Silverstein F, Buchanan K, Johnston M V
Neurosci Lett. 1984 Aug 31;49(3):271-7. doi: 10.1016/0304-3940(84)90301-x.
Exposure of immature rats to 8% oxygen after unilateral carotid artery ligation (UCL) causes metabolic, neurochemical and histopathological changes in the ipsilateral forebrain that resemble those in human perinatal hypoxic-ischemic encephalopathy. Regional cerebral perfusion in this model was examined by visual analysis of India ink trapped in cerebral vessels and measurement of [14C]iodoantipyrine [( 14C]IAP) and [3H]flunitrazepam extraction into the brain. UCL alone reduced [14C]IAP accumulation in the ipsilateral hemisphere by 20% and hypoxia superimposed on UCL progressively reduced ipsilateral hemisphere perfusion by 71% at 2 h. Hypoxia probably injures neurons in this model by causing a critical reduction in cerebral perfusion, an effect which also appears to be important in the human disorder.
对单侧颈动脉结扎（UCL）后的幼鼠暴露于8%的氧气中，会在同侧前脑引起代谢、神经化学和组织病理学变化，这些变化类似于人类围产期缺氧缺血性脑病中的变化。通过对滞留在脑血管中的印度墨水进行视觉分析以及测量[14C]碘安替比林[（14C）IAP]和[3H]氟硝西泮进入脑内的摄取量，来检测该模型中的局部脑灌注情况。单独的UCL使同侧半球中[14C]IAP的积累减少了20%，而叠加在UCL上的缺氧在2小时时使同侧半球灌注逐渐减少了71%。在该模型中，缺氧可能通过导致脑灌注的严重减少来损伤神经元，这种作用在人类疾病中似乎也很重要。
