Ito U, Ohno K, Nakamura R, Suganuma F, Inaba Y
Stroke. 1979 Sep-Oct;10(5):542-7. doi: 10.1161/01.str.10.5.542.
The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
采用蒙古沙鼠的左脑半球来阐明脑缺血期间以及短暂缺血后脑血流恢复时发生脑水肿的机制。通过组织干燥法测量含水量。用火焰光度法测量钠和钾离子浓度。用γ闪烁计数器测量131I - 白蛋白(RISA)从血液到脑实质的通透情况。我们的研究结果表明,在缺血期间以及脑血流恢复后的短时间内会出现单纯的细胞毒性水肿。由于血脑屏障受损导致血浆成分从血液中漏出而加速的血管源性水肿,在脑血流恢复后出现。缺血少于1小时后,脑血流的恢复显著降低了脑水肿的程度。然而,缺血超过3小时后,脑血流的恢复使脑水肿大大加重。