd:YAG laser system and an automatically controlled high-frequency current system were investigated on 15 rabbits. Changes of the intracerebral temperature were registered at 4 different distances from the energy source. The intracerebral temperature was increased to 42.5 degrees C at a distance of 5 mm to the heat source and maintained at this level for a period of 60 min. The contact Nd:YAG laser system reached 42.5 degrees C at 3 W of output power. Using higher laser output power, brain tissue herniation (brain edema) through the burrhole was observed. The automatically controlled high-frequency current system reached 42.5 degrees C at 18.75 W of output current. A very small herniation of brain tissue could be observed using higher output current. Both heat sources presented an exponential decrease of the temperature profile depending on the distance. The tissue heat clearance was compensated for by intermittent laser or high-frequency current application. Both systems proved efficient for inducing hyperthermia as needed for antitumoral therapy.
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PMID:Induced hyperthermia in brain tissue in vivo. 797 3

Mild to moderate hypothermia (30-33 degrees C) reduces brain injury after brief (< 2-h) periods of focal ischemia, but its effectiveness in prolonged temporary ischemia is not fully understood. Thirty-two Sprague-Dawley rats anesthetized with 1.5% isoflurane underwent 3 h of middle cerebral artery occlusion under hypothermic (33 degrees C) or normothermic (37 degrees C) conditions followed by 3 or 21 h of reperfusion under normothermic conditions (n = 8/group). Laser-Doppler estimates of cortical blood flow showed that intraischemic hypothermia reduced both postischemic hyperperfusion (p < or = 0.01) and postischemic delayed hypoperfusion (p < or = 0.01). Hypothermia reduced the extent of blood-brain barrier (BBB) disruption as estimated from the extravasation of Evans blue dye at 6 h after the onset of ischemia (p < or = 0.01). Hypothermia also reduced the volume of both brain edema (p < or = 0.01) and neuronal damage (p < or = 0.01) as estimated from Nissl-stained slides at both 6 and 24 h after the onset of ischemia. These results demonstrate that mild intraischemic hypothermia reduces tissue injury after prolonged temporary ischemia, possibly by attenuating postischemic blood flow disturbances and by reducing vasogenic edema resulting from BBB disruption.
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PMID:Mild intraischemic hypothermia reduces postischemic hyperperfusion, delayed postischemic hypoperfusion, blood-brain barrier disruption, brain edema, and neuronal damage volume after temporary focal cerebral ischemia in rats. 801 9


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