Dudra-Jastrzębska Monika, Ułamek-Kozioł Marzena, Andres-Mach Marta, Łuszczki Jarogniew J, Januszewski Sławomir, Czuczwar Stanisław J, Pluta Ryszard
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.
Pharmacol Rep. 2015 Jun;67(3):417-20. doi: 10.1016/j.pharep.2014.10.022. Epub 2014 Nov 18.
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.
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.
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.
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.
实验数据表明,心脏骤停及随后的全脑缺血存活大鼠会诱发对听源性惊厥的易感性。本研究旨在探究大鼠心脏骤停是否会在该事件发生后的1个月和2个月长期内影响惊厥易感性。通过电惊厥和戊四氮诱导惊厥来评估惊厥易感性。
对34只心脏骤停存活大鼠和34只假手术动物进行实验,假手术动物也接受了手术,但心脏未停跳。在每组5 - 6只大鼠的3组中计算电惊厥和戊四氮的阈值。电惊厥的终点是强直性后肢伸展,戊四氮的终点是全身性阵挛性惊厥。
结果表明,心脏骤停在手术后1个月或2个月均未改变电惊厥阈值。另一方面,心脏骤停1个月后,戊四氮惊厥阈值显著降低。戊四氮的半数惊厥剂量从52.47mg/kg(假手术大鼠)降至34.03mg/kg以诱导阵挛性惊厥活动。心脏骤停2个月后未观察到这种效应。
显然,全脑缺血与戊四氮惊厥阈值的短暂降低有关,而电惊厥阈值保持不变。