Nikolov R, Milanova D
Methods Find Exp Clin Pharmacol. 1982;4(4):221-8.
The effects of exogenously applied prostaglandin F2 alpha (PGF2 alpha) and prostacyclin (PGI2) on asphyxic anoxia was studied in curarized and artificially ventilated cats. Anoxia was induced by stopping the ventilation and checking the changes in the EcoG. Cortical resistance (CRs) was evaluated as time between stopping the ventilation and the extinction of ECoG. Cortical recovery (CRc) was expressed as time between restitution of ventilation and reappearance of brain activity. Anoxia resistance index (ARI) was defined as the ratio between these two parameters (CRs/CRc). PGF2 alpha was applied by 5 minute i.v. and intracarotid (i.c.) infusion in a dose of 10 micrograms/kg/min, and PGI2 in a dose of 250 ng/kg/min for 15 minutes intracarotidly. The results show that both the i.c. and i.v. infusion with PGF2 alpha led to a significant decrease of CRs and prolongation of CRc resulting in decrease of ARI. The changes are more expressed at i.v. infusion, PGI2 does not improve the ECoG changes evoked by hypoxia. Suggestions for the possible mechanism of PGF2 alpha action and for the failure of PGI2 to protect the brain are made.
在箭毒化并人工通气的猫身上,研究了外源性应用前列腺素F2α(PGF2α)和前列环素(PGI2)对窒息性缺氧的影响。通过停止通气并检查脑电图(EcoG)的变化来诱导缺氧。皮层抵抗(CRs)以停止通气至EcoG消失的时间来评估。皮层恢复(CRc)表示为恢复通气至脑活动重新出现的时间。缺氧抵抗指数(ARI)定义为这两个参数的比值(CRs/CRc)。PGF2α通过静脉内(i.v.)和颈内动脉(i.c.)以10微克/千克/分钟的剂量输注5分钟,PGI2以250纳克/千克/分钟的剂量经颈内动脉输注15分钟。结果表明,PGF2α经颈内动脉和静脉内输注均导致CRs显著降低和CRc延长,从而使ARI降低。静脉内输注时变化更明显,PGI2不能改善缺氧引起的EcoG变化。对PGF2α作用的可能机制以及PGI2未能保护大脑的原因提出了建议。