Kostron H, Fischer J
Surg Neurol. 1983 Jul;20(1):48-54. doi: 10.1016/0090-3019(83)90105-2.
The regional, cellular, and subcellular distribution of [3H]dexamethasone in brain edema of rats was studied. Edema was induced either by occlusion of the right carotid artery or by a cold lesion of the right temporal lobe. [3H]dexamethasone (0.3 mCi) was injected intravenously. After 30 minutes (unless otherwise stated) the brains and other desired organs were removed. In the control animals, 51% of the total [3H]dexamethasone activity was found in the cerebral hemispheres (27% in the right, 24% in the left), 24% in the cerebellum, and 24% in the brainstem. Time-course studies revealed a rapid decline of [3H]dexamethasone content in all regions of the brain. After 48 hours of ligation of the right carotid artery, 80% of the [3H]dexamethasone could be found in the cerebral hemispheres (48% in the right, 32% in the left), 10% in the cerebellum, and 9% in the brainstem. In the series in which cold lesions were induced, 74% of the [3H]dexamethasone was recovered in the cerebral hemispheres (40% in the right (lesion), 34% in the left (control]. Before the trauma, 75% of the dexamethasone was found in astrocytes and 25% in neurons; after the trauma, 48% was bound to astrocytes and 42% to neurons. At the subcellular level, accumulation took place in the microsomal, lysosomal, and cytoplasmic fractions of the damaged cells. These data demonstrate an increased uptake of dexamethasone into ischemic damaged brain tissue and into neurons, microsomes, and lysosomes.
研究了[3H]地塞米松在大鼠脑水肿中的区域、细胞及亚细胞分布。通过结扎右颈动脉或右颞叶冷损伤诱导水肿形成。静脉注射[3H]地塞米松（0.3毫居里）。30分钟后（除非另有说明）取出脑及其他所需器官。在对照动物中，[3H]地塞米松总活性的51%存在于大脑半球（右侧27%，左侧24%），24%存在于小脑，24%存在于脑干。时间进程研究显示，脑内所有区域的[3H]地塞米松含量迅速下降。右颈动脉结扎48小时后，80%的[3H]地塞米松可在大脑半球中发现（右侧48%，左侧32%），10%在小脑，9%在脑干。在诱导冷损伤的系列实验中，74%的[3H]地塞米松在大脑半球中回收（右侧（损伤侧）40%，左侧（对照侧）34%）。创伤前，75%的地塞米松存在于星形胶质细胞中，25%存在于神经元中；创伤后，48%与星形胶质细胞结合，42%与神经元结合。在亚细胞水平，受损细胞的微粒体、溶酶体和细胞质部分出现积聚。这些数据表明，地塞米松在缺血性损伤脑组织、神经元、微粒体和溶酶体中的摄取增加。
