Dwyer B E, Nishimura R N, Fujikawa D G
Epilepsy Research Laboratory, Veterans Administration Medical Center, Sepulveda, California 91343.
Exp Neurol. 1988 Mar;99(3):772-7. doi: 10.1016/0014-4886(88)90192-6.
We used a model of perinatal hypoxic/ischemic brain damage which combines unilateral common carotid artery ligation and hypoxia (8% O2). Protein synthesis inhibition and cell loss were found in the ipsilateral forebrain of 11-day-old rats when hypoxia was initiated 4 h but not 24 h after carotid ligation. [14C]Iodoantipyrine uptake studies suggest that compensating vascular changes which protect the ipsilateral forebrain occur within 24 h of carotid ligation.
我们使用了一种围产期缺氧/缺血性脑损伤模型,该模型结合了单侧颈总动脉结扎和缺氧(8%氧气)。当在颈动脉结扎后4小时而非24小时开始缺氧时,在11日龄大鼠的同侧前脑发现了蛋白质合成抑制和细胞丢失。[14C]碘安替比林摄取研究表明,在颈动脉结扎后24小时内会出现保护同侧前脑的代偿性血管变化。