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)

The cardiovascular effects of opioid peptides have been studied. Leucine-enkephalin (Leu-ENK) produced blood pressure (BP) increases following administration into the lateral brain ventricles (i.v.t.), into the cisterna magna (i.c.i.), and following intravenous (i.v.) administration. Heart rate (HR) increases were observed following all routes of administration (threshold for BP and HR effects at 0.3 nmole, maximum at 360 nmoles). The cardiovascular effects were independent of generalized seizures, which may occur at higher doses of enkephalins (ENK). D-alanine-enkephalin (D-Ala-ENK) attenuated the vagal component of the baroreceptor reflex in cats. This was indicated by the findings that HR did not decrease following D-Ala-ENK-induced BP increases and that the compensatory decreases in HR following i.v. pressor doses of angiotensin II (ANG II) were markedly attenuated in cats treated with i.v.t. D-Ala-ENK. Naloxone inhibited the BP and HR effects following i.c.i. and i.v., but not following i.v.t., administration of Leu-ENK. The i.v.t. Leu-ENK effect were inhibited by beta-adrenergic receptor blockade. Bratteboro rats homozygous for hereditary diabetes insipidus with total absence of antidiuretic hormone (ADH) synthesis responded with BP decreases following i.v.t. Leu-ENK, while BP increases were observed in control Long-Evans rats. Blood pressure increases to i.v.t. Leu-ENK were markedly greater in spontaneously hypertensive rats of the stroke-prone strain (SHR-sp) than in normotensive control rats; SHR-sp exhibit a humoral pattern of increased ADH, ACTH, and catecholamines, presumably due to central peptidergic stimulation. The known effects of opioid peptides on these hormones and the observed cardiovascular responses suggest a possible participation of this peptide system in the maintenance of high BP in the SHR-sp.
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PMID:Enkephalin effects on blood pressure, heart rate, and baroreceptor reflex. 739 23

Ethanol dependence was achieved in male, Long-Evans rats after 8 days on a balanced liquid diet that supplied 4.5% ethanol. After 1-h access to a solution of 10% ethanol (95%)/5% sucrose, the rats were deprived of food, water, and ethanol for 9 h. Following 30-s key jingling, about 80% of the animals exposed to ethanol experienced tonic-clonic seizures. Neurochemical analyses of striatal tissues revealed a significant (p < 0.05) increase in dopamine (DA) and a significant decrease in serotonin (5-HT) in the ethanol-exposed rats that had seizures compared to control rats. Homovanillic acid concentrations of the ethanol-treated rats with seizures were significantly higher than the levels found in ethanol-treated animals that had experienced no seizures. Daily average ethanol intake of the rats that had seizures vs. those that did not was almost the same at 16 g/kg/day. The findings indicate that rats experiencing ethanol withdrawal-induced seizures manifest opposite alterations in dopaminergic and serotoninergic activity compared to controls. The present results do not reveal if the striatal changes are caused by ethanol rather than by the seizures.
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PMID:Simultaneous changes in striatal dopamine, serotonin, and metabolites after withdrawal seizures in rats from dependence on alcohol. 763 60

The changes in the permeability of the blood-brain barrier during pentylenetetrazol (PTZ)-induced seizures were investigated in normothermic and hypothermic rats. Six groups of rats were studied: (I) normothermic control; (II) hypothermic control; (III) normothermia plus PTZ (80 mg/kg); (IV) normothermia plus PTZ (160 mg/kg); (V) hypothermia plus PTZ (80 mg/kg); (VI) hypothermia plus PTZ (160 mg/kg). The rats were anesthetized with diethyl ether. In the hypothermic animals, colonic temperature was reduced to 20 +/- 1 degree C by submerging the animals in ice water. In normothermic animals, distinct Evans-blue leakage was observed in the occipital cortex, thalamus, hypothalamus, substantia nigra, corpus striatum, and medulla oblongata in both PTZ groups. However, hypothermic animals which received a high dose of PTZ showed the most severe blood-brain barrier breakdown. Mean levels of Evans blue in the brains of low-dose (80 mg/kg) PTZ-treated animals were 8.7 +/- 2.2 micrograms/g and 5.7 +/- 1.4 micrograms/g in the normothermic and hypothermic groups, respectively. This difference was significant (P < 0.01). The levels in the high dose (160 mg/kg) PTZ-treated animals were 10.2 +/- 3.5 micrograms/g and 15.9 +/- 3.6 micrograms/g in the normothermic and hypothermic groups, respectively (P < 0.02). In conclusion, deep hypothermia prevents the blood-brain barrier disruption induced by 80 mg/kg pentylenetetrazol and aggravates the increase in permeability after 160 mg/kg pentylenetetrazol.
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PMID:The effect of profound hypothermia on blood-brain barrier permeability during pentylenetetrazol-induced seizures. 769 98

This study reports comparative dose-response data for kainic acid (KA) induced seizures in juvenile (35-40 days old) and adult (70-90 days old) Wistar-Furth (WF), Fisher 344 (F344), Sprague-Dawley (SD) and Long-Evans Hooded (LEH) rats. Juvenile male WF (n = 51), F344 (n = 55), SD (n = 60), LEH (n = 50) and adult male WF (n = 48), F344 (n = 52), SD (n = 52), LEH (n = 53) rats were given KA 6, 8, 10, 12 or 14 mg/kg, sc. As previously demonstrated adult WF and F344 rats showed the greatest sensitivity and most reliable convulsant responses to kainic acid; SD and LEH rats were less sensitive and showed more variable convulsant responses. Regardless of strain, all juvenile rats exhibited greater sensitivity and less variable convulsant response to KA compared to adults. This was most evident in juvenile SD and LEH rats. Results suggest that while seizure sensitivity to KA decreases with age, genetic factors may regulate the expression of this resistance.
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PMID:Rat strain and age differences in kainic acid induced seizures. 775 May 11

The effect of pregnancy on blood-brain barrier permeability was investigated during bicuculline-induced seizure in Wistar rats, using Evans-blue as a tracer. The experiments were carried out with two methods to investigate the integrity of the blood-brain barrier, i.e. Evans-blue albumin extravasation was determined as a macroscopical finding. A quantitative estimation with a spectrophotometer using homogenized brain to release the dye was performed to evaluate the macroscopical findings in a separate group of animals. During convulsions the mean arterial blood pressure increased in both pregnant and nonpregnant rats. The extravasation of Evans-blue was more pronounced in the nonpregnant rats. Mean values for Evans-blue dye were found to be 0.29 +/- 0.07 mg% whole brain in nonpregnant control female rats and 0.30 +/- 0.09 mg% whole brain in pregnant rats. This difference was not significant (P > 0.05). Mean values for Evans-blue dye were 1.02 +/- 0.30 mg% whole brain in nonpregnant female rats, and 0.60 +/- 0.12 mg% in the pregnant rats during bicuculline-induced seizures. This difference was significant (P < 0.01). The severe protein leakage was seen in the thalamus, midcaudate, hypothalamus and mesencephalon bilaterally in the nonpregnant rats. However, in pregnant rats, Evans-blue leakage was similar to that of female rats except that the intensity of blood-brain barrier breakdown was less after convulsion.
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PMID:Influence of pregnancy on blood-brain barrier integrity during seizures in rats. 814 31

We compared the efficacy of four different classes of anesthetics to arrest the progression of brain damage after chemoconvulsant-induced seizures in rats. In two series of experiments, ventilated, paralyzed Long-Evans rats were subjected to 30 or 45 min of continuous seizures induced by intravenous (IV) mercaptopropionic acid (MPA) or inhaled flurothyl, respectively. In the first series, seizures produced with MPA were treated with: 1) thiopental, 15 mg/kg IV bolus (controls); 2) thiopental, 27 mg/kg IV followed by 20.9 mg.kg-1.h-1 for 2 h; 3) isoflurane 4% inhaled concentration for 1 min followed by 1%-2% for 2 h; 4) ketamine 30 mg/kg IV followed by 9.12 mg.kg-1.h-1 for 2 h; 5) midazolam 25 mg/kg IV followed by 9.7 mg.kg-1.h-1 for 2 h. In a second series, seizures were produced by flurothyl and, based on suggestive results in the MPA series, control rats were compared with rats receiving midazolam 25 mg/kg IV followed by 9.7 mg.kg-1.h-1. In all instances, seizure activity, recorded by electroencephalograph, stopped with anesthetic treatment. In MPA-treated rats extranigral damage was mild, with no differences apparent between anesthetics. Control animals sustained severe lesions in the substantia nigra pars reticulata (SNPR). No statistically significant differences between anesthetic groups were present, although an effect was suggested for midazolam to decrease SNPR lesional area (P = 0.06). In flurothyl-treated rats, there were significant reductions in SNPR neuropathologic grade (P = 0.025) and lesional area (P = 0.025) with midazolam. We conclude that midazolam attenuates postseizure SNPR damage in rats.
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PMID:Effect of anesthetics on neuropathologic sequelae of status epilepticus in rats. 834 34

The effect of i.c.v. administration of Evans blue to sound sensitive DBA/2 mice and to genetically epilepsy-prone rats was studied. In mice, Evans blue (3.3-52 nmol) induced: hyperlocomotion, wild running, scratching, clonic muscle spasms, tonic seizure (latency 10-45 min), followed by death or recovery. The CD50 value for clonic seizures for Evans blue was 35(23-53) nmol. Pretreatment (45 min) with Evans blue (13-52 nmol, i.c.v.) dose-dependently reduced the incidence of sound-induced seizures in DBA/2 mice (ED50 value against clonic seizures = 30 [15-58] nmol, i.c.v). In rats, Evans blue (104 nmol, i.c.v.) induced electroencephalographic seizures in the hippocampus and cortex and behavioural limbic seizures with a latency of 15-20 min. A reduction in the mean score (from 5 to 2-3) for behavioural seizures was observed which lasted for 4-5 days in rats electrically-kindled daily in the hippocampal CA3 subsector. Sound-induced clonic seizures in kindled and non-kindled rats were reduced for 3-4 days after administration of Evans blue (104 nmol, i.c.v.).
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PMID:Proconvulsant and anticonvulsant effects of Evans blue dye in rodents. 834 7

1. Magnesium sulphate (MgSO4) has been used for many years in the prevention of eclamptic seizures, but its mechanism of action has never been elucidated. Recent studies suggest that cerebral vasospasm is an important feature of eclampsia and we have developed and tested the hypothesis that MgSO4 can reverse cerebral vasoconstriction. 2. Studies were performed in conscious, male Long Evans rats with pulsed Doppler probes sutured around both common carotid arteries after the external carotid artery had been ligated on the left, thus allowing simultaneous measurement of changes in common and internal carotid blood flow. Intravascular catheters were placed in the abdominal aorta for measurement of systemic blood pressure and in the right jugular vein for administration of drugs. Mean arterial blood pressure and mean Doppler shift signals were used to calculate percentage changes in common and internal carotid vascular conductance. 3. After a period of recovery the animals were infused with endothelin-1, angiotensin II, neuropeptide-Y or NG-nitro-L-arginine methyl ester alone or in combination, and MgSO4 in low or high dose was infused when the effects of the vasoconstrictors had become established. 4. MgSO4 itself, at the low dose, had no effect on carotid vascular conductance. Endothelin-1, angiotensin II and neuropeptide-Y all reduced common and internal carotid vascular conductance and this effect was significantly attenuated by low dose MgSO4. The carotid vasoconstrictor action of endothelin-1 was completely abolished by high dose MgSO4.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnesium sulphate reverses the carotid vasoconstriction caused by endothelin-I, angiotensin II and neuropeptide-Y, but not that caused by NG-nitro-L-arginine methyl ester, in conscious rats. 840 87

Global ischemia was used to induce a sensitivity to sound-triggered generalized seizures in 24 male Long-Evans rats. All showed a generalized seizure when exposed to a 108 dB bell for 1 min. They were assigned randomly to 3 groups of 8, and received 30 additional sound exposures. The early treatment group was injected with valproate (200 mg/kg i.p) 1 h prior to each of the first 10 sound exposures. The late treatment group received the same treatment during the second set of 10 sound exposures after 10 sound exposures without treatment. The third group was untreated. Both early and late treated groups had a significant reduction in seizure incidence during the treatment period, i.e. both groups showed seizure control. However, in the late group seizures returned promptly when valproate treatment was discontinued, while the early group showed a sustained reduction in seizure susceptibility. Since this outcome corresponds to seizure remission, the findings of this study favor early treatment.
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PMID:Early, but not late, antiepileptic treatment reduces relapse of sound-induced seizures in the post-ischemic rat. 852 2

External stimuli may contribute to seizure occurrence in at least two ways. First, the aberrant neuronal activity that precipitates a seizure could be elicited by certain external events; and second, external events could cue the organism to an impending seizure and result in a compensatory response that is, in effect, 'anti-convulsant'. While previous research has been aimed at addressing these issues, the results have been inconclusive. The present study was conducted to clarify and extend this prior work. Adult male Long-Evans hooded rats were chronically implanted with a kindling electrode and randomly assigned to one of two groups. The Tone group was presented with a 2-s auditory stimulus (Tone) beginning one second prior to and overlapping with the 1-s kindling stimulus. Animals in the No Tone group received only the kindling stimulus. Antecedent tone presentation significantly delayed the rate of amygdala kindling. The Tone group required significantly more stimulations to reach a Stage 5 seizure than did the No Tone group. The possibility of this phenomenon providing a means to study the mechanisms underlying anti-epileptogenesis is discussed.
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PMID:Antecedent tone presentation significantly delays rate of amygdala kindling. 856 65


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