内洋地黄素介导脑缺血-再灌注损伤

Endoxin mediated cerebral ischemic-reperfusion injury

目的 观察大鼠脑缺血 再灌注损伤时内洋地黄素水平变化及内洋地黄素拮抗药地高辛抗血清对脑缺血 再灌注损伤的防治作用。方法 采用Kameyama s三动脉夹闭法制作双侧大脑半球缺血模型。缺血 30分钟后再灌注。于再灌注同时 ,尾静脉注射不同剂量内洋地黄素拮抗药地高辛抗血清。再灌注 60分钟后取血分离血清 ,同时断头取脑制作脑匀浆。测定血清CK含量、血清和脑组织内洋地黄素含量以及脑组织ATP酶活性。结果 脑缺血 再灌注时 ,脑组织和血清内洋地黄素水平明显升高 ,血清CK活性显著增高 ,而脑组织ATP酶活性显著下降。地高辛抗血清能显著降低脑组织内洋地黄素水平降低血清CK活性 ,但血清内洋地黄素水平却显著提高 ;大、中剂量地高辛抗血清能明显提高脑组织ATP酶活性。结论 脑缺血再灌注时内洋地黄素水平显著升高 ,内洋地黄素是介导脑缺血 再灌注损伤的重要因子。内洋地黄素拮抗药地高辛抗血清通过拮抗内洋地黄素而减轻脑缺血 再灌注损伤 ,对脑缺血

Objective To evaluate the changes of endoxin during cerebral ischemic reperfusion injury,and the prevention and treatment effect of anti digoxin antiserum(endoxin antagonist)on bilateral cerebral hemisphere ischemic reperfusion inury.Methods The global cerebral ischemic reperfusion model in SD rats was prepared by Kameyamas manner.After ischemia for 30min,reperfusion was established,and different does of anti digoxin antiserum were injected via caudal vein.The blood samples were collected at 60min of reperfusion.The rats were killed,and cerebral hemisphere was removed for preparing homogenate.The levels of serum CK,serum and brain tissue endoxin,brain tissue ATPase activities were examined respectively.Results The levels of serum and brain tissue endoxin in ischemic reperfusion group were significantly higher than those in false operation group,while serum CK activity increased outstandingly,ATPase activity in brain tissue had a significant decrease.Anti digoxin antiserum remarkably decreased the level of brain tissue endoxin and serum CK activity,but made the level of serum endoxin increased significantly.The high and middle concentration of anti digoxin antiserum had a significant effect of raising brain tissue ATPase activity.Conclusion Cerebral ischemic reperfusion could increase the level of brain tissue and serum endoxin.Endoxin is a major factor mediated brain ischemic reperfusion injury.Anti digoxin antiserum can attenuate brain injury and has a protection and treating effect on cerebral ischemic reperfusion injury by antagonizing endoxin. [