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Seizure susceptibility to electroconvulsions or pentylenetetrazol after complete cerebral ischemia in rats due to cardiac arrest
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نویسنده
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dudra-jastrzębska m. ,ułamek-kozioł m. ,andres-mach m. ,łuszczki j.j. ,januszewski s. ,czuczwar s.j. ,pluta r.
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منبع
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pharmacological reports - 2015 - دوره : 67 - شماره : 3 - صفحه:417 -420
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چکیده
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Background experimental data provide evidence on the induction of a susceptibility to audiogenic seizures in rats surviving cardiac arrest and subsequent global brain ischemia. the aim of this study was to find out whether cardiac arrest in rats could affect seizure susceptibility in the long-term period of one and two months,following this event. seizure susceptibility was evaluated against electroconvulsions and pentylenetetrazol-induced seizures. methods experiments were conducted on 34 rats surviving cardiac arrest and 34 sham-operated animals which also had surgery but their hearts were not stopped. the threshold for electroconvulsions and pentylenetetrazol was calculated in 3 groups of 5-6 rats. the endpoint for electroconvulsions was the tonic hindlimb extension and for pentylenetetrazol-generalized clonic seizure. results the results indicate that cardiac arrest did not modify the threshold for electroconvulsions either one or two months,following the surgery. on the other hand,a significant reduction in the seizure threshold for pentylenetetrazol was noted one month after cardiac arrest. the median convulsive dose of pentylenetetrazol was decreased from 52.47 mg/kg (sham-operated rats) to 34.03 mg/kg of the convulsant for the induction of clonic seizure activity. this effect was not observed at two months after cardiac arrest. conclusions it is evident that global brain ischemia is associated with a transient reduction in the convulsive threshold for pentylenetetrazol whilst the threshold for electroconvulsions remains unchanged. © 2014 institute of pharmacology,polish academy of sciences.
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کلیدواژه
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Brain ischemia; Cardiac arrest; Electroconvulsions; Pentylenetetrazol; Seizures
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آدرس
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department of pathophysiology,medical university of lublin,lublin,poland,department of physiopathology,institute of rural health,lublin, Poland, laboratory of ischemic and neurodegenerative brain research,mossakowski medical research centre,polish academy of sciences,warszawa, Poland, isobolographic analysis laboratory,institute of rural health,lublin, Poland, department of pathophysiology,medical university of lublin,lublin,poland,isobolographic analysis laboratory,institute of rural health,lublin, Poland, laboratory of ischemic and neurodegenerative brain research,mossakowski medical research centre,polish academy of sciences,warszawa, Poland, department of pathophysiology,medical university of lublin,lublin,poland,department of physiopathology,institute of rural health,lublin, Poland, laboratory of ischemic and neurodegenerative brain research,mossakowski medical research centre,polish academy of sciences,warszawa, Poland
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Authors
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