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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 forced cooling was studied as applied to the contents of ammonia, glutamine, glutaminic, asparaginic and alpha-amino butyric acids in the brain of sousliks woken-from hibernation. The cooling of the woken sousliks to the body temperature of 30, 20 and 25 degrees C decreased to some extent the ammonia content in the brain. A deeper hypothermia (10 degrees C) causes its 60,4% decrease as compared to the ammonia amount in woken animals. The cooling of the animals to 30, 25, 20 and 10 degrees C considerably decreases the contents of glutamine, glutaminic acid and GABA in the brain tissue.
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PMID:[Effect of hypothermia on the ammonia-glutamine-glutamic acid system in ground squirrels after hibernation]. 54 34

The content of ammonia, glutamine, dicarboxylic amino acids and GABA was studied in the brain under 1, 2, 4-fold separate and simultaneous effect of hypothermia (19-20 C) and hyperoxia (3 atm.). A two-fold hypothermia of rats is accompanied by a greater increase of ammonia in the brain than a three-fold one. The content of glutamine under two-fold cooling is unchanged and under three-fold cooling it is twice as low as compared to its content in the brain of the control rats. The content of glutamic acid decreased after two-fold hypothermia is almost unchanged by the third seance of hypothermia. The repeated actions of hyperoxia also cause a considerable increase in the ammonia content but the dynamics of changes in the content of the nitrogenous metabolic products is contary to that in animals subjected to repeated seances of hypothermia. A simultaneous combined action of hypothermia and hyperoxia produces no additive effect on the system ammonia-glutaminic acid.
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PMID:[Effect of hypothermia and hyperoxia on the ammonia-glutamic acid system in the brain of rats]. 96 Feb 39

A purine degradation study, thermography and near infrared spectroscopy of the extremities were performed on 2 young males with Fabry disease and 2 healthy controls. Two-minute semi-ischemic forearm exercise caused a distinct increase in lactate in all subjects, but venous hypoxanthine and ammonia were greatly increased only in the Fabry patients, suggesting a relatively hypoxic state of the extremities. Limb thermograms of the patients revealed glove and stocking type disturbance at rest. Poor recovery of the skin temperature of the hands and forearms after exercise was observed in the patients, but the sharp increase in oxygenated hemoglobin after total ischemia was found to be normal or near infrared spectroscopy. Neurotropin showed an analgesic effect, i.e. a strong and selective heat-productive action on the painful lesions, and suppressed the hypoxanthine level after exercise in 1 patient. Although the pathophysiology of the pain in Fabry disease has not been clearly elucidated, a relatively hypoxic state with peripheral hypothermia might play an important role in triggering of a painful attack or chronic burning paresthesia.
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PMID:Relative hypoxia of the extremities in Fabry disease. 145 89

L-Methionine sulfoximine (MSO) intraperitoneally injected at subconvulsive and convulsive doses induced a rectal hypothermia in the restrained rat maintained at an ambient temperature of 23 degrees C; this hypothermia developed during the preconvulsive period, and it was not suppressed by simultaneous injection of L-methionine which antagonized the behavioral effects of ammonia elevated contents in the central nervous system. The development of rectal hypothermia was faster when the injection of MSO was made into the lateral cerebral ventricle and particularly into the third ventricle. MSO-induced hypothermia seemed to be a poikilothermia-like state in the cold environment with retention of a normal regulation in the heat environment. Infusion of MSO into the anterior hypothalamic/preoptic (AH/PO) area induced a rapid rectal hyperthermia, but infused into the mammillary region MSO had no effect on rectal temperature. It is suggested that rectal hypothermia induced by MSO may be directly related to a depressive effect on glucose oxidative metabolism in cell structures, maybe astroglial cells, located in the vicinity of the ventricle or the capillary walls.
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PMID:Study of the hypothermia induced by methionine sulfoximine in the rat. 325 71

The changes of hepatic energy metabolism during normothermic and hypothermic ischemia were investigated using rats with portajugular shunt. In addition, some blood parameters were estimated as to whether they could reflect the changes in hepatic energy level (represented by energy charge, EC). In this study, [pyruvate]/[lactate] x 1/K(K = 1.11 x 10(-4)) and [2-oxoglutarate] x [ammonia]/[glutamate] x 1/K(K = 3.87 x 10(-3) mmole) were used as indexes of cytosolic and mitochondrial redox state, respectively. The following results were obtained. 1) Though hepatic EC recovered after 30 minutes of ischemia, it didn't recover after 60 minutes of normothermic ischemia. 2) The recovery of the hepatic EC even after 60 minutes of ischemia was observed in hypothermic condition. 3) Mitochondrial redox state changed like hepatic EC, however, some dissociations were observed between cytosolic redox state and hepatic EC in hypothermic ischemia. 4) The changes of mitochondrial and cytosolic redox state were reflected in those of arterial ammonia and lactate level, respectively. As a result, hypothermia can prolong the safe ischemic period due to its stabilizing effect on mitochondrial redox state. In addition, the changes of the hepatic EC are reflected in those of arterial ammonia and lactate level. In hypothermic condition, however, ammonia seemed a better parameter than lactate in assessing hepatic EC.
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PMID:[Study of the ischemic effect on the hepatic energy metabolism]. 341 4

The May 1986 Mt. Hood climbing disaster presented Portland area hospitals the opportunity to initiate a trial of extracorporeal rewarming using cardiopulmonary bypass in ten severely hypothermic patients (two survivors). The data from this experience as well as others previously reported can yield prognostic indicators of survival in cases of accidental hypothermia. These are demonstrated to include: the presence of underlying medical illness, duration of cold exposure, initial core temperature, mental status, the presence of spontaneous respirations, presenting cardiac rate and rhythm, and arterial oxygen tension. Profound hyperkalemia and markedly elevated serum ammonia levels indicate cell lysis; significant hypofibrinogenemia suggests intravascular thrombosis and each laboratory marker predicts a dire outcome. The treatment of choice for severe accidental hypothermia is felt to be rapid core rewarming on cardiopulmonary bypass.
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PMID:Prognostic factors in severe accidental hypothermia: experience from the Mt. Hood tragedy. 366 5

1. Hypothermia in midwinter revealed a marked increase in GABA and glutamine due to active decarboxylation and amidation of glutamic acid. This influenced the glutamate-aspartate pathway and resulted in a significant drop in levels of both acids. 2. Elevated levels of GABA and taurine during hibernation pointed to their role as inhibitory neurotransmitters. 3. Amidation of glutamate induced a noticeable drop in ammonia concurring with increased urea and low uric acid levels. 4. Hypothermia in summer revealed a significant role of temperature as a determining factor in the hibernation cycle. Arousal was a repeated, though reversed, phenomenon in this cycle.
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PMID:Hibernation hypothermia and metabolism in hedgehogs--changes in free amino acids and related compounds. 612 98

Cardiac muscle biopsy specimens were obtained from 33 patients undergoing open-heart surgery under K+-induced ischemic arrest in hypothermia (cardioplegic right atrial and right ventricular muscles) or under hypothermic ischemic arrest without K+-cardioplegia (noncardioplegia right atrial muscle), and sequential patterns of changes in the myocardial metabolism were studied by standard enzymatic techniques. The concentrations of the high energy phosphates were not only adequately preserved but actually exceeded the initial values in the cardioplegic muscles during the 40-min period of the ischemic arrest. In addition, elevated ammonia levels were neutralized by these muscles, and excessive variations in the myocardial intermediary metabolism were prevented. The levels of ATP were also adequately preserved by the noncardioplegic right atrial muscle during the 12-min period of ischemic arrest. But this protection was achieved at the expense of a 20% reduction in the myocardial creatine phosphate levels and other associated severe intracellular metabolic derangements. Changes in the myocardial intermediary metabolism, at the end of 12 min of ischemic arrest and at the end of 40 min of K+-cardioplegic arrest, were almost identical. The results of these studies suggest that, in contrast to the hypothermic arrest alone, K+-cardioplegia in hypothermia offers a superior myocardial metabolic preservation over an extended period of time.
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PMID:Effect of potassium-induced cardioplegia in hypothermia on myocardial energy, ammonium, and intermediary metabolism in man. 742 61

Keeping a patient with fulminant hepatic failure (FHF) alive until a donor liver is available for transplantation can be a problem. We describe an 18-year-old woman with paracetamol-induced FHF, who was treated by total hepatectomy, hypothermia, plasma exchange, and extracorporeal liver support. The patient was anhepatic for 14 h. The liver-support system consisted of plasma separation and perfusion through a charcoal filter and a hollow-fibre module seeded with matrix-attached porcine hepatocytes. With artificial liver treatment there was reversal of severe neurological dysfunction, normalisation of intracranial pressure, and decreased serum ammonia. The patient underwent emergency transplantation with an ABO-incompatible liver, followed by transplantation with a compatible organ eight days later. The patient has fully recovered and is neurologically intact.
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PMID:Control of cerebral oedema by total hepatectomy and extracorporeal liver support in fulminant hepatic failure. 810 68

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26


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