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作 者:魏岚[1] 王玲[1] 欧阳雪松 王正荣[1] 刘柏林[1]
出 处:《中国应用生理学杂志》1999年第1期8-11,共4页Chinese Journal of Applied Physiology
基 金:国家自然科学基金
摘 要:目的和方法:本文通过DOCA硅胶管皮下埋入法建立大鼠心力衰竭模型,比较正常与心衰大鼠心肌收缩力的变化。采用RNAslotblot杂交从基因转录水平检测正常与心衰大鼠心肌组织中心肌收缩蛋白分子基因αcardiacactin与αMHC表达的变化。结果:(1)心衰大鼠心肌收缩力较正常大鼠明显降低;(2)心衰大鼠与正常大鼠相比,心肌收缩蛋白分子基因αcardiacactin表达水平未见有统计学意义的变化,而αMHC表达水平呈显著降低(下降21.30%,P<0.05);(3)αMHCmRNA的含量与心肌收缩力的大小存在线性正相关(r=0.4143,n=43,P<0.05)。结论:αMHC基因表达水平的下降是心衰时心肌收缩力减退的主要分子基础之一。Aim and Mcthods: The animal model of heart failure was set up by means of deoxycorticosterone acetate impregnated silicone rubber implants in Wistar rats. Cardiac contractility in normal and heart failure rats were examined, and gene expression of its myocardial contractile protein, α cardiac actin and α MHC,were quantitatively analyzed at gene transcription level by using RNA slot blot hybridization. Results: (1) The cardiac contractility in the heart failure rats was lower than that in the normal. (2)There was no significant difference in α cardiac actin mRNA levels between normal and failing rat heart, while α MHC mRNA levels in the failing rat heart was significantly lower than that in the normal rat heart (21.30%, P <0.05).(3) The regressive analysis shows that cardiac contractility is positively correlated with the gene expression of its myocardial contractile protein, α MHC,( r =0.4143, n =43, P <0.05). Conclusion:The above results indicated that the gene expression level of α MHC is one of the key molecular basis for determining the cardiac contractility.
分 类 号:R541.6[医药卫生—心血管疾病] R337.2[医药卫生—内科学]
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