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用ＮＡＤＰＨｄ 组织化学和电镜技术研究了汉防己碱（Ｔｅｔ）对大鼠缺血再灌流脑一氧化氮合酶（ＮＯＳ）活性及超微结构变化的作用。结果发现，缺血１５ ｍ ｉｎ，再灌流２ ｈ 后，海马超微结构出现明显的病理学损害，主要包括核周出现髓鞘样变，核周间隙增大，胞核均质化，大量片状软化灶，毛细血管周围水肿。Ｔｅｔ １０ 和２０ｍ ｇ／ｋｇ 缺血前３０ ｍ ｉｎ 腹腔注射可明显改善或避免出现上述缺血组织学改变。缺血１５ ｍ ｉｎ，再灌流２４ ｈ 后，皮层和海马ＮＯＳ阳性细胞数目显著增多，Ｔｅｔ５，１０ 和１５ ｍ ｇ／ｋｇ 缺血前３０ ｍ ｉｎ 腹腔注射，浓度依赖地抑制缺血再灌流所致的ＮＯＳ阳性细胞数目增加。这些结果提示，Ｔｅｔ可抑制缺血再灌流脑ＮＯＳ活性，减少ＮＯ产生，这可能与Ｔｅｔ减轻脑缺血再灌流的损害有关。
The effect of tetrandrine on the activity of NOS and the ultrastructure of cerebral ischemia-reperfusion injury were studied by NADPH-d histochemistry and electron microscopy. The results showed that the ultrastructure of the hippocampus showed obvious pathological damage after 15 min of ischemia and 2 h of reperfusion, including mainly myelin-like changes in the peri-nucleus, increased perinuclear space, homogenization of nuclei, Softening the shape of the capillary around the edema. Intraperitoneal injection of Tet 10 and 20 m g / kg 30 min before ischemia significantly improved or prevented the above ischemic histological changes. The number of NOS positive cells in cortex and hippocampus increased significantly after ischemia 15 min and reperfusion for 24 h. Tet5, 10 and 15 m g / kg were injected intraperitoneally 30 min before ischemia in a concentration-dependent manner to inhibit ischemia-reperfusion The number of NOS positive cells increased. These results suggest that Tet can inhibit cerebral NOS activity and reduce NO production after ischemia-reperfusion, which may be related to the protection of Tet against ischemia-reperfusion injury.