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本研究用Ｓ－Ｄ大鼠，在其一侧筛孔（ＥＦ）处切断支配脑血管的副交感神经舒血管神经，看是否能增加该侧大脑中动脉栓塞后脑梗塞的体积。脑梗塞体积的测量在栓塞后２４ｈ由６层切面之和求得。４组动物中除Ｄ组（假手术组）未见到梗塞外，其余３组的（Ａ组为神经切断加大脑中动脉栓塞；Ｂ组为暴露出神经但未切断大脑中动脉栓塞，Ｃ组为单纯大脑中动脉栓塞）梗塞体积（平均数±标准差）分别为（１５３±４２）ｍｍ３、（１４７±４２）ｍｍ３和（１４８±４５）ｍｍ３，方差分析结果，无差别（Ｐ＞０．０５）。同时也没有看到各组间梗塞部位的差别。本研究未能证实副交感神经纤维在脑缺血这一病理生理过程中的作用。
In this study, we used S-D rats to cut off the sympathetic vasodilatory vessels that dominated cerebrovascular vessels at one side of the mesh (EF) to see if they could increase the volume of cerebral infarction after the middle cerebral artery occlusion. Measurement of cerebral infarction volume 24h after embolization obtained by the sum of 6 slices. In the 4 groups of animals, except for group D (sham operation group), no infarction was observed, the other 3 groups (Group A: nerve cut-off plus middle cerebral artery occlusion; Group B: nerve-exposed but not cut-off middle cerebral artery occlusion; Group C Infarct volume (mean ± standard deviation) were (153 ± 42) mm3, (147 ± 42) mm3 and (148 ± 45) mm3, respectively, with no difference in ANOVA (P> 0.05). 05). At the same time, we did not see the difference between the infarction sites in each group. This study failed to confirm the role of parasympathetic nerve fibers in the pathophysiology of cerebral ischemia.