Ito U, Ohno K, Suganuma Y, Suzuki K, Inaba Y
Stroke. 1980 Mar-Apr;11(2):166-72. doi: 10.1161/01.str.11.2.166.
Mongolian gerbils were observed for the effects of beta-methasone on ischemic brain edema which developed during ischemia or after blood flow restoration. The severity of brain edema was determined by measuring water content of the ischemic cerebral hemisphere, using the wet and dry methods. Sodium and potassium ions were extracted from homogenized brains with 0.75N HNO2 and ion concentration measured by flame photometry. Passage of RISA from blood into the cerebral parenchyma, as an indicator of blood-brain barrier change, was determined with a gamma-scintillation counter. In the cytotoxic edema model, animals were killed after 9 h permanent ischemia or 3 h after 1 h ischemia. In the simultaneous cytotoxic and vasogenic edema model, the animals were killed either 20 h or 3 days following 1 h ischemia, or 3 h after blood flow restoration following 6 h ischemia. Steroid treatment was ineffective in ischemic brain edema of the cytotoxic or vasogenic type.
观察了蒙古沙鼠中倍他米松对缺血期间或血流恢复后发生的缺血性脑水肿的影响。脑水肿的严重程度通过采用干湿法测量缺血性脑半球的含水量来确定。用0.75N HNO₂从匀浆脑中提取钠和钾离子，并用火焰光度法测量离子浓度。用γ闪烁计数器测定作为血脑屏障变化指标的放射性碘血清白蛋白（RISA）从血液进入脑实质的情况。在细胞毒性水肿模型中，动物在永久性缺血9小时后或缺血1小时后3小时处死。在同时存在细胞毒性和血管源性水肿的模型中，动物在缺血1小时后20小时或3天处死，或在缺血6小时后血流恢复3小时后处死。类固醇治疗对细胞毒性或血管源性缺血性脑水肿无效。
