Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma glucose and glucagon concentrations were measured in edible dormice during the bout of hibernation, arousal and active periods. During lethargy, plasma glucose and glucagon were low, compared to active values and did not fluctuate throughout the phase. During rewarming, plasma glucose regularly increased from 17 degrees to 37 degrees C while plasma glucagon rose after the 17 degrees C stage and reached the higher values at 26 degrees C, then slightly decreased at 37 degrees C. During arousal, plasma levels of free amino acids progressively increased. The effect of temperature and secretagogue (glucose and arginine) on glucagon secretion was studied using perfused pancreas from hibernating edible dormouse. In vitro rewarming of pancreas induced an increase in glucagon secretion. Glucagon secretion was regulated by glucose (inhibitory effect) and by arginine (stimulating effect) up to 25 degrees C. The effect of temperature and glucagon on oxygen uptake of hibernating edible dormouse brown fat was studied using an in vitro technique. Rewarming strongly increased oxygen consumption from 10 to 37 degrees C. Glucagon enhanced oxygen consumption up to 20 degrees C.
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PMID:Glucagon secretion in the hibernating edible dormouse (Glis glis). 286 68

Seven English Springer Spaniels (6 adult males and 1 female) with chronic hemolysis and sporadic intravascular hemolytic crises were determined to have a deficiency in erythrocyte phosphofructokinase (PFK) activity, a key regulatory enzyme of anaerobic glycolysis. Intermittent severe pigmenturia concomitant with weakness, lethargy, and anorexia were the major clinical signs and commonly were related to exercise or other stressful situations that caused panting or barking (hyperventilation). Pale or icteric mucous membranes, fever, mild hepatosplenomegaly, and muscle wasting sometimes were evident. Results of routine laboratory testing indicated a persistent marked bilirubinuria and reticulocytosis with normal PCV, to severe anemia and intermittent hemoglobinuria and hyperkalemia. Erythrocyte PFK activities were severely reduced to 8% to 22% of values for control dogs. The block of glycolysis at the PFK step caused a markedly diminished erythrocyte 2,3-diphosphoglycerate content, resulting in an increased hemoglobin-oxygen affinity and compensatory accelerated erythrocyte production. Phosphofructokinase-deficient erythrocytes had increased alkaline fragility in vitro and in vivo. Hemolytic crises were induced in vivo by hyperventilation that caused transient, mild alkalemia. Studies of family members of a PFK-deficient dog suggested an autosomal recessive mode of inheritance. Carrier dogs with half-normal erythrocyte PFK activities appeared clinically normal.
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PMID:Hemolysis caused by phosphofructokinase deficiency in English springer spaniels: seven cases (1983-1986). 295 37

Myonecrosis is an unusual sequelae to carbon monoxide poisoning with only 16 cases having been reported in the English-language literature. At the University of Illinois Hospital, we encountered a 25-year-old fire academy student who presented to our Emergency Department with a carboxyhemoglobin level of 16% following a training exercise in a smoke-filled room. The patient was not wearing a self-contained breathing apparatus and his duration of exposure was 7-8 min, by which time he had blacked out for about 1 min. Upon arrival, the patient was lethargic, with a moderate inhalation burn. The patient was treated with hyperbaric oxygen at 2 1/2 ATA. Following 90 min of hyperbaric oxygen, slight flexor compartment weakness, along with tenderness of the proximal lower extremities was noted. CPK was elevated to 65,998 (100% mm) with urine dipstick being positive for blood and only occasional rbc's seen in the urine sediment. The patient did well with forced diuresis and alkalinization of the urine. No oliguria was noted and the CPK fell to 893 five days later. This is the only case in the English-language literature who developed myonecrosis from carbon monoxide, despite hyperbaric oxygen treatment. We believe that this case demonstrates that hyperbaric oxygen cannot prevent the development of myonecrosis induced by carbon monoxide.
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PMID:Myonecrosis in carbon monoxide poisoning. 335 79

Measurement of regional cerebral blood flow (rCBF) using the i.v. 133Xe technique was carried out during resection of a right temporooccipital arteriovenous malformation (AVM) with ipsilateral middle and posterior cerebral arterial supply. Intraoperatively, a rCBF detector was in place over the right frontotemporal area, about 5 to 6 cm from the border of the AVM. Anesthesia was 0.75% isoflurane in oxygen and nitrous oxide. After dural exposure, the rCBF was 27 ml/100 g/min at a pCO2 of 29 mm Hg and a mean arterial pressure (MAP) of 90 mm Hg. The pCO2 was then elevated to 40 mm Hg, and the rCBF was increased to 55 ml/100 g/min at a MAP of 83 mm Hg. After AVM removal, the rCBF rose to 50 ml/100 g/min at a pCO2 of 27 mm Hg and a MAP of 75 mm Hg. The pCO2 was elevated to 33 mm Hg and the rCBF increased to 86 ml/100 g/min at a MAP of 97 mm Hg. During skin closure, the rCBF was 94 ml/100 g/min at a pCO2 of 26 mm Hg and a MAP of 97 mm Hg. The patient was neurologically normal postoperatively except for a mild, new visual field defect. After 2 to 3 days, the patient gradually developed lethargy, confusion, and nausea with relatively normal blood pressure. An angiogram revealed residual enlargement of the posterior cerebral artery feeding vessel. Computed tomography showed edema extending from the area of AVM resection as far as the frontal region, producing a significant midline shift anteriorly. Intraoperative rCBF monitoring revealed significant hyperperfusion after AVM resection, which was associated with signs and symptoms of the normal perfusion pressure breakthrough syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:133Xe blood flow monitoring during arteriovenous malformation resection: a case of intraoperative hyperperfusion with subsequent brain swelling. 337 91

Bilirubin inhibits in vitro oxidative phosphorylation and glycolysis. This study investigated the in vivo effect of bilirubin on cerebral oxygen, glucose, and lactate uptake in newborn piglets. Seventeen 2- to 4-day-old piglets were divided into three groups and examined as follows: group 1 = control (C); group 2 = control with sulfisoxazole; and group 3 = experimental, given bilirubin with sulfisoxazole. In the experimental group, bilirubin was infused for 4 h. The cerebral bilirubin content in the bilirubin-infused group was 11.0 +/- 1.4 nmol/g of cerebral cortex (mean +/- SEM), consistent with levels found in infants with kernicterus. However, this level of brain bilirubin had no major, acute effects on cerebral uptake of oxygen, glucose, or lactate despite producing lethargy and ataxia which were consistent with bilirubin intoxication. This suggests that mitochondrial changes may not be involved in vivo in acute bilirubin encephalopathy.
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PMID:The in vivo effect of bilirubin and sulfisoxazole on cerebral oxygen, glucose, and lactate metabolism in newborn piglets. 365 36

To determine whether treatment with hyperbaric oxygen (HBO) or dimethyl sulfoxide (DMSO) could mitigate the fatal effects of cerebral ischemia, we anesthetized 68 gerbils with ketamine, ligated the right carotid artery (CA), and placed a snare occluder around the left CA. After 48 hours, 30 gerbils that were neurologically normal or had suffered only mild deficits were subjected to left CA occlusion without anesthesia for periods of 2 to 60 minutes. The onset of circling, posturing, falling, and lethargy began immediately; seizures and coma ensued 4 to 5 minutes later and persisted until release of the left CA occluder. All gerbils recovered after 2-minute staged bilateral CA occlusions. The mortality rate was 33% after both 5- and 10-minute occlusions and 100% after 20- and 60-minute bilateral occlusions. Twelve gerbils were placed in an HBO chamber (100% oxygen at 1.5 atmospheres) for 15 minutes during 20-minute bilateral occlusion; only 2 died (16% mortality rate). Thus, HBO therapy conferred significant protection against death from untreated ischemia (P less than 0.001). Histological examination showed that the extent of patchy bilateral ischemic neuronal damage was much less in surviving gerbils that received HBO therapy than in those that died after 20-minute occlusions. Fourteen gerbils were treated with DMSO, 2.5 g/kg intraperitoneally, during 5- or 10-minute bilateral CA occlusion; 12 died (86% mortality rate). Thus, DMSO provided no protection against fatal cerebral infarction; in fact, the results in the 10-minute reperfusion group suggest that DMSO may have a deleterious effect.
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PMID:Effect of hyperbaric oxygen therapy or dimethyl sulfoxide on cerebral ischemia in unanesthetized gerbils. 371 99

We report a series of 28 pediatric carbon monoxide exposures. Sixteen patients (57%) were judged to have potentially toxic carboxyhemeglobin (COHb) levels (greater than 15%). In this group the range of COHb blood levels was 16.7% to 44.0% (mean = 26.5%). An unusually high incidence of syncope (56.3%, 9/16) and lethargy (68.7%, 11/16) was observed. Every patient with a COHb level greater than or equal to 24% experienced syncope; a marked departure from published adult values. Lethargy was reported at a mean COHb concentration of 25.9%. All patients with levels over 25% COHb, neurologic findings, acidosis, or syncope were considered candidates for hyperbaric oxygen therapy (HBOT). No morbidity from HBOT was encountered. Eighty-nine percent (25/28) of the patients are reportedly doing well, with no late sequelae identified. Delayed neurologic sequelae in three patients include chronic headaches, memory difficulties, or decline in school performance.
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PMID:Pediatric carbon monoxide toxicity. 383 44

Methylene chloride is a chlorinated hydrocarbon used widely in home and industry. Its intentional abuse has not been reported previously. We describe the case of a 14-year-old boy who presented with lethargy, nausea, and chills six hours after the intentional inhalation of a household product containing methylene chloride. The patient's elevated carboxyhemoglobin level responded well to 100% oxygen therapy. The pathophysiology and treatment of methylene chloride are discussed.
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PMID:Methylene chloride inhalation: an unusual form of drug abuse. 402 92

We report here on a case of primary alveolar hypoventilation in a 9 yr old child. From the age of 8 years, the patient has suffered from episodes of bronchopneumonia associated with severe respiratory insufficiency and lethargy. After recovery, cyanosis developed during the night and, later on, during the day. On two occasions, serious respiratory depression followed ketamine sedation for cardiac catheterization and total anaesthesia for cerebral angiography. Pulmonary function tests showed normal volumes and normal mechanics of breathing; blood gas analysis revealed a slight hypercapnic acidosis and hypoxia. The ventilatory response to CO2 was virtually absent, whereas voluntary hyperventilation normalized blood gas values. A polygraphic recording during sleep showed a marked worsening of hypoventilation, which occurred soon after falling asleep and continued throughout all sleep stages; sporadic central apnoeas, at times prolonged, were recorded only during light sleep. The patient, now 14 yr old, is maintained in satisfactory condition with low flow nocturnal oxygen administration combined with the use of a body respirator during sleep twice a week.
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PMID:A polygraphic study of one case of primary alveolar hypoventilation (Ondine's curse). 672 66

Two morbidly obese patients were described as having severe obstructive sleep apnea syndrome with several apneic periods occurring during sleep that produced substantial oxygen desaturation and, in one patient, cardiac arrhythmias. These patients, by dieting, had noted specific "trigger" weights at which they would manifest symptoms of lethargy, hypersomnolence, and snoring. Both were treated with tracheostomy, and after several days without apnea their cardiac and respiratory status stabilized and they underwent loop gastric bypass. Successful weight loss ensued and repeated sleep studies disclosed no further apneic periods (with the tracheostomies occluded), and so their tracheostomies were removed. We consider sleep apnea syndrome to be an indication for bariatric surgery.
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PMID:Obstructive sleep apnea in the morbidly obese. An indication for gastric bypass. 674 16


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