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作 者:高夏[1] 袁丽娜[2] 苑星[1] 王平凡[1] 孙芳[1] 孟宪慧[1] 张虹妍[1]
机构地区:[1]河南省胸科医院心外科,河南郑州450008 [2]河南省疾病控制中心,河南郑州450003
出 处:《河南医学研究》2010年第4期392-395,共4页Henan Medical Research
基 金:河南省科技厅基础与前沿技术研究项目(092300410109)
摘 要:目的:研究核因子-kB在左心室机械辅助减负荷模型中的表达及其意义,探讨左心室减负荷后,心肌逆向重构的分子机制。方法:选用Lew is大鼠,结扎冠状动脉左前降支诱导心力衰竭,4周后,心力衰竭后的心脏及右肺移植到受体大鼠的腹部(通过供体的升主动脉与受体的降主动脉吻合)。移植两周后,评价心脏重量,左心室重量,心肌细胞直径大小,核因子-kB的表达。结果:心力衰竭后增大的心脏,左心室重量,左心室心肌细胞直径,移植后趋于正常;心力衰竭后左心室核因子-kB的表达明显增高;移植后核因子-kB的表达趋于正常。结论:左心室减负荷后,心肌逆向重构的过程伴随着心肌细胞分子水平的改变如核因子-kB表达的改变,可能与左心室辅助后心脏功能的恢复有关。Objective: To study the expression and significance of nuclear factor-kB in the model of left ventricular mechanical unloading.To explore the molecular mechanism of cardiomyocyte reverse remodel.Methods: Heart failure was induced in Lewis rats by ligating left anterior descending(LAD) artery.After four weeks,the failing hearts and right lungs were heterotopically transplanted into the abdomen of the recipients by anatomizing their ascending aorta to the recipients' abdominal aorta.Two weeks after transplantation,myocardial hypertrophy were detected by pathological studies,as well as nuclear factor-kB of the left ventricle.Results: The increased heart weight,left ventricular weight and myocyte diameter of the failing hearts were decreased to normal after transplantation.The levels of nuclear factor-kB increased significantly after heart failure,and decreased to normal after transplantation.Conclusion: Myocardium reverse remodeling after left ventricular unloading was accompanied by the change of cardiomyocyte in molecular level,such as the change of nuclear factor-kB,which may involved in the improvement heart function after supported by left ventricular assist device.
分 类 号:R54[医药卫生—心血管疾病]
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