急慢性脑血管痉挛发生机制的研究。

K Jiang
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引用次数: 0

摘要

采用放射免疫法、荧光显微镜、透射电镜对前列腺素(PG)、脂质过氧化(LPO)及超微结构进行了研究。新鲜动脉血(成像急性痉挛)引起基底动脉痉挛强烈(+ + +)和血管壁空泡恶化,但6-酮- pgf1 α和TXB2、PGE2和LPO没有变化。培养动脉血(表现慢性痉挛)也明显引起基底动脉痉挛(+ + +)。血管壁空泡恶化,6-酮- pgf1 α水平明显降低(P < 0.01), LPO含量显著升高(P < 0.01), TXB2和PGE α水平无明显变化。提示急性痉挛与慢性痉挛发生机制不同。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[The study of occurrence mechanism in acute and chronic cerebral vasospasm].

Using radioimmunoassay, fluorescence and transmittal++ electronmicroscopy, we studied the of prostaglandin(PG), lipid peroxidation(LPO) and ultrastructure. Fresh arterial blood (imaging acute spasm) produced basilar arterial spasm strongly(+ + +) and vacuole deterioration in vascular walls but there were no changes in 6-keto-PGF1 alpha and TXB2 and PGE2 and LPO. Incubated arterial blood (imaging chronic spasm) produced basilar arterial spasm markedly (+ + +) also. Vacuole deterioration in vascular walls either, and decreased the level of 6-keto-PGF1 alpha apparently (P < 0.01) and elevated the content of LPO significantly (P < 0.01) and there were no changes in the level of TXB2 and PGE alpha. This experiment suggests that the mechanism of acute spasm and chronic spasm is different.

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