Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fructose-1,6-diphosphate has been shown to improve neurologic recovery following resuscitation from cardiac arrest and to restore brain electrical activity during hypoglycemic coma in rabbits. In view of these findings, we determined whether fructose-1,6-diphosphate protects the brain during ischemia-hypoxia. We subjected 16 rabbits to hypotension, hypoxemia, and bilateral common carotid artery occlusion. Five minutes after the onset of isoelectric electroencephalograms, seven randomly selected rabbits received 10% fructose-1,6-diphosphate (350 mg/kg bolus followed by 10 mg/kg/min infusion for 90 minutes) and the remaining nine rabbits (controls) received an equal volume of 1.5% NaCl (3.5 ml/kg bolus followed by 0.1 ml/kg/min infusion for 90 minutes). After isoelectricity lasting 7.86 +/- 0.8 minutes (mean +/- SEM) in the treated group and 6.44 +/- 0.38 minutes in the control group, the rabbits were reinfused with autologous shed blood and reoxygenated and the carotid artery occluders were removed. Treated rabbits recovered electrical activity more rapidly than the controls (p less than 0.005), and all seven treated rabbits survived. Only two controls (22%) survived (p less than 0.001), and they were severely disabled. Histology showed extensive cortical necrosis and focal necrosis in the hippocampi and cerebellum of brains from the two surviving controls. Brains from two treated rabbits exhibited minimal neuronal loss limited to the neocortex, and the brains from the remaining five treated rabbits were normal. This study suggests that fructose-1,6-diphosphate protects the brain from ischemic-hypoxic insults.
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PMID:Prevention of ischemic-hypoxic brain injury and death in rabbits with fructose-1,6-diphosphate. 232 42

Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 20 patients with diabetes mellitus but without disturbance of consciousness and five who recovered from hypoglycaemic coma. CSF lactate was slightly but significantly higher in diabetes mellitus (1.78, SEM 0.04 m mol/l) than that in 15 control subjects (1.40, SEM 0.05 m mol/l). In those who recovered from hypoglycaemic coma, CSF lactate was markedly elevated to 2.45-4.43 m mol/l. CSF glucose concentrations, however, were substantially the same between treated hypoglycaemic and diabetes mellitus groups. These findings indicate that CSF lactate levels increase with glycaemic levels in diabetes mellitus owing to enhanced glucose influx into glycolytic pathway of the brain, and also increases in treated hypoglycaemic coma probably due to mitochondrial dysfunction or damage.
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PMID:Cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma. 292 23

The effect of alpha-adrenergic stimulation by IV adrenaline and propranolol infusion upon basal insulin and growth hormone secretion was studied in six chronic alcoholics during alcohol withdrawal, two alcoholics recently admitted to hospital with alcohol-induced hypoglycaemia and twelve healthy subjects. In all healthy subjects a decline in basal insulin (mean +/- SEM decremental area 166 +/- 19) and an increase in growth hormone (mean +/- SEM incremental area 527 +/- 164) was found. In the two alcoholics admitted to hospital with alcohol hypoglycaemia, no consistent change occurred in basal insulin and basal growth hormone concentrations during alpha-adrenergic stimulation. In the other alcoholics a decrease in basal insulin (mean +/- SEM decremental area 91 +/- 13.5) was found, but this decrease was significantly less (p less than 0.05) than in healthy subjects. Growth hormone did not change significantly in these alcoholics. It is concluded that disturbances in the alpha-adrenergic modulation of basal insulin and growth hormone secretions are common in alcoholics in a withdrawal state. The implication of this finding for the occurrence of alcohol-induced hypoglycaemic coma is discussed.
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PMID:Disturbed alpha-adrenergic modulation of insulin and growth hormone secretion in chronic alcoholics. 698 94