心梗后心力衰竭大鼠心脏基因表达谱及益气活方对其血流动力学影响的研究

Cardiac Gene Expression Spectrum of the Rat with Heart Failure after Myocardiac Infarction: Effects of the Formula for Benefiting Qi and Activating Blood Circulation on Cardiac Hemodynamics

目的 观察益气活血方对心梗后心力衰竭模型大鼠心脏血流动力学的影响。方法 以大鼠左冠状动脉结扎术造成心梗后心衰模型。对心衰形成 (术后 10d)、稳定 (8周 )二期的大鼠左心室梗塞区、非梗塞区和同期假手术组左心室分别取材并提取总RNA ,以 6张大鼠 4 0S基因芯片 (4 0 96个基因 张芯片 )对其进行检测 ;术后 4周以益气活血方对模型大鼠治疗至 8周 ,以卡托普利作为阳性对照药 ;经阻抗法观察给药前后大鼠心脏功能的变化。结果 ①检测基因表达谱芯片 ,发现心衰模型大鼠心肌有参与能量代谢、心肌细胞骨架及纤维等 13类共千余条表达上调和下调的基因 ,在梗塞区差异表达基因形成期最多 (10 86条 )、稳定期次之 (72 4条 ) ;而非梗塞区为形成期最多 (196条 ) ,稳定期较少 (97条 )。②心梗后心衰大鼠经治疗后心功能明显改善 ,卡托普利组SV(mL 次 )由0 0 96± 0 0 2 6改善为 0 319± 0 0 82 (P <0 0 1) ,CO(mL min)由 4 2 80± 11 0 2变为 136 90± 35 12 (P<0 0 1) ,CI[mL (min·kg) ]由 10 2 34± 31 0 0改善为 2 84 0 9± 6 5 74 (P <0 0 1) ;益气活血组SV由0 0 99± 0 0 30改善为 0 340± 0 0 70 (P <0 0 1)、CO由 4 4 14± 11 90变为 14 1 4 9± 19 36 (P <0 0 1) ,CI由 10 8 2 4±

Objective To observe the cardiac gene expression spectrum of the rat with heart failure after myocardiac infarction (HFMI) and the effects of the formula for benefiting qi and activating blood circulation (FBQABC) on cardiac hemodynamics in the rat model of HFMI. Methods The rat model of HFMI was established by left coronary artery ligation. The total RNA was extracted from the samples of the infarct area and non infarct area of the left ventricle of the rats in the model group and from the samples of the left ventricle of the rats in the sham operation group, respectively, at the heart failure formation stage (10 days after the operation) and the heart failure stable stage (8 weeks after the operation); the extracted total RNA was detected with 6 rat 40S gene chips (4096 genes/a chip). From the 4th weeks after the operation, the rats in the model group were treated with FBQABC until to the 8th week, with captopril as a positive control, and the changes in the rat cardiac function were observed by an impedance method before and after the administration. Results The detection with gene chips showed that there were more than 1000 genes in 13 types, the expressions of which were either up regulated or down regulated, involving energy metabolism, the frame of the cardiac muscle cell and the cardiac muscle fiber; there were 1086 differential expression genes in the infarct area at the heart failure formation stage and 724 differential expression genes at the heart failure stable stage; and there were 196 differential expression genes in the non infarct area at the heart failure formation stage and 97 differential expression genes at the heart failure stable stage. After the treatment of captopril and FBQABC, the SV, CO and CI in the HFMI rats were all improved markedly ( P <0 01). Conclusion The mechanism of FBQABC for treating heart failure in HFMI rats may be its regulating the cardiac energy metabolism related genes, hence, causing the improvement of the cardiac function.