Journal Browser Advanced Search Help
Journal Browser Advanced search HELP
J Korean Child Neurol Soc. 1998 Oct;6(1):47-54. Korean. Original Article.
Choi BJ , Kim YI , Whang KT .
Department of Pediatrics, Catholic University Medical College, Seoul, Korea.
Department of Neurology, Catholic University Medical College, Seoul, Korea.
Abstract

PURPOSE: Nonsteroidal anti-inflammatory drugs inhibit the synthesis of prostaglandin(PG) through inhibition of the enzyme, cyclooxygenase. Some of the arachidonic acid metabolites may influence the spread of electrocortical activity, and delay the pentylenetetrazol(PTZ)-induced seizures. The purpose of the present study was to evaluate systematically the effect of pretreatment with PG synthetase inhibitors on PTZ-induced seizures. METHODS: To evaluate the effects of pretreatment with PG synthetase inhibitors on seizures produced by 30mg/kg, 60mg/kg PTZ, free-moving Sprague-Dawley rats weighing 250-300gm with chronically-implanted supracortical electrodes were used. Electrocorticogram was recorded for 1hr prior to pretreatment administration of either saline (control) or PG synthetase inhibitor and 1hr after administration of PTZ. RESULTS: 1) A 30mg/kg dose of PTZ produced bursts of high voltage activity after a latency of 616+/-72sec. Although the animals showed spontaneous movements throughout the test period, they were motionless or myoclonus. The number of high voltage bursts during the first hr of the test period was 368+/-31.2) A 30mg/kg of PTZ produced high voltage bursts after a latency of 1118+/-35sec which was significantly greater for the ibuprofen-pretreated groups receiving 90mg/kg when compared to the saline-pretreated group. In addition, the number of high voltage bursts(173+/-17) which occurred during the first hr of the test period was significantly smaller than that recorded from the saline-pretreated group. 3) After pretreatment with a 450mg/kg dose of paracetamol, a 30mg/kg of PTZ produced bursts of electrocortical activity with onset latencies of 665+/-112sec which were not significantly different than those recorded from the saline-pretreated group. The number of high voltage bursts during the first hr of the test period was 141+/-30 which was significantly smaller than that recorded from the saline-pretreated group. 4) A 50mg/kg dose of mefenamic acid pretreatment caused 30mg/kg PTZ-induced high voltage bursts after latency of 227+/-47sec which was significantly shorter than that recorded from the saline-pretreated group. The number of high voltage bursts during the first hr of the test period was 522+/-42 which was significantly greater than that recorded from the saline-pretreated group.5) A 60mg/kg dose of PTZ produced bursts of high voltage activity after a latency of 79+/-14sec. An electrocortical seizure with concurrent convulsions appeared subsequently by 129+/-30sec. 6) A 60mg/kg of PTZ produced high voltage bursts after a latency of 217+/-38sec which was significantly greater for the ibuprofen-pretreated groups receiving 90mg/kg when compared to the saline-pretreated group. An electrocortical seizure with concurrent convulsions appeared subsequently by 287+/-30sec.7) After pretreatment with paracetamol(450mg/kg), a 60mg/kg of PTZ produced bursts of electrocortical activity with onset latencies of 143+/-36sec which were significantly different than those recorded from the saline-pretreated group. There was no convulsive or no electrocortical seizure.8) A 50mg/kg mefenamic acid pretreatment caused 60mg/kg PTZ-induced high voltage bursts after latency of 35+/-5sec which was significantly shorter than that recorded from the saline-pretreated group. An electrocortical seizure appeared subsequently by 58+/-10sec which was significantly different than that recorded from the saline-pretreated group. CONCLUSION: It is possible that the delay and/or block of convulsions induced by the higher doses of PTZ was the result of PG synthesis inhibition. However, the PG synthetase inhibitors had a more differential effect on general PTZ-induced excitation of the CNS evidenced by changes in electrocortical activity. The mechanism underlying this action could be either through inhibition of the activity of cyclooxygenase in tissues which play a role in the manifestation of seizure activity or through an action not related to their common action on cyclooxygenase.

Copyright © 2019. Korean Association of Medical Journal Editors.