地高辛抗血清拮抗内洋地黄素介导的脑缺血再灌注损伤的实验研究

目的　观察脑缺血再灌注损伤时血清和脑组织内洋地黄素水平变化和内洋地黄素拮抗剂地高辛抗血清对脑缺血再灌注损伤的干预作用。方法　采用Kameyama’s的三动脉夹闭法制作双侧大脑半球缺血模型。SD大鼠 5 6只 ,随机分成 7组 ,每组 8只。假手术组 ,缺血再灌注模型组 ,阴性对照组 ,尼莫地平组 ,小剂量、中剂量、大剂量地高辛抗血清组。各组于再灌注 6 0min后取血分离血清 ,同时断头取脑制作脑匀浆和光镜标本。结果　脑缺血再灌注时 ,血清CK活性增高 ;脑组织SOD活性下降 ,MDA水平升高 ;脑组织和血清内洋地黄素水平明显升高 ;脑组织ATP酶活性下降 ;脑线粒体内总Ca2 + 水平升高 ,Mg2 + 水平下降 ;脑组织存在炎症性改变和片状坏死区 ,细胞层次不清 ,锥体细胞形态异常。地高辛抗血清能降低血清CK活性 ;拮抗缺血再灌注所致的脑组织SOD活性下降和MDA水平的升高 ;能降低脑组织内洋地黄素水平 ;大、中剂量地高辛抗血清组能明显提高脑组织ATP酶活性 ,拮抗缺血再灌注所致的脑组织线粒体内离子水平的异常 ;能减轻神经元细胞变性。结论　脑缺血再灌注时脑组织内洋地黄素水平升高 ,增高的内洋地黄素是介导脑缺血再灌注损伤的重要因子。地高辛抗血清通过拮抗内洋地黄素的作用而减轻脑损伤 ,对脑缺血再灌注损伤有防治作用

Anti-digoxin antiserum antagonized cerebral ischemic-reperfusion injury induced by endoxin

AIM To evaluate the changes of serum and brain tissue endoxin in model of bilateral cerebral hemisphere ischemic reperfusion injury, and effect of anti digoxin antiserum (an antagonist of endoxin). METHODS The bilateral cerebral hemisphere ischemic model was prepared by ligating three vascular by Kameyama's manner. SD rats were randomly divided into 7 groups and each group had 8 rats. Sham group, ischemic reperfusion group, negative control group, nimodipine group, low concentration anti digoxin antiserum group, middle concentration anti digoxin antiserum group, high concentration anti digoxin antiserum group. The blood was collected at the end of reperfusion, meanwhile rats were killed, and the bilateral cerebral hemisphere were took out and used to prepare encephlon homogenate and made into samples of light microscope. RESULTS Compared with sham group, the serum CK content increased; Brain tissue SOD activity reduced and MDA content increased importantly in ischemia reperfusion group; The levels of serum and brain tissue endoxin in ischemia reperfusion group were significantly higher, while ATPase activity in brain tissue decreased; Mitochondrial Ca 2+ content in brain tissue increased significantly and Mg 2+ content decreased significantly. In brain tissue,there was some inflammatory change and local necrosis;The rank order and structure of cell wasn't clear;The morphology of pyramidal cell was abnormal. Compared with ischemic reperfusion group, Anti digoxin antiserum reduced serum CK content; It antagonized lowering of SOD activity and increase of MDA content in brain tissue; It remarkably reduced the level of brain tissue endoxin; It reduced abnormal ion content of brain tissue mitochondrion induced by cerebral ischemic reperfusion injury; The high and middle concentration anti digoxin antiserum had a significant effect on raising brain tissue ATPase activity. It reduced neuron denaturation. CONCLUSION Cerebral ischemic reperfusion can increase the level of brain tissue and serum endoxin and higher endoxin can promote brain injury. Endoxin is a major factor involved in cerebral ischemic reperfusion injury. Anti digoxin antiserum can reduce brain tissue injury and had a protective and treatment effect on cerebral ischemic reperfusion injury by antagonizing the effect of endoxin.