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Side 1 fra 64 resultater
Adaptation to chronic hypoxia during diet-induced ketosis.
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It is recognized that brain oxygen deprivation results in increased glycolysis and lactate accumulation. Moreover, glucose metabolism is altered during starvation or diet, resulting in increased plasma ketones (acetoacetate + beta-hydroxybutyrate; BHB). We investigated glucose and lactate adaptation
Butanediol induced ketosis increases tolerance to hypoxia in the mouse.
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In previous studies from our laboratory a positive correlation between elevated blood ketone levels and the survival time (ST) during hypoxia (4-5% oxygen) was observed in fasted and alloxan diabetic mice. To test the hypothesis that ketosis was somehow increasing the tolerance of mice to hypoxia,
Relation of colloid osmotic pressure to arterial hypoxemia and cerebral edema during crystalloid volume loading of patients with diabetic ketoacidosis.
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The effect of crystalloid volume loading on serum colloid osmotic pressure, arterial oxygen (Po2), alveolar-arterial oxygen gradient (A-aDo2), and cerebral lateral ventricle dimensions was prospectively studied in 18 patients with diabetic ketoacidosis. Serial measurements showed concomitant
Ketosis may promote brain macroautophagy by activating Sirt1 and hypoxia-inducible factor-1.
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Ketogenic diets are markedly neuroprotective, but the basis of this effect is still poorly understood. Recent studies demonstrate that ketone bodies increase neuronal levels of hypoxia-inducible factor-1α (HIF-1α), possibly owing to succinate-mediated inhibition of prolyl hydroxylase activity.
[Ketoacidosis, hyperoxia and hypoxia].
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Effect of phosphate on oxygen-hemoglobin affinity, diphosphoglycerate and blood gases during recovery from diabetic ketoacidosis.
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The effects of intravenous phosphate administration on the hemoglobin-oxygen affinity, the 2,3 diphosphoglycerate level and blood gases were investigated in twenty severe diabetic patients with ketoacidosis in the intensive care unit. Ten received phosphate (mean total amount for each patient = 300
Noncardiogenic pulmonary edema complicating diabetic ketoacidosis.
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OBJECTIVE
To alert physicians to the possibility of pulmonary edema as a complication of diabetic ketoacidosis.
METHODS
We report a case of adult respiratory distress syndrome after resuscitative efforts to compensate the first episode of diabetic ketoacidosis in a previously healthy young
Diabetic ketoacidosis (DKA): treatment guidelines.
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Diabetic ketoacidosis (DKA), resulting from severe insulin deficiency, accounts for most hospitalization and is the most common cause of death, mostly due to cerebral edema, in pediatric diabetes. This article provides guidelines on management to restore perfusion, stop ongoing ketogenesis, correct
Alcoholic ketoacidosis presenting with extreme hypoglycemia.
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A 66-year-old man with a history of chronic alcoholism presented with Kussmaul respirations following several days of fasting accompanied by vomiting, in the presence of continued ethanol intake. He was subsequently found to have a serum glucose level of <20 mg/dL and an anion gap of 36. Despite his
Ketoacidosis.
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The pathogenesis and treatment of diabetic ketoacidosis has been discussed. Insulin deficiency leads to increased rates of hepatic ketogenesis and gluconeogenesis with resultant hyperglycemia and ketonemia. Treatment consists of insulin and fluid replacement. Insulin therapy is titrated against the
Haemodynamic and metabolic effects in diabetic ketoacidosis in rats of treatment with sodium bicarbonate or a mixture of sodium bicarbonate and sodium carbonate.
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To examine factors determining the haemodynamic and metabolic responses to treatment of diabetic ketoacidosis with alkali, groups of anaesthetised and ventilated rats with either diabetic ketoacidosis (mean arterial pH 6.86-6.96, mean arterial blood pressure 63-67 mm Hg) or hypovolaemic shock due to
Six cases of sudden cardiac arrest in alcoholic ketoacidosis.
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We report herein 6 cases of sudden cardiac arrest in alcoholic ketoacidosis (AKA). All cases displayed evidence of prolonged excessive alcohol consumption and elevated beta-hydroxybutyric acid levels and exhibited pulseless electrical activity (PEA) upon collapse. Severe metabolic acidosis was also
Chronic in vitro ketosis is neuroprotective but not anti-convulsant.
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The ketogenic diet (KD), used successfully to treat a variety of epilepsy syndromes in humans and to attenuate seizures in different animal models, also provides powerful neuroprotection in various CNS injury models. Yet, a direct role for ketone bodies in limiting seizure and neuronal damage
Brain tissue oxygenation-guided management of diabetic ketoacidosis induced cerebral edema*.
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OBJECTIVE
Type 1 diabetes mellitus is the most common chronic disease of childhood. Diabetic ketoacidosis is a well-known complication of diabetes mellitus and can be associated with devastating cerebral edema resulting in severe long-term neurologic disability. Despite the significant morbidity and
Lactic acidosis, ketoacidosis, and energy turnover: "figure" you made the correct diagnosis only when you have "counted" on it--quantitative analysis based on principles of metabolism.
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Three cases are presented to illustrate that quantitative analysis based on physiologic principles can help resolve certain controversies in clinical medicine. For example, in case 1, a patient with severe hypoxia, the rate of production of lactic acid is so high that only restoration of delivery of
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