Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the newborn lamb's cerebral cellular activity and metabolism following acute insulin-induced hypoglycemia. Eleven animals received an insulin bolus followed by a continuous infusion to maintain a plasma glucose of 1 mM/l for 2 h, while 8 other animals received an equivalent dose of saline. Following the induction of hypoglycemia, the animals became quiet and transient seizures were observed in 3 animals. A significant increase in heart rate (p less than 0.01), and a decrease in arterial PaCO2 at 30 min (p less than 0.01), and pH at 2 h (p = 0.02), following hypoglycemia, were observed in the experimental group. Hypoglycemia did not significantly alter the cerebral blood flow, mitochondrial respiratory control ratio or the state-3 activity. The cerebral arteriovenous difference (CAVD) for oxygen did not change, while the glucose CAVD was significantly reduced from 0.47 +/- 0.21 to 0.24 +/- 0.16 mM/l (p less than 0.05) at the end of the hypoglycemia period, suggesting consumption of alternate substrates of energy by the brain. Insulin-induced hypoglycemia was associated with a significant increase in arterial lactate (p less than 0.01), and a significant correlation (p less than 0.01) between arterial and CAVD for lactate and beta-hydroxybutyrate (BOB) was observed. Cerebral consumption of alternate substrates of energy was inconsistent, and only observed for lactate in 5 and for BOB in 3 experimental animals following hypoglycemia. These data indicate that the newborn lamb's cerebral cellular activity is not affected by the degree of hypoglycemia achieved in these studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral metabolic response and mitochondrial activity following insulin-induced hypoglycemia in newborn lambs. 265 16

In spite of significant advances made in the technology to image the intracranial contents and to measure the metabolic activity of discrete brain sites, the factor(s) responsible for the death of ischemic neurons remains unresolved. Several potential culprits have been tried: (1) "energy failure", or depletion of high-energy phosphates, occurs very quickly after ischemia, but energy metabolites recover even in tissues where functional return does not occur; (2) "tissue lactacidosis" enhances ischemic cell necrosis, but this factor is not the indispensable cause of neuronal necrosis because acidosis is minimal or nonexistent under conditions of hypoglycemia and seizures; (3) "impairment of the microcirculation" may be a contributing factor, but such microcirculatory impairment cannot be the initiating event as it is known that irreversible neuronal injury precedes the development of microcirculatory abnormalities; (4) the effects of "excitatory neurotransmitters", especially glutamate, may explain the "delayed neuronal death" or the protracted necrosis of neurons in the CA1 sector of the hippocampus; (5) ionic pump alterations: studies of experimental myocardial ischemia tend to support a contributory role of Ca2+ in the aggravation of cell necrosis; however, lack of an experimental model in which steady-state conditions can be maintained has left unresolved the potential participation of calcium ions in ischemic cell necrosis; (6) the same statement, concerning the lack of an experimental model, can be made about the role of free-radical species; oxygen free radicals and superoxides are abundant in the reperfusion stage of ischemic injury, but it is unclear how significant their contribution might be as initiators of ischemic necrosis; and (7) the "ischemic penumbra" is a zone or portion of brain tissue that is sufficiently hypoperfused as to be functionless, but where the cells are likely to recover once normal perfusion is reestablished. Further understanding of the "penumbra" may prove crucial in future studies of brain ischemia.
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PMID:Physiopathology of cerebral ischemia. 265 39

Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.
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PMID:Adenosine in the control of the cerebral circulation. 270 69

The hypocalcaemia observed in infants and children may have different causes, the most common being vitamin D deficiency rickets, which still exists, and hypoparathyroidism, which is rare. The clinical manifestations of hypocalcaemia may be neurological disorders, such as seizures, respiratory disorders with possible laryngospasm or severe cardiac disorders that may result in sudden death. Pronounced or symptomatic hypoglycaemia requires hospitalization and active therapy. Treatment has now been improved by the 1-hydroxyle derivatives of vitamin D.
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PMID:[Hypocalcemia in infants and children]. 271 66

To characterize further the hypoglycemic effect of intrathecally (i.t.) administered morphine, species and drug specificity, effects of morphine-induced tolerance and pentobarbital-induced anesthesia and effects on liver glycogen were studied in nonfasted animals. In rats, morphine (125 micrograms i.t.) produced the same behavioral toxicity (scratching, biting, seizures) and hypoglycemia as previously reported in mice. In mice, the glycine antagonist strychnine (5 micrograms i.t.) and the morphine metabolite morphine-3-glucuronide (2 micrograms i.t.) mimicked the behavioral, but not the hypoglycemic, effects of high-dose i.t. morphine. Kainic acid (0.1 micrograms i.t.), which caused high-frequency hindlimb movements, also did not cause hypoglycemia. Naltrexone (1 mg/kg/ s.c.) or the s.c. implantation of morphine pellets for 3 days attenuated the hypoglycemic effect, but not the behavioral effects, of morphine (40 micrograms i.t.). The hyperglycemic effect of s.c. morphine(20 mg/kg) was blocked by i.t. morphine. Anesthesia with pentobarbital (75 mg/kg i.p.) attenuated the hypoglycemic effect of morphine (40 micrograms i.t.). Morphine i.t. also caused a time- and dose-dependent decrease in liver glycogen levels and was more potent in causing glycogenolysis (30 min ED50 = 19 micrograms) than in causing hypoglycemia (30 min ED50 = 30 micrograms). It is concluded that the hypoglycemic effect of i.t. morphine appears to be independent of its behavioral effects, displays tolerance and is accompanied by hepatic glycogen depletion.
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PMID:Studies on the mechanism of hypoglycemia induced by intrathecal morphine: dissociation from behavioral effects, effects of tolerance and depletion of liver glycogen. 273 44

Defective activity of carnitine palmitoyltransferase I was demonstrated in fibroblasts derived from a patient with hypoketotic hypoglycemia. The level of activity observed was approximately 10% of the control mean. Oxidation of palmitate by intact fibroblasts was reduced to 5% of control values. The patient presented at age 14 months with seizures and was found to have marked hypoglycemia and no ketones in the urine. In response to fasting, she developed hypoglycemia, but the curves for acetoacetate and 3-hydroxybutyrate were flat. Administration of medium-chain triglycerides relieved the hypoglycemia and generated a brisk ketogenesis.
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PMID:Deficiency of carnitine palmitoyltransferase I. 276 84

The influence of hyperglycemia and moderate hypoglycemia plus electroconvulsive seizure on the permeability of the blood-brain barrier to protein was studied in rats. Evans blue was used as a blood-brain barrier tracer. Following a single electroconvulsive seizure, slight staining of brain tissue was seen. After 10 electroconvulsive stimuli followed by sustained seizure activity, this phenomenon was more pronounced in moderate hypoglycemic animals. In this group, Evans blue albumin extravasation occurred in all regions of the hemispheres, but the most severe protein leakage was seen in the thalamus, hypothalamus, amygdala nuclei, and frontal, parietal, and occipital cortex. Ten repeated electroconvulsive stimuli applied in case of hyperglycemia made no important difference in blood-brain barrier dysfunction according to normoglycemic group. Our results suggest that moderate hypoglycemia provokes the effect of electroconvulsive seizure on the permeability of the blood-brain barrier.
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PMID:Blood-brain barrier permeability after electrically induced seizure in normoglycemic, hypoglycemic, and hyperglycemic rats. 279 94

Human carnitine palmitoyltransferase (CPT) deficiency results in 2 clinical forms: a more common "muscular form" with myoglobinuria with or without delayed or impaired ketogenesis and a rare "hepatic form" with hypoketotic hypoglycemia, encephalopathy and seizures without muscular manifestations. We present 2 patients, a male (patient 1) and a female (patient 2) with infantile "hepatic" CPT deficiency and previously documented CPT1 deficiency in fibroblasts. In patient 2, a deficiency of "total" CPT activity in liver had also been previously documented. We set up an isotope exchange assay system that effectively differentiated CPT1 and CPT2 activities in muscle. We found normal CPT1 and CPT2 activities in our patients under near saturating substrate conditions. The CPT1 and CPT2 activities were suppressed to a strikingly similar degree under different kinetic conditions as compared to control muscle and were found to have similar Km values for carnitine and PCoA. With Km concentrations of carnitine, the mean residual activities of CPT1 for patients 1 and 2 were 49 and 44%, respectively (control range 40-53%); the mean residual activities of CPT2 were 60 and 46%, respectively (control range 49-59%). With Km concentrations of PCoA, the mean residual activities of CPT1 for patients 1 and 2 were 52 and 58%, respectively (control range of 52-59%); mean residual activities of CPT2 were 54% and 56%, respectively (control range of 51-68%). When the Vmax concentration of PCoA was doubled and bovine serum albumin reduced to 0.1%, the mean residual activities of CPT1 for patients 1 and 2 were 69 and 63%, respectively (control range 60-80%). In "muscular" patients, a marked absolute deficiency of CPT2 activity (less than 12% residual) was found with an apparent increased sensitivity to suppression of enzymatic activity when the Km concentration of carnitine was used. We suggest that CPT1 and CPT2 may be separate proteins. Furthermore, CPT1 itself may exist as tissue-specific isoforms being the same protein in liver and fibroblasts and a different protein in muscle. Either could be encoded for by the same or closely related genes.
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PMID:Normal muscle CPT1 and CPT2 activities in hepatic presentation patients with CPT1 deficiency in fibroblasts. Tissue specific isoforms of CPT1? 280 20

Plasma epinephrine, norepinephrine, and dopamine responses were studied in insulin-dependent diabetic patients at rest, on standing and during insulin-induced hypoglycemia. beta-Adrenergic sensitivity was evaluated by the isoproterenol sensitivity test. Five men who had adrenergic symptoms during hypoglycemia and no severe hypoglycemic accidents (coma, seizures) (group A) and five men who had repeated severe hypoglycemic accidents but lack of adrenergic symptoms of hypoglycemia (group B) were studied. The mean resting plasma epinephrine was lower in group B (147 +/- 22 pmol/L, SEM) than in group A (398 +/- 98 pmol/L, P less than 0.02). On standing plasma epinephrine increased significantly in both groups. During hypoglycemia blood glucose decreased identically in the two groups; plasma epinephrine and norepinephrine increased significantly and to the same extent in both groups; the mean maximal heart rate was significantly greater in group A than in group B. Isoproterenol sensitivity (defined as the dose of isoproterenol required to increase heart rate by 25 beats/min) was lower in group B (5.87 +/- 1.12 micrograms) than in group A (2.37 +/- 0.22 micrograms, P less than 0.01). The group B patients had significantly fewer hypoglycemic symptoms during insulin-induced hypoglycemia than did group A patients. We conclude that decreased beta-adrenergic sensitivity contributes to the lack of adrenergic symptoms of hypoglycemia in insulin-dependent diabetic patients.
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PMID:Lack of hypoglycemic symptoms and decreased beta-adrenergic sensitivity in insulin-dependent diabetic patients. 282 5

A nine-year-old mixed breed dog was presented with a history of mild generalized seizures, weakness, and muscle fasciculations, following periods of excitement and exercise. Investigative procedures included haematology, chemical pathology, faecal analysis, urinalysis, cerebrospinal fluid analysis, hormone assays, computerized axial tomography and scintigraphic imaging. Results of these investigations revealed hypoglycaemia (blood glucose 1.9 mmol l-1, hyperinsulinism (111 muu ml-1) and an amended insulin-glucose ratio of 2643. The glucagon tolerance test was typical for an insulin producing pancreatic islet cell tumour and pancreas scintigraphic imaging revealed focal lesions in the pancreas and liver. Seizures were initially controlled by dietary means and by limiting exercise. Eventual control was obtained by treatment with prednisolone (1 mg kg-1 on alternate days) and diazoxide (10 mg kg-1 in divided doses daily). Post mortem examination confirmed the presence of a pancreatic islet cell adenocarcinoma with hepatic metastasis.
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PMID:An insulinoma causing hypoglycaemia and seizures in a dog: case report and literature review. 285 64


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