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本实验采用堤式颅窗软脑膜微循环实验方法，利用去甲肾上腺素和α，β－受体阻断剂，研究了交感神经在缺氧性脑血管扩张反应（ＨＣＶ）中的作用。去甲肾上腺素（１０－７ｍｏｌ／Ｌ和１０－６ｍｏｌ／Ｌ）对软脑膜微动脉无明显作用。β－受体阻断剂普萘洛尔（局部用药，下同）对ＨＣＶ无明显影响，而用１０－６ｍｏｌ／Ｌ哌唑嗪阻断软脑膜微动脉α－受体可明显增强ＨＣＶ（由２１．５±９．８％增至３０．６±９．２％，Ｐ＜０．０１）。结果提示，正常情况下交感神经对脑血管影响较小，但在缺氧时，交感神经对脑血管有收缩作用。交感神经可能通过增加其末梢释放去甲肾上腺素，作用于α－受体，限制微劝脉扩张而在缺氧性脑血管扩张反应中起调节作用。
In this study, we used dike cranial window parenchyma microcirculation experimental method, the use of norepinephrine and α, β-blockers to study the role of sympathetic nerve in hypoxic cerebrovascular dilatation (HCV). Norepinephrine (10-7mol / L and 10-6mol / L) had no significant effect on the pia mater arterioles. Propranolol, a β-receptor blocker (topical application, the same below), had no significant effect on HCV, whereas blockade of pial arteriolar α-receptor with 10-6mol / L prazosin markedly increased HCV 21.5 ± 9.8% to 30.6 ± 9.2%, P <0.01). The results suggest that sympathetic nerves have less effect on cerebrovascular under normal conditions, but during hypoxia, sympathetic nerves have a contractile effect on cerebrovascular. Sympathetic nerves may play a regulatory role in hypoxic cerebrovascular dilatation by increasing the release of norepinephrine and acting on the alpha-receptors, limiting the dilation of the dilational pulse.