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作 者:李树清[1]
机构地区:[1]昆明医学院病理生理教研室
出 处:《微循环学杂志》1997年第3期3-5,共3页Chinese Journal of Microcirculation
基 金:国家自然科学基金
摘 要: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 microregional cortex(25μm2), 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.
分 类 号:R743.320.2[医药卫生—神经病学与精神病学]
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