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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of intraperitoneal and intrahippocampal 2-chloroadenosine and caffeine were examined in fully kindled amygdaloid rats. Intraperitoneal administration of 2-chloroadenosine (5 and 10 mg/kg) decreased afterdischarge duration, stage 5 seizure duration and prolonged time taken to reach stage 4 seizure. Only the 10 mg/kg dose induced a significant reduction in seizure stage. Intraperitoneal administration of caffeine (50 mg/kg) increased both afterdischarge duration and stage 5 seizure duration but did not significantly alter other parameters. Intrahippocampal microinfusion of 2-chloroadenosine (1 mM) or caffeine (2 mM) did not alter any of the measured seizure parameters. Intraperitoneal but not intrahippocampal pretreatment of animals with caffeine (50 mg/kg and 2 mM, respectively) blocked the anticonvulsant effects induced by intraperitoneal administration of 2-chloroadenosine. It may therefore be concluded that the adenosine A1 receptors of the CA1 region of the hippocampus do not play a role in mediating the anticonvulsant effects of intraperitoneally administered 2-chloroadenosine in amygdaloid kindled rats.
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PMID:Effect of intraperitoneal and intrahippocampal (CA1) 2-chloroadenosine in amygdaloid kindled rats. 909 13

The influence of adenosine, its analogs: (-)N6-(R-phenylisopropyl)-adenosine (R-PIA), N6-cyclohexyladenosine (CHA), 5-(N-ethylcarboxamido)-adenosine (NECA), adenosine uptake inhibitor-dipyridamole, and theophylline and caffeine (adenosine receptor antagonists) on ethanol withdrawal syndrome was investigated in rats. Adenosine (100 mg/kg ip), all adenosine analogs and dipyridamole (30 mg/kg ip) reduced the number of rats in which audiogenic convulsions appeared. Caffeine and theophylline (5-25 mg/kg ip) did not influence significantly the audiogenic seizures, but they antagonized the depressing effects of adenosine analogs on these withdrawal symptoms. The results suggest that adenosine mechanisms in the brain may be implicated in the development of ethanol withdrawal syndrome.
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PMID:Influence of adenosinergic drugs on ethanol withdrawal syndrome in rats. 911 97

The essential oil obtained from the leaves of Psidium guyanensis Pers. (Myrtaceae) was studied against lethal seizures induced by intraperitoneal injection of pentylenetetrazole (80 mg/kg), picroptoxin (6 mg/kg), and strychnine (2 mg/kg) in mice. At oral doses of 100, 200, and 400 mg/kg, the essential oil attenuated the severity of pentylenetetrazole-induced seizures and offered a dose-related protection but it was found to be ineffective against convulsions induced by picrotoxin and strychnine. The blockade of its protective effect on pentylenetetrazole lethal seizures by caffeine (10 and 50 mg/kg, i.p.) suggests a probable participation of endogenous adenosine in its mechanism. Furthermore, a peripheral mechanism also appears to be involved as the essential oil (5-20 micrograms/ml) was able to block selectively the acetylcholine (1.65 x 10(-6) M) induced contractions but not those evoked by high potassium (80 mM) or caffeine (2 x 10(-3) M) on isolated toad rectus abdominis muscle.
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PMID:The leaf essential oil of Psidium guyanensis offers protection against pentylenetetrazole-induced seizures. 914 Feb 26

The present study investigated the effects of nitric oxide synthase (NOS) inhibitors on the seizure threshold of DMCM in mice. The seizure threshold of DMCM was evaluated using an intravenous infusion technique. The threshold of DMCM was significantly decreased by pretreatment with N-nitro-L-arginine (NOARG; 8 mg/kg) and N-nitro-L-arginine methyl ester (L-NAME; 100 mg/kg), but not with D-NAME. Furthermore, these NOS inhibitors also decreased the threshold for pentylenetetrazole-induced seizure. However, the threshold for caffeine-induced seizure was not affected by NOARG. These results suggest that the endogenous NO system may play an important role in the expression of seizure by GABA(A) receptor inhibitory agents (DMCM and PTZ).
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PMID:Aggravation of DMCM-induced seizure by nitric oxide synthase inhibitors in mice. 918 Mar 70

The behavioural and electrocorticographic (ECoG) convulsant effects of several xanthine derivatives injected intraperitoneally (i.p.) were studied in genetically-epilepsy prone rats. The aim of the study was to evaluate the relationship among convulsant potency, molecular structure and lipophilicity of some xanthines. Animals were injected i.p. with various doses (250-1000 micromol/kg) and a different convulsant potency was observed among the various xanthines tested. IBMX (3-isobutyl-1-methylxanthine), theophylline (1,3-dimethylxanthine) and caffeine (1,3,7-trimethylxanthine) induced an epileptogenic pattern that consisted in an initial phase characterized by wet-dog shakes followed by head tremor, nodding, clonic convulsion and they appeared to be the most potent xanthines among those studied. During seizures, the electrocortical activity was usually characterized by single or multiple sharp- or spike-wave episodes followed by polyspike discharges. After the highest doses of IBMX, theophylline and caffeine, the animals react with falling down, transient tonic clonic seizures, escape response and generalized seizures followed by post-ictal period. Equimolar doses of 8-chlorotheophylline and theobromine (3,7-dimethylxanthine) produced less evident epileptic responses in comparison to previous compounds, whereas no epileptic signs were observed following the administration of enprofylline (3-propylxanthine), etofylline [7-(2-hydroxyethyl)theophylline], diprophylline [7-(2,3-dihydroxy-propyl)theophylline] and doxofylline [7-(1,3-dioxolan-2-ylmethyl) theophylline]. Lipophylicity of the compounds was determined, but no convincing correlations were found between the rank order of lipophilicities and the convulsant potencies of the compounds studied. On the other hand, structure-activity relationship was also investigated. We suggest that the substitution pattern on the xanthine nucleus may explain, in part, the different convulsant potency of the compounds studied. Furthermore, a selective antagonism of adenosine subtype receptors should be considered.
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PMID:Convulsant effects of some xanthine derivatives in genetically epilepsy-prone rats. 922 89

Caffeine is used and abused on a daily basis in different beverages, OTC products, and as a prescribed medication. The strength varies widely from negligible in decaffeinated drinks to medicinal grade of 200 mg/tablet. A total of 7,655 exposures were recorded in 1995 by the AAPCC Toxic Exposure Surveillance System with no fatality. However, within a 4-mo period, the Panhandle Poison Center recorded 2 deaths due to caffeine overdose. The abrupt onset of intractable seizures needs to be anticipated in order to appropriately manage the victims and to prevent the adverse outcome.
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PMID:Acute caffeine ingestion fatalities: management issues. 925 Nov 73

In adult rat brain, adenosine A2A receptors and dopamine D2 receptors are known to be located on the same cells where they interact in an antagonistic manner. In the present study we wanted to examine when this situation develops and compared the postnatal ontogeny of the binding of the adenosine A2A receptor agonist [3H]CGS 21680, the binding of the dopamine D1 receptor antagonist [3H]SCH 23390 and the dopamine D2 receptor antagonist [3H]raclopride. All three radioligands bound to the striatum at birth and this binding increased several-fold during the postnatal period. [3H]SCH 23390 binding developed first (mostly during the first week), followed by [3H]raclopride binding (first to third week) and [3H]CGS 21680 binding (only during second and third week). For all three radioligands the binding tended to decrease between 21 days and adulthood. This occurred earlier and was more pronounced in the globus pallidus than in the other examined structures. The increase in [3H]CGS 21680 binding from newborn to adult was mainly due to four-fold increase in the number of binding sites. The pharmacology of [3H]CGS 21680 binding to caudate-putamen was similar in newborn, one-week-old and adult animals, and was indicative of A2A receptors. The binding was inhibited by guanylyl imidodiphosphate at all ages, indicating that A2A receptors are G-protein-coupled already at birth. In contrast to the large increase in [3H]CGS 21680 binding, there was a decrease in the levels of A2A messenger RNA during the postnatal period in the caudate-putamen. In cerebral cortex [3H]CGS 21680 bound to a different site than the A2A receptor. From birth to adulthood cortical binding of [3H]CGS 21680 increased four-fold and that of the adenosine A1 agonist [3H]cyclohexyladenosine 19-fold. During early postnatal development [3H]SCH 23390 binding was higher in deep than in superficial cortical layers, but this difference disappeared in adult animals. There was binding of both [3H]CGS 21680 and [3H]cyclohexyladenosine to the olfactory bulb, suggesting a role of the two adenosine receptors in processing of olfactory information. [3H]CGS 21680 binding was present in the external plexiform layer and glomerular layer, and increased during development, but the density of binding sites was about one tenth of that seen in caudate putamen. [3H]cyclohexyladenosine showed a very different labelling pattern, resembling that observed with [3H]SCH 23390. Postnatal changes in adenosine receptors may explain age-dependent differences in stimulatory caffeine effects and endogenous protection against seizures. Since A2A receptors show a co-distribution with D2 receptors throughout development, caffeine may partly exert such actions by regulating the activity of D2 receptor-containing striatopallidal neurons.
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PMID:Distribution and postnatal ontogeny of adenosine A2A receptors in rat brain: comparison with dopamine receptors. 928 70

The seizure-modulating effects of 2-chloroadenosine (2-CLA) infused directly into the amygdala were investigated. Different groups of amygdala-kindled rats were infused (1 microliter) with 2-CLA (0.25, 1, 10 and 25 nM), caffeine (200 microM and 2 mM), a combination of the two or artificial cerebrospinal fluid (ACSF) applied directly through a cannula located in the amygdala. Infusion of 2-CLA dramatically suppressed seizure stage (SS), after discharge duration (ADD) and stage 5 seizure duration (S5D), while the latency to bilateral forelimb clonus (S4L) was significantly prolonged. These anticonvulsant effects were evident after 5 min, reached a maximum at the 60 min time point and were still detectable 360 min post-2-CLA infusion. Pretreatment with caffeine blocked the anticonvulsant effects of 2-CLA dose-dependently. These results may suggest that in amygdaloid-kindled rats, adenosine receptors located in the amygdala play a major role in the expression of the anticonvulsant activity of 2-CLA.
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PMID:Intra-amygdala infusion of 2-chloroadenosine suppresses amygdala-kindled seizures. 943 26

1. Despite advances in the art and science of fluid balance, exertional heat illness -- even life-threatening heat stroke -- remains a threat for some athletes today. 2. Risk factors for heat illness include: being unacclimatized, unfit, or hypohydrated; certain illnesses or drugs; not drinking in long events; and a fast finishing pace. 3. Heat cramps typically occur in conditioned athletes who compete for hours in the sun. They can be prevented by increasing dietary salt and staying hydrated. 4. Early diagnosis of heat exhaustion can be vital. Early warning signs include: flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion. 5. Pitfalls in the diagnosis of heat illness include: confusion preventing self-diagnosis; the lack of trained spotters; rectal temperature not taken promptly; the problem of "seek not, find not;" and the mimicry of heat illness. 6. Heat stroke is a medical emergency. Mainstays of therapy include: emergency on-site cooling; intravenous fluids; treating hypoglycemia as needed; intravenous diazepam for seizures or severe cramping or shivering; and hospitalizing if response is slow or atypical. 7. The best treatment is prevention. Tips to avoiding heat illness include: rely not on thirst; drink on schedule; favor sports drinks; monitor weight; watch urine; shun caffeine and alcohol; key on meals for fluids and salt; stay cool when you can; and know the early warning signs of heat illness.
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PMID:Treatment of suspected heat illness. 969 24

The aim of this study was to determine the interaction potential of the new antiepileptic drug felbamate (2-phenyl-1,3-propanediol dicarbamate) with three Ca2+ channel blockers (nicardipine, nifedipine, and flunarizine), one Ca2+ channel activator (Bay K 8644; 1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl)-phenyl]-3-pyridi ne carboxylic acid), and two methylxanthines (caffeine and aminophylline (theophylline2 . ethylenediamine)) which are all known to markedly change protective effects of conventional antiepileptic drugs. To do so, the maximal electroshock seizure test in mice (an experimental model predicting drug efficacy in the treatment of human generalized tonic-clonic seizures) was employed to (1) quantify changes in the protective efficacy and potency of felbamate produced by adjunct drugs and (2) assess the ability of aminophylline and caffeine to affect protective efficacy afforded by a submaximal protective dose of felbamate against maximal electroshock-induced seizures. Doses of adjunct drugs were selected based on their effects on the threshold for electroconvulsions and on appropriate literature. Nicardipine (10-30 mg/kg), nifedipine (5-20 mg/kg), flunarizine (2.5-10 mg/kg), Bay K 8644 (2.5-5 mg/kg), and aminophylline (50-75 mg/kg) did not change the protective efficacy and potency of felbamate against maximal electroshock-induced tonic convulsions. Aminophylline in the dose of 100 mg/kg, however, diminished the protective potency of felbamate as evidenced by a statistically significant increase in the protective ED50 value of felbamate (a dose, in mg/kg, predicted to protect 50% of mice against convulsive stimulus) from 79.6 to 118 mg/kg; P < 0.05). Aminophylline and caffeine only at high doses (100 and 161.7 mg/kg, respectively) significantly diminished the protective efficacy of felbamate (110 mg/kg) from 96% to 27% and 40% (P < 0.05), respectively. In conclusion, felbamate shows low interaction potential with Ca2+ channel modulators and methylxanthines. Such low interaction potential clearly differentiates felbamate from conventional antiepileptic drugs where protective effects are readily altered by the compounds tested in the present study.
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PMID:Felbamate demonstrates low propensity for interaction with methylxanthines and Ca2+ channel modulators against experimental seizures in mice. 971 56


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