肥厚型心肌病患者左室心肌收缩期应变率的速度向量成像定量分析

目的:应用速度向量成像(VVI)技术,探讨肥厚型心肌病(HCM)患者左室心肌收缩期应变(ε)、应变率(SR)的改变.方法:选取20例室间隔肥厚的HCM患者和20例年龄配对的健康志愿者,在VVI模式下,分别取心尖四腔、三腔和二腔切面,分析左室18个室壁节段的ε和SR曲线,测量收缩期峰值.结果:对照组左室心肌收缩期SR值为(-1.06±0.09)/s,HCM组为(-0.74±0.16)/s,HCM组左室心肌各节段收缩期SR较对照组明显减低,差异有统计学意义(P<0.05).HCM组各节段收缩期SR减低不仅仅限于肥厚部位,也存在于非肥厚部位.结论:HCM患者左室心肌收缩期ε和SR明显低于对照组,HCM患者收缩期ε和SR的减低不仅限于肥厚部位.     

Panax notoginseng saponins inhibit ischemia-induced apoptosis by activating PI3K/Akt pathway in cardiomyocytes

Aim of this study

The panax notoginseng saponins (PNS) have been clinically used for the treatment of cardiovascular diseases and stroke in China. Evidences demonstrated that PNS could protect cardiomyocytes from injury induced by ischemia, but the underlying molecular mechanisms of this protective effect are still unclear. This study was aimed to investigate the protective effect and potential molecular mechanisms of PNS on apoptosis in H9c2 cells in vitro and rat myocardial ischemia injury model in vivo.

Materials and methods

H9c2 cells subjected to serum, glucose and oxygen deprivation (SGOD) were used as in vitro models and SD rats subjected to left anterior descending (LAD) coronary artery ligation were used as in vivo models. The anti-apoptotic effect of PNS was evaluated by Annexin V/PI analysis or TUNEL assay. Mitochondrial membrane potential (Δψm) was detected by JC-1 analysis. The expression of Akt and phosphorylated Akt (p-Akt) were detected by western blot assay.

Results

PNS exhibited anti-apoptotic effect both in H9c2 cells and in ischemic myocardial tissues. However, the effect was blocked in vitro by LY294002, a specific PI3K inhibitor. The anti-apoptotic effect of PNS was mediated by stabilizing Δψm in H9c2 cells. Furthermore the indices of the left ventricular ejection fractions (EF), left ventricular fractional shortening (FS), left ventricular dimensions at end diastole (LVDd) and left ventricular dimensions at end systole (LVDs) suggested that PNS improved rats cardiac function. PNS significantly increased p-Akt both in H9c2 cells and in ischemic myocardial tissues and this effect was also blocked by LY294002 in H9c2 cells.

Conclusion

Results of this study suggested that PNS could protect myocardial cells from apoptosis induced by ischemia in both the in vitro and in vivo models through activating PI3K/Akt signaling pathway.