Objectives To observe the protective effects of left ventricular function in diabetic cardiomyopathy rats after delivery of acidic fibroblast growth factor (aFGF) to myocardium by using ultrasound-targeted microbubble destruction (UTMD) and investigate the possible therapeutic mechanism.
Methods Twenty-four rats were induced to be DCM model by streptozotocin through intraperitoneal injecting and were randomly divided into the DCM group and the aFGF therapy group, and twelve normal rats were included as normal control group in the study. The aFGF therapy group animals were infused with SonoVue-aFGF mixed fluids through tail vein and simultaneous using UTMD. Four weeks after intervention, all rats underwent the cardiac catheter exam to obtaine the left ventricular contraction end pressure (LVESP), left ventricular end-diastolic pressure (LVEDP) and the maximal rate of pressure increase/decrease (± dp/dtmax). At last, myocardial tissue of all rats were stained with immunohistochemistry to quantify myocardial microvascular density, improved Masson staining of collagen to determination the myocardial collagen volume fraction (CVF), TUNEL method to detect the myocardial tissue apoptosis index (AI).
Results Four weeks after intervention, the LVESP and LV ± dp/dtmax in the aFGF therapy group were significantly increased than in DCM group (P < 0.01), and the LVEDP in the aFGF therapy group were significantly lower than in the DCM group (P <0.01). The MVD in the aFGF therapy group were significantly increased than in DCM group (P < 0.01), but the CVF and AI in the aFGF therapy group were significantly lower than in the DCM group (P < 0.01).
Conclusions Delivery of aFGF to diabetic myocardium by using UTMD could improve the left ventricular function and may be a new feasible therapeutic method for DCM.