Tomabechi M, Sako K, Yonemasu Y
Department of Neurosurgery, Asahikawa Medical College, Hokkaido Japan.
Neurol Med Chir (Tokyo). 1994 Feb;34(2):76-80. doi: 10.2176/nmc.34.76.
The distribution of exogenous 45Ca in the focal ischemia rat model (middle cerebral artery occlusion) was studied using 45Ca autoradiography. High 45Ca accumulations were observed in the frontal cortex and caudate-putamen corresponding with morphological damage shown by HE staining. Regional 45Ca concentrations were calculated from the optical density on the 45Ca autoradiograms. Rapid uptake of 45Ca in the ischemic brain occurred during the first 5 hours, and continued more slowly between 5 and 24 hours after ischemia. The area of 45Ca accumulation was also expanded between 5 and 24 hours. An area of low 45Ca concentration around the area of high accumulation developed 5 hours after ischemia, which presumably accumulated 45Ca between 5 and 24 hours after ischemia. The lower concentration of 45Ca in the periphery of ischemia may result from: 1) a decrease in the total amount of calcium due to narrowing of extracellular space accompanied by cytotoxic edema, and 2) delayed accumulation of exogenous 45Ca due to reduced clearance of extracellular fluid.
利用⁴⁵Ca放射自显影技术研究了局灶性缺血大鼠模型（大脑中动脉闭塞）中外源性⁴⁵Ca的分布情况。在额叶皮质和尾状核 - 壳核观察到⁴⁵Ca的高积累，这与苏木精 - 伊红（HE）染色显示的形态学损伤相对应。根据⁴⁵Ca放射自显影片上的光密度计算局部⁴⁵Ca浓度。缺血脑中⁴⁵Ca在最初5小时内快速摄取，并在缺血后5至24小时之间以较慢速度持续摄取。⁴⁵Ca积累区域在5至24小时之间也有所扩大。缺血5小时后，在高积累区域周围出现了一个⁴⁵Ca浓度较低的区域，该区域可能在缺血后5至24小时积累了⁴⁵Ca。缺血周边区域较低的⁴⁵Ca浓度可能是由于：1）细胞毒性水肿伴随细胞外间隙变窄导致钙总量减少，以及2）细胞外液清除减少导致外源性⁴⁵Ca积累延迟。
