血小板活化及钙超载在光化学诱导的大鼠血栓性脑损伤中的作用

Role of Platelet Activation and Calcium Overload in Photochemically Induced Ischemic Brain Damage

用光化学诱导大鼠血栓性脑缺血，研究脑血栓形成的组织形态学特点，观察脑皮层微区（２５μｍ２）内钠（Ｎａ＋）、钾（Ｋ＋）、钙（Ｃａ２＋）及镁（Ｍｇ２＋）含量（电子探针显微分析）及全血血小板聚集（阻抗法）的改变并探讨其在脑缺血发病中的作用。结果表明，光化学反应后４ｈ全血血小板聚集明显升高（Ｐ＜０．０５），皮层实质血管内大量血小板堆积；２４ｈ后神经元坏死乃继发于血栓形成所致的脑缺血。缺血区Ｎａ＋、Ｃａ２＋含量增加（Ｐ＜０．０５）不仅是脑缺血时能量衰竭的结果，也是导致脑损伤的重要原因。

photochemical model was established to induce thrombotic cerebral ischemia in rats. Using light and electron microscopy electron probe microanalysis and impedance technique, the features of histopathology and the changes of sodium(Na^+), potassuim(K^+), calcium(Ca^2+) and magnesuim(Mg^2+) content in the microregional cortex(25μm2), and whole blood platelet aggregation were observed before and after cerbral thrombosis. The results showed that whole blood platelet aggregation increased significantly(P<0.05) 4 hours after photochemical reaction. A numerous platelet aggregation within the parenchymal vessels of the right cortex and neuron necrosis may be secondary to the cerebral ischemia caused by thrombosis. The increased Na^+ and Ca^2+ levels during cerebral ischemia are not only the cause of brain damage but also the results of platelet activation and energy failure. 