Nikolov R, Nikolova M
Methods Find Exp Clin Pharmacol. 1982 Aug-Sep;4(6):397-402.
The protective effect of piracetam against PGF2 alpha-impaired cerebral resistance to hypoxia was investigated by EEG study in relaxed and artificially ventilated cats. Asphyxic anoxia was performed after 5 min of intracarotid (i.c.) or i.v. infusion of 10 micrograms/kg/min PGF2 alpha before and 30 min after piracetam (100 mg/kg i.v.). The following parameters were determined: cortical resistance (CRs)--as time between stopping the ventilation and the extinction of EEG; cortical recovery (CRc) - as time between restitution of ventilation and reappearance of brain activity; anoxia resistance index (ARI) - as the ratio between these two parameters (CRs/Crc). Both the i.c. and i.v. infusion of PGF2 alpha led to a significant decrease in CRs and lengthening of CRc which resulted in a decrease in ARI. Piracetam reverses the PGF2 alpha-induced changes in asphyxic anoxia. The possible mechanism of piracetam's effect and the probable therapeutic value of the latter are considered.
通过脑电图研究，在放松且人工通气的猫身上探究了吡拉西坦对PGF2α损害的脑缺氧耐受性的保护作用。在静脉注射（i.v.）或颈内动脉（i.c.）输注10微克/千克/分钟PGF2α 5分钟后，以及在吡拉西坦（100毫克/千克静脉注射）给药前和给药后30分钟进行窒息性缺氧实验。测定了以下参数：皮层耐受性（CRs）——即停止通气至脑电图消失之间的时间；皮层恢复时间（CRc）——即恢复通气至脑活动重新出现之间的时间；缺氧耐受指数（ARI）——即这两个参数的比值（CRs/CRc）。颈内动脉和静脉输注PGF2α均导致CRs显著降低以及CRc延长，进而导致ARI降低。吡拉西坦可逆转PGF2α诱导的窒息性缺氧变化。文中还探讨了吡拉西坦作用的可能机制及其可能的治疗价值。
