论文部分内容阅读
目的研究内洋地黄素在离体大鼠心脏缺氧复氧损伤中的变化,观察内洋地黄素特异性拮抗剂地高辛抗血清对大鼠心脏缺氧复氧损伤的保护作用,明确内洋地黄素在心脏缺氧复氧损伤中的作用与机制。方法制备离体大鼠心脏缺氧复氧损伤模型,SD大鼠随机分为6组(n=10):正常对照组,缺氧复氧损伤组,维拉帕米组,小剂量、中剂量、大剂量地高辛抗血清组。连续记录各组心外膜ECG、HR、LVDP、±dp/dtmax。各组于复氧灌流结束时,取左心室心肌组织测定心肌匀浆中内洋地黄素含量、MDA含量、细胞膜Na+K+ATP酶活性以及线粒体内Ca2+水平。结果缺氧复氧损伤组ECG表现为ST段显著抬高,心率减慢,LVDP和±dp/dtmax显著降低,于复氧灌流早期出现严重室性心律失常;心肌组织内洋地黄素水平和MDA含量明显升高,细胞膜Na+K+ATP酶活性明显下降,线粒体内Ca2+水平显著升高。中、大剂量地高辛抗血清能明显降低心肌组织内洋地黄素水平和MDA含量,恢复心肌细胞膜Na+K+ATP酶活性,降低线粒体内Ca2+水平,改善心肌缺血性ST段抬高,显著改善血流动力学,拮抗再灌注引起的室性心律失常。结论地高辛抗血清通过拮抗内洋地黄素,恢复心肌细胞膜Na+K+ATP酶活性,减轻细胞内Ca2+超载,对缺氧复氧损伤心肌有明显的保护作用。表明内洋地黄素是介导心肌缺氧复氧损伤的重要?
Objective To study the changes of endoxin in the anoxia-reoxygenation injury in isolated rat hearts and to observe the protective effect of digoxin antiserum specific to endoxin on rat heart anoxia-reoxygenation injury Effect and mechanism of digitalis on cardiac hypoxia and reoxygenation injury. Methods The isolated rat heart model of hypoxia-reoxygenation injury was established. The SD rats were randomly divided into 6 groups (n = 10): normal control group, hypoxia-reoxygenation injury group, verapamil group, , High-dose digoxin antiserum group. The epicardial ECG, HR, LVDP, ± dp / dtmax were recorded continuously. At the end of reperfusion perfusion, the content of endoxin, MDA, membrane Na + K + ATPase activity and mitochondrial Ca2 + level in myocardium homogenate were measured by left ventricular myocardial tissue. Results In hypoxia-reoxygenation injury group, the ECG showed significant elevation of ST segment, slow heart rate, significant decrease of LVDP and ± dp / dtmax, serious ventricular arrhythmias in early reperfusion perfusion; The content of Na + K + ATPase obviously decreased and the level of Ca2 + in mitochondria increased significantly. Medium and high doses of digoxin antiserum can significantly reduce the level of endoxin and myocardial MDA content, restore myocardial cell membrane Na + K + ATPase activity, reduce mitochondrial Ca2 + levels, improve myocardial ischemic ST segment elevation, Significantly improves hemodynamics and antagonizes ventricular arrhythmias caused by reperfusion. Conclusion Digoxin antiserum can antagonize endoxin and restore the activity of Na + K + ATPase in myocardial cell membrane, and reduce the overload of intracellular Ca2 +, which has a significant protective effect on myocardium induced by hypoxia-reoxygenation. That endoxin is mediated myocardial hypoxia reoxygenation injury important?