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)

Aminophylline, 285.7 +/- 2.19 mg/kg infused intravenously in unanaesthetized rats produced onset of seizures within 3.2 +/- 0.99 minutes. Seizures were repetitive and death occurred in 10.5 +/- 1.75 minutes. Pretreatment of rats with carbamazepine, sodium valproate and diazepam at doses that prevented electroshock induced seizures were effective in significantly postponing seizures and death, but did not reduce mortality. Concomitant EEG studies in aminophylline infused rats showed that cortical excitability evidenced by initial cortical spiking occurred at 42 secs and polyspiking at 165 seconds. Following diazepam, the initial cortical spike was delayed 50 fold, appearing after 36 minutes. Antiepileptic drugs and EEG monitoring may prove useful in patients with status asthmaticus receiving intravenous aminophylline.
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PMID:Antiepileptic drugs delay the onset of seizures induced by aminophylline in conscious rats. 159 41

Focal injection of 2-chloroadenosine into the substantia nigra protects Sprague-Dawley rats against electroshock seizures (50 mA. 60 Hz, 0.2 s) and genetically epilepsy prone rats against audiogenic seizures. 2-Chloroadenosine infusion into the substantia nigra pars reticulata provided significant protection against electroshock seizures (1.66, 8.33 and 25 nmol) and audiogenic seizures (66, 331 pmol and 1.66 nmol). High doses of 2-chloroadenosine injected into the substantia nigra pars compacta resulted in a similar suppression of electroshock seizure activity (8.33 nmol) and audiogenic seizures (1.66 nmol). No anticonvulsant activity was observed when 2-chloroadenosine was infused into the entopeduncolar nucleus. Lower doses of 2-chloroadenosine provided significant protection against audiogenic seizures (66 and 331 pmol) when injected into the inferior colliculus. Aminophylline antagonised these effects, indicating that purinergic mechanisms are involved in both audiogenic and electroshock seizures. In addition, the similarity of these effects to those elicited by excitatory amino acid antagonists in the inferior colliculus and substantia nigra pars reticulata is consistent with 2-chloroadenosine acting by reducing excitatory transmission.
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PMID:Anticonvulsant action of 2-chloroadenosine injected focally into the inferior colliculus and substantia nigra. 206 May 98

The mechanism of action of aminophylline in prolonging seizures was tested in amygdala-kindled rats. Aminophylline prolonged the afterdischarge duration of kindled seizures. This seizure-prolonging action of aminophylline was strongly antagonized by the adenosine A1 agonist cyclohexyladenosine and partially antagonized by the benzodiazepine partial agonist RO 15-1788. However, the specific benzodiazepine antagonist CGS 8216 did not affect the seizure-prolonging action of aminophylline. Also, the potent anticonvulsant effect of diazepam on kindled seizures, which was completely antagonized by CGS 8216, was unaffected by aminophylline. Furthermore, a range of benzodiazepine inverse agonists, GABA antagonists, phosphodiesterase inhibitors and xanthines did not prolong afterdischarge durations. These results demonstrate that the seizure-prolonging action of aminophylline is due to block of A1 adenosine receptors since it is prevented by adenosine A1 agonists.
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PMID:Adenosine receptor antagonism accounts for the seizure-prolonging effects of aminophylline. 221 1

Interaction of two well known methyl xanthines, aminophylline--an antiasthmatic agent--and caffeine--commonly present in beverages, on the seizure protective ability of carbamazepine (CBZ) against electrically and chemically induced seizures in rats was investigated. Aminophylline (75 mg/kg, ip) did not alter the activity of CBZ (10 mg/kg, ip; ED100) on maximal electroshock seizures while dose dependent antagonism of CBZ efficacy was seen at 100 and 150 mg/kg, ip. Similar effects were observed with caffeine (200 and 250 mg/kg, ip). At the highest tolerated doses, aminophylline (150 mg/kg, ip) and caffeine (250 mg/kg, ip) produced antagonism of CBZ protection against pentylenetetrazole seizures. These observations support the possibility that the antagonism due to the interaction of these drugs could be related to their action at adenosine receptor sites in the brain.
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PMID:Inhibition of anticonvulsant action of carbamazepine by aminophylline and caffeine in rats. 263 65

Aminophylline (A) is a proconvulsant in adult rats. We studied the effect of A on amygdala kindling in 15-day-old rat pups. Production of generalized seizures was significantly promoted by A at doses ranging from 10 to 100 mg/kg. Terminal status epilepticus (TSE) was produced in 33% of pups receiving 25 mg/kg A, 75% of pups receiving 50 mg/kg A, and 100% of pups receiving 100 mg/kg A. The number of stimuli needed to produce a stage 4-5 generalized seizure was significantly smaller in animals receiving 10 mg/kg A (5.7 +/- 3.4), 25 mg/kg A (3.4 +/- 2.4), 50 mg/kg A (1.9 +/- 1.4), or 100 mg/kg A (1.9 +/- 1.6) than in saline-treated controls (12.3 +/- 3.7) (P less than 0.001). In addition, 16% of pups receiving 50 mg/kg and 33% of pups receiving 100 mg/kg A and never stimulated developed TSE. These seizure-promoting effects of A in rat pups undergoing amygdala kindling are far more dramatic and occur at far lower doses than those previously reported in adults.
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PMID:Proconvulsant effects of aminophylline during amygdala kindling in developing rats. 272 Sep 53

Aminophylline (50 and 100 mg/kg) and CGS 8216 (20 and 40 mg/kg) decreased the anticonvulsant potency of diazepam (5 and 10 mg/kg) against electroshock-induced seizures. It should be emphasized that aminophylline moderately affected the protective action of the benzodiazepine at a dose of 5 mg/kg, whereas it was equipotent with CGS 8216 with regard to diazepam at a dose of 10 mg/kg. Consequently, participation of a purinergic component in the anticonvulsant action of diazepam is suggested. On the other hand, the use of aminophylline in epileptic patients suffering from asthma seems unjustified.
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PMID:Aminophylline and CGS 8216 reverse the protective action of diazepam against electroconvulsions in mice. 300 Jul 60

Two xanthine derivatives, aminophylline and enprofylline, were tested on the protective activity of phenobarbital, 20 mg/kg i.p. (60 min before the test) against amygdala-kindled seizures in female rats. Enprofylline, 27.8 mg/kg i.p. (0.143 mmol/kg) 30 min, and aminophylline, 10 mg/kg i.p. (0.043 mmol/kg) 30 min, did not modify any kindling parameter. Aminophylline, 30 mg/kg (0.143 mmol of theophylline/kg), considerably increased seizure and afterdischarge durations. Aminophylline, 30 mg/kg, abolished the effect of phenobarbital (20 mg/kg) upon these seizure parameters. Both values reached the level observed in animals treated with aminophylline alone. Aminophylline, 10 mg/kg, only moderately increased afterdischarge duration in phenobarbital (20 mg/kg)-treated group. Enprofylline, 27.8 mg/kg, was devoid of any action upon the protection offered by phenobarbital in this model of epilepsy.
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PMID:Effects of aminophylline and enprofylline on the protective activity of phenobarbital against amygdala-kindled seizures in rats. 350 99

Rats were implanted with chronic electrodes to stimulate the perforant path and record the elicited monosynaptic evoked potentials from the dentate gyrus of the hippocampal formation. Dentate responses were examined in awake and anesthetized animals after exposure to saline and aminophylline (100 mg/kg, IP). In the awake animal, aminophylline treatment did not significantly alter the threshold or elicited amplitude of either the excitatory post-synaptic potential (EPSP) or the population spike (PS). Aminophylline pretreatment markedly enhanced the length and severity of elicited seizures from hippocampal (dentate gyrus) or perforant pathway stimulation. After daily perforant pathway stimulations which established "kindled" seizures, aminophylline significantly increased only the amplitude of the evoked PS in awake animals. In animals anesthetized with chloropent, aminophylline increased significantly before kindling the amplitude of both the EPSP and PS without effecting thresholds for each. After perforant pathway kindling, only the PS amplitude was increased significantly by aminophylline. Inhibition, thought to be from GABA-mediated recurrent collaterals, was found to be increased rather than decreased by kindling. Further, aminophylline treatment did not result in reduction of this inhibition before or after kindling. These data suggest that at this dose of aminophylline neither enhanced transmitter release at this synapse as measured by the amplitude of the EPSP, nor reduced recurrent collateral inhibition significantly contributed to the prolongation of elicited seizure afterdischarge. The increase in PS amplitude reflecting an increased number of granule cells excited to discharge with perforant path stimulation after aminophylline was noted in awake animals but was greatest in the anesthetized animals. Although the number of granule cells excited to discharge was increased by aminophylline, the small increase in amplitude seen compared to the effects of other neurotoxins on this synapse makes this an unlikely explanation for the profound increased seizure response seen after aminophylline.
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PMID:Modification of excitation and inhibition evoked in dentate gyrus by perforant path stimulation: effects of aminophylline and kindling. 394 69

To test the hypothesis that kindling is restrained by the inhibitory neuromodulator, adenosine, the adenosine uptake blocker, papaverine, or the adenosine antagonist, aminophylline, were injected systemically into rats 20 min before each daily electrical stimulation of the amygdala. The effects on amygdala-triggered seizures of papaverine, adenosine, 2-chloroadenosine, and the adenosine antagonists, isobutylmethylxanthine and caffeine, were also investigated at seizure threshold. Papaverine inhibited kindling, whereas aminophylline accelerated kindling. The adenosine agonists had anticonvulsant effects on seizures, and the antagonists had proconvulsant effects which involved, primarily, the lengthening of afterdischarge duration. Aminophylline injected repeatedly, in the absence of electrical stimulation, induced seizures. These results support the hypothesis that adenosine can modulate kindling and affect the seizure process.
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PMID:Adenosine modulation of amygdala kindling. 672 86

Aminophylline-induced seizures were studied in 166 male albino rats in five age groups--7, 12, 18, 25 and 90 days old. Aminophylline injected in doses from 150-350 mg/kg i.p. elicited both minimal, clonic and major, i.e. generalized tonic-clonic seizures during the 60-min observation period. The pattern of minimal seizures did not change during development; major seizures exhibited changes in proportion to their three phases--running, tonic and clonic phases. Dependence on the dose of aminophylline was observed in the incidence of major seizures as well as in shortening of latencies of both types of seizures. More marked convulsant effects of aminophylline in 7-, 12- and 18-day-old rat pups than in older animals might be due to pharmacokinetic as well as pharmacodynamic factors.
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PMID:Aminophylline exhibits convulsant action in rats during ontogenesis. 781 24


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