Simon R P, Griffiths T, Evans M C, Swan J H, Meldrum B S
J Cereb Blood Flow Metab. 1984 Sep;4(3):350-61. doi: 10.1038/jcbfm.1984.52.
Light and electron microscopy has been used to study the cytopathological changes in the rat hippocampus directly after a 30-min period of forebrain ischemia and after 30 or 120 min of reperfusion. The fine structural localization of calcium has been demonstrated using the oxalate/pyroantimonate procedure. Cellular changes considered typical of ischemia (swelling of astrocytic processes, distention of mitochondria, condensation of cytoplasm, "ischemic cell change") are most prominent after 30 min of reperfusion. At this time, dense calcium pyroantimonate deposits are evident in swollen mitochondria in pyramidal and hilar neurons. After 120 min of reperfusion, substantial restitution has occurred; most mitochondria appear normal and there are few calcium deposits. However, a small number of selectively vulnerable neurons (hilar and pyramidal neurons) show dense condensation (ischemic cell change) with multiple vacuoles containing calcium deposits. The role of excessive calcium entry and mitochondrial calcium overload during the reperfusion period in determining the death of selectively vulnerable neurons is discussed.
利用光镜和电镜研究了大鼠前脑缺血30分钟后以及再灌注30或120分钟后海马体的细胞病理学变化。采用草酸盐/焦锑酸盐法证实了钙的精细结构定位。被认为是典型缺血性的细胞变化(星形细胞突起肿胀、线粒体扩张、细胞质浓缩、“缺血性细胞变化”)在再灌注30分钟后最为明显。此时,在锥体细胞和门区神经元肿胀的线粒体中可见致密的焦锑酸钙沉积。再灌注120分钟后,已发生实质性恢复;大多数线粒体看起来正常,钙沉积很少。然而,少数选择性易损神经元(门区和锥体细胞)显示出致密浓缩(缺血性细胞变化),伴有多个含有钙沉积的空泡。文中讨论了再灌注期钙过度内流和线粒体钙超载在决定选择性易损神经元死亡中的作用。