Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study effects of catecholamines on cerebral oxygen consumption (CMRo2) and blood flow (CBF), rats maintained on 75% N2O and 25% O2 were infused i.v. with noradrenaline (2, 5, or 8 microgram.kg-1.min-1) or adrenaline (2 or 8 microgram.kg-1.min-1) for 10 min before CBF and CMRo2 were measured. In about 50% of animals infused with 2--8 microgram.kg-1.min-1 of noradrenaline, CMRo2 (and CBF) rose. However, there was no dose-dependent response, and CMRo2 did not exceed 150% of control. The effects of noradrenaline in a dose of 5 microgram.kg-1.min-1 on CMRo2 and CBF were blocked by propranolol (2.5 mg.kg-1). In animals infused with adrenaline (8 microgram.kg-1.min-1) CMRo2 was doubled and, in many, CBF rose 4- to 6-fold. It is concluded that, when given in sufficient amounts, catecholamines have pronounced effects on cerebral metabolism and blood flow, the effects of adrenaline on CMRo2 and CBF resembling those observed in status epilepticus.
 ...
PMID:Influence of intravenously administered catecholamines on cerebral oxygen consumption and blood flow in the rat. 69 50

Twenty-four adult male Wistar rats were used in this study. Status epilepticus was provoked in 10 rats by embedding coriaria lactone particle into the left cerebral motor cortex. In the controls were embedded particles without coriaria lactone. After 6 h of continuous seizure, the locus coeruleus was studied with the noradrenaline (NA) fluorescence histochemical technique and enzyme histochemical test for monoamine oxidase (MAO). The intensity of NA fluorescence was detected with fluorescent microscope autoexposuremeter and analysed with MIAS-200 Image Analyser. The study group showed a parallel increase of NA fluorescence as compared with that of the control group by both measurements. NA plays an inhibitory role in the cortex. Our data suggest that the increase of NA in locus coeruleus may be due to the reduction of NA release from axon terminal. Reduction in inhibition could be one of the mechanisms of seizure activity. The intensity of MAO was detected with MIAS-200 Image Analyser. The regulation of monoamine metabolism by MAO in the central nervous system and the increase of MAO activity in the continuous seizure group may be induced by the accumulation of NA in the locus coeruleus soma.
 ...
PMID:[Histochemical and image-analytic study of the rat locus coeruleus during status epilepticus]. 145 44

Selective lesions of the noradrenergic locus coeruleus (LC) system have recently been shown to aggravate both ischemic and epileptic brain damage. This study explores the possibility that the LC system also influences hypoglycemic brain injury. Bilateral 6-hydroxydopamine lesions of the LC projection to the forebrain were found to cause no change in the degree of neuronal necrosis in the neocortex, hippocampal formation and caudate-putamen following 30 min of reversible insulin-induced hypoglycemic coma. We propose that selective neuronal necrosis in ischemia and status epilepticus is due to the action of excitatory amino acids at synaptic sites, which can be partly counteracted by noradrenaline release from inhibitory LC terminals. In hypoglycemia, excitatory amino acids probably cause brain damage via a local and more diffuse toxic effect which is not significantly influenced by the activation of the LC system.
 ...
PMID:Mechanisms of hypoglycemic brain damage. Evidence against a significant role of the noradrenergic locus coeruleus system. 314 10

To determine the role of noradrenaline, dopamine, and serotonin in the brain of patients with infantile spasms, levels of respective major metabolites in cerebrospinal fluid were examined. Homovanillic acid levels were significantly increased in these patients, while 3-methoxy-4-hydroxyphenylethylene glycol and 5-hydroxyindoleacetic acid were not significantly altered, as compared with controls. In patients with febrile convulsion and status epilepticus who were examined during or within a few hours after convulsions the same phenomenon was evident. The increased level of dopamine metabolite was closely related to the occurrrence of convulsions and is considered to be a secondary phenomenon.
 ...
PMID:Elevated homovanillic acid in cerebrospinal fluid of children with infantile spasms. 615 22

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
 ...
PMID:Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model. 646 70

Rats subjected to structural brain damage induced by sustained convulsions triggered by systemic administration of pilocarpine (PILO) are a useful model for investigation of the mechanisms essential for seizure generation and spread in rodents. After PILO administration, three distinct phases are observed: (a) an acute period of 1-2 days' duration corresponding to a pattern of repetitive limbic seizures and status epilepticus; (b) a seizure-free (silent) period characterized by a progressive return to normal EEG and behavior of 4-44 days' duration; and (c) a period of spontaneous recurrent seizures (SRS) starting 5-45 days after PILO administration and lasting throughout the animal's life. PILO (320-350 mg/kg intraperitoneally, i.p.) was administered to rats, and the content of hippocampal monoamines and amino acids was measured in the acute, silent, and SRS periods by liquid chromatography. Norepinephrine (NE) level was decreased during all periods whereas dopamine (DA) content was increased. Serotonin (5-hydroxytryptamine, 5-HT) was increased only in the acute period. Utilization rate measurement of monoamines showed increased NE consumption and decreased DA consumption during all phases. 5-HT utilization rate was increased only in the acute period. Amino acid content showed a decrease in aspartate (ASP) and glutamate (GLU) concentrations associated with increased gamma-aminobutyric acid (GABA) level during the acute period. The silent phase was characterized by a decrease in glycine (GLY) and GABA levels and an increase in GLU concentration. The SRS period showed an increase in all amino acid concentrations. These findings show important neurochemical changes in the course of establishment of an epileptic focus after brain damage induced by status epilepticus triggered by pilocarpine.
 ...
PMID:Spontaneous recurrent seizures in rats: amino acid and monoamine determination in the hippocampus. 811 29

The GABA-withdrawal syndrome (GWS) is a model of local status epilepticus following the interruption of a chronic GABA infusion into the rat somatomotor cortex. GWS is characterized by focal epileptic electroencephalographic discharges and associated contralateral myoclonus. In neocortical slices obtained from GWS rats, most neurons recorded in the GABA-infused area are pyramidal neurons presenting bursting properties. The bursts are induced by white-matter stimulation and/or intracellular depolarizing current injection and correlate with a decrease of cellular sensitivity to GABA, caused by its prolonged infusion. This effect is related to a calcium influx that may reduce the GABAA receptor-mediated inward current and is responsible for the bursting properties. Here we present evidence for the involvement of calcium- and NMDA-induced currents in burst genesis. We also report modulatory effects of noradrenaline appearing as changes on firing patterns of bursting and nonbursting cells. Complementary histochemical data reveal the existence of a local noradrenergic hyperinnervation and an ectopic expression of tyrosine hydroxylase mRNAs in the epileptic zone.
 ...
PMID:The GABA-withdrawal syndrome: a model of local status epilepticus. 1070 10

Behavioural changes, muscarinic and dopaminergic receptors density and levels of monoamines were measured in striatum of rats after pilocarpine-induced status epilepticus (SE). Wistar rats at the age of 21 days were treated with pilocarpine (400mg/kg; subcutaneously) whilst the control group was treated with 0.9% saline (s.c.). Both groups were sacrificed 1h following the treatment. SE induced a muscarinic receptor downregulation of 64% in pilocarpine group. This effect was also observed to be 57% in D(1) and 32% in D(2). In the dissociation constant (K(d)) values in muscarinic and D(1) receptor no alterations were verified. On the other hand, the K(d) value for D(2) was observed to increase 41%. High performance liquid chromatography determinations showed 63, 35, 77 and 64% decreases in dopamine, 3-methoxy-phenylacetic acid, serotonin and 5-hydroxyindoleacetic acid contents, respectively. The homovanilic acid level was verified to increase 119%. The noradrenaline content was unaltered. A direct evidence of monoamine levels alterations can be verified during seizure activity and receptor density changes appear to occur in an accentuated way in immature brain during the estabilishment of SE induced by pilocarpine.
 ...
PMID:Pilocarpine-induced status epilepticus: monoamine level, muscarinic and dopaminergic receptors alterations in striatum of young rats. 1587 89

Electroconvulsive therapy (ECT) is the most effective treatment for therapy-refractory depression. Usually, prior antidepressant medication will be continued during ECT. However, the seizure threshold may be influenced by psychotropic drugs. We report a patient who received right unilateral ECT under concomitant treatment with bupropion, a selective noradrenaline- and dopamine-reuptake inhibitor. After the fourth session, a focal status epilepticus occurred, which was pharmacoresistant for the duration of 12 days. We assume that the induction of a status may be facilitated by a lowering of the seizure threshold due to bupropion. An evaluation of drug therapy and control of EEG before and during ECT are recommended, especially when the drug treatment has an influence on the seizure threshold.
 ...
PMID:Partial status epilepticus after electroconvulsive therapy and medical treatment with bupropion. 2197 24

In the management of epilepsy, AT1 receptor antagonists have been suggested as an additional treatment strategy. A hyperactive brain angiotensin (Ang) II system and upregulated AT1 receptors are implicated in the cerebrovascular alterations in a genetic form of hypertension. Uncontrolled hypertension could also, in turn, be a risk factor for a seizure threshold decrease and development of epileptogenesis. The present study aimed to assess the effects of the selective AT1 receptor antagonist ZD7155 on kainic acid (KA)-induced status epilepticus (SE) development and accompanying changes in the hippocampal extracellular (EC) neurotransmitter levels of noradrenaline (NAD), serotonin (5-HT), and dopamine (DA) in spontaneously hypertensive rats (SHRs) and their parent strain Wistar-Kyoto (WKY) rats, since monoamines are well-known neurotransmitters involved in mechanisms of both epilepsy and hypertension. Status epilepticus was evoked in freely moving rats by a repetitive intraperitoneal (i.p.) administration of KA in subconvulsant doses. In the treatment group, ZD7155 (5mg/kg i.p.) was coadministered with the first KA injection. Spontaneously hypertensive rats exhibited higher susceptibility to SE than WKY rats, but the AT1 receptor antagonist did not alter the development of SE in SHRs or in WKY rats. In vivo microdialysis demonstrated significant KA-induced increases of the hippocampal NAD and DA levels in SHRs and of NAD, 5-HT, and DA in WKY rats. Although SHRs developed more severe seizures while receiving a lower dose of KA compared to WKY rats, AT1 receptor antagonism completely prevented all KA-induced increases of hippocampal monoamine levels in both rat strains without affecting seizure development per se. These results suggest a lack of direct relationship between KA-induced seizure susceptibility and adaptive changes of hippocampal NAD, 5-HT, and DA levels in the effects of ZD7155 in WKY rats and SHRs.
...
PMID:Effects of AT1 receptor antagonism on kainate-induced seizures and concomitant changes in hippocampal extracellular noradrenaline, serotonin, and dopamine levels in Wistar-Kyoto and spontaneously hypertensive rats. 2592 88


1