Objective: To research the relationship between diaschisis and nitric oxide synthase (NOS)neuron loss, vasoconstriction subsequent to excitotoxin lesion. Methods: Local microinjection of kainic acid into parietal cortex of rats and stained with β-NADPH histochemistry and EA50 histological staining. Results:1 h post-lesion, there was degeneration of NOS neurons and some of non-NOS neurons in bilateral cortex,hippocampus and cerebellar cortex. By 4 h post-lesion, there was a 32%～39% reduction in diameter of microvasculature that was strictly confined to the areas of NOS neuronal degeneration. By 8 h, the NOS nerve terminals become dust-like and lose of nerve fiber density was seen throughout the ipsilateral cortex. Within 1 d, NOS neuronal degeneration was seen in bilateral hippocampus, ipsilateral diencephalons and mesencephalon. 2～5 d post-lesion, concomitant with the NOS containing neurons-degeneration, induced NOS activity was faintly visible in neurons of cerebral cortex and hippocampus, and large number of neurons were lost in CA3 and CA4 subfieds of hippocampus in 7 d post-lesion. Conclusion: These findings suggested that diaschisis is related to excitotoxic death of NOS and non-NOS neurons. The loss of NO contributes to vasoconstriction which is responsible for the reduced blood flow and metabolism in affected regions.%目的研究局部皮质注射海仁酸导致NOS神经元损伤及血管收缩与神经功能联系障碍的关系.方法将微量海仁酸注射到大鼠顶叶,β-NADPH组织化学及EA50组织学染色.结果注射后1 h双侧大脑皮质、海马和小脑皮质均可见NOS神经元和一些非NOS神经元溃变;4 h后NOS阳性神经元损伤区域微血管的直径缩小了32%～39%;8 h后NOS阳性神经末梢溃变呈细颗粒状;1 d后双侧海马和伤侧间脑等部位的NOS神经元溃变;2～5 d后皮质、海马等部位的部分神经元诱导表达NOS活性;7 d后双侧海马CA3和CA4大量神经元丢失.结论神经功能联系障碍与兴奋性神经毒所致的跨突触NOS神经元和非NOS神经元损伤有关,NOS神经元损伤所致的NO减少导致血管收缩,引起受损区域的脑血流减少及代谢功能障碍.
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