地高辛抗血清对大鼠心肌缺氧复氧损伤心功能的影响及机制研究  

Effects and mechanism of anti-digoxin antiserum on heart function in myocardial anoxia-reoxygenation injury in rats

作　　者：汪和贵[1] 柯永胜[1] 王德国[1] 杨尚印[1] 

机构地区：[1]皖南医学院弋矶山医院心内科,安徽芜湖241001

出　　处：《中国药理学通报》2007年第5期662-666,共5页Chinese Pharmacological Bulletin

基　　金：安徽省自然科学基金资助项目(No01043902050430707)

摘　　要：目的研究内洋地黄素特异性拮抗剂地高辛抗血清对大鼠心肌缺氧复氧损伤心功能的影响及其作用机制。方法制备离体大鼠心肌缺氧复氧损伤模型,60只SD大鼠随机分为6组,每组10只。对照组,缺氧复氧组,维拉帕米组,小剂量、中剂量、高剂量地高辛抗血清组。连续纪录各组ECG、HR、LVDP、±dp/dtmax。各组于复氧结束后测定心肌组织中内洋地黄素水平、线粒体内Ca2+含量和冠脉流出液中NO含量。电镜观察心肌线粒体及血管内皮细胞结构的变化。结果缺氧复氧组心肌组织内洋地黄素水平升高,线粒体内Ca2+含量升高,NO含量降低,心肌线粒体及内皮细胞明显损伤,心功能明显受抑制。中、高剂量地高辛抗血清能降低心肌组织内洋地黄素水平和线粒体内Ca2+含量,升高NO含量,减轻缺氧复氧所致的心肌线粒体及内皮细胞的损伤,改善心肌收缩和舒张功能。结论地高辛抗血清抑制心肌缺氧复氧损伤所致的心功能减弱,其机制可能与拮抗内洋地黄素,减轻线粒体内Ca2+超载,升高NO浓度,保护了线粒体及内皮细胞功能有关。Aim To investigate effects and the mechanism of endoxin special antagonist anti-digoxin antiserum on heart function in myocardial anoxia-reoxygenation injury in rats. Methods The isolated Langendorff perfused rat heart model was established. Sixty Sprague Dawley（SD） rats were randomly divided into six groups and each group had 10 rats： control group, anoxia-reoxygenation group, verapamil group, low, middle, high dose anti-digoxin antiserum groups. ECG, HR, LVDP and ± dp/dtmax were continuously recorded. The endoxin levels and intramitochondrial Ca^2＋ contents in myocardial tissues and nitric oxide （NO） contents in coronary artery fluence were measured after reoxygenation. Structures of mitochondrial and endothelial cells were observed by microscope. Results The anoxia-reoxygenation group showed a remarkable increase in endoxin level and intramitochondrial Ca^2＋ content, an obvious decrease NO content, an obvious injury of mitochondrial and endothelial cell, an obvious inhibition of heart function. Middle, high dose of anti-digoxin antiserum group could remarkably decrease endoxin level and intramitochondrial Ca^2＋ content; increase NO content; obviously relieve the injury of mitochondrial and endothelial cells; remarkably improve the discovery of heart function. Conclusion Anti-digoxin antiserum could inhibit the failure of heart function induced by myocardial anoxia-reoxygenation injury. Its mechanism may be related to antagonize endoxin, relieve mitochondrial Ca^2＋ overload, increase NO contents, and protect the function of mitochondrial and endothelial cells.

关 键 词：内洋地黄素 地高辛抗血清 缺氧复氧/心肌 一氧化氮 心功能 

分 类 号：R-332[医药卫生] R322.11