Wallenstein M C, Bito L Z
Electroencephalogr Clin Neurophysiol. 1979 Jan;46(1):106-9. doi: 10.1016/0013-4694(79)90055-5.
Suprafusion of 125 microliter 6% KCl solution over the visual cortex of rabbits 2-24 h after they suffered a prostaglandin (PG) E1-induced epileptic seizure was found to cause a recurrence of seizure activity. The initial seizure was induced by the cortical suprafusion of PGE1 over the left visual cortex of PG transport inhibitor-pretreated rabbits. Control animals that were not pretreated with PG transport inhibitors (bromcresol green or probenecid), or received suprafusion of saline or PGF2 alpha rather than PGE1, did not show initial seizure activity. In these animals, and in animals that had PG-induced seizures 72 h before KCl administration, the KCl solution caused only inhibition of the visually evoked response but no seizure activity. The results are interpreted to indicate that under appropriate conditions PGE1 can create a latent epileptogenic focus which can be reactivated by KCl. It is suggested that since PGE1 is produced by the brain normally, and in increased amounts as the result of overstimulation, irritation or trauma, this potent autacoid may play a role in the spontaneous development of latent epileptogenic foci or the recurrence of epileptic seizures.
在前列腺素(PG)E1诱导的癫痫发作后2至24小时,对兔视觉皮层超灌注125微升6%氯化钾溶液,发现会导致癫痫活动复发。最初的癫痫发作是通过对经PG转运抑制剂预处理的兔左侧视觉皮层超灌注PGE1诱导的。未用PG转运抑制剂(溴甲酚绿或丙磺舒)预处理、或接受盐水或PGF2α而非PGE1超灌注的对照动物,未表现出初始癫痫活动。在这些动物以及在给予氯化钾前72小时有PG诱导癫痫发作的动物中,氯化钾溶液仅引起视觉诱发电位的抑制,而无癫痫活动。结果被解释为表明在适当条件下,PGE1可产生一个潜在的致痫灶,该致痫灶可被氯化钾重新激活。有人提出,由于PGE1通常由脑产生,且在过度刺激、刺激或创伤后产量增加,这种强效自分泌物质可能在潜在致痫灶的自发形成或癫痫发作复发中起作用。