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实验性脑缺血时血小板醣化蛋白（ＧＭＰ－１４０）比对照组有显著升高，随缺血时间延长，ＧＭＰ－１４０呈渐进性升高，至缺血２４ｈ有显著下降，但ＴＸＢ２仍然呈升高趋势；缺血急性期的神经元及微血管循环障碍的病理变化与ＧＭＰ－１４０的演变过程有相关性，随水肿及循环障碍改善，ＧＭＰ－１４０显著下降，而ＴＸＢ２２４ｈ后仍然呈增高改变。结果表明急性脑缺血时ＧＭＰ－１４０的升高原因仅可能与血小板激活后的分解有关。它的动态变化趋势与急性循环损害的相关性表明ＧＭＰ－１４０在内皮依赖性血管舒缩障碍中有一定的意义，而ＴＸＢ２则受血小板在内的多种因素影响。
The level of GMP-140 in experimental cerebral ischemia was significantly higher than that in control group. With prolongation of ischemia, GMP-140 increased gradually and reached the level of 24h after ischemia, but TXB2 still increased There was a correlation between the pathological changes of neuronal and microvascular circulatory disorders in acute phase of ischemia and GMP-140. With the improvement of edema and circulatory disturbance, GMP-140 decreased significantly, but still increased after TXB224h. The results show that the cause of elevated GMP-140 in acute cerebral ischemia may only be related to the decomposition after platelet activation. The relationship between its dynamic changes and acute circulatory damage suggests that GMP-140 has some significance in endothelium-dependent vasomotor disorders, while TXB2 is affected by many factors including platelets.