GW24-e1365 Effects of renal sympathetic denervation on ventricular remodelling in canine

Objectives To access the therapeutic effects of renal sympathetic denervation (RSD) onpost-myocardial infarction (MI) ventricular remodelling in canine, the most optimal time for treatment, and discuss its possible mechanism. Methods Thirty canines were randomly assigned to RSD1w + MI (MI 1 week after RSD, n = 6), MI1w + RSD(RSD one week after MI, n = 6), MI2w + RSD (RSD two weeks after MI, n = 6), Ngroup (Normal, n = 6), MI group (MI, n = 6). Establishing a canine model of precise acute myocardial infarction by ligating the left anterior descending (LAD) coronary artery, The first three groups of dogs received RSD 1 week before and 1 week, 2 weeks after myocardial infarction. And Blood samples were taken pre-embolization and 4 weeks after embolization, detection of endothelin-1(ET-1) and brain natriuretic peptide (BNP) levels. At the same time, echocardiography was performed to know cardiac function and heart size. Sacrificed all the dogs at end of experiment and the samples of cardiac and renal arteries was obtained. The expression of MMP-2, MMP-9 in the cardiac and the expression of TH in renal arteries were got by immunohistochemistry. Results (1) In MI group, the left ventricular ejection fraction of significantly declined (from 0.57 ± 0.03 to 0.41 ± 0.05, P < 0.05), plasmaBNP (from 27.91 ± 2.81 to 455.67 ± 47.88 pg/ml,P < 0.01), ET-1 (from 52.92 ± 10.53 to 99.47 ± 16.66 pg/ml, P < 0.05) and the expression of MMP-2, MMP-9 in cardiac was elevated; (2) Compared with MI group, the LVEF in RSD1w + MI, MI1w + RSD and MI2w + RSD group was significantly improved, respectively (all P < 0.05); LVEDd was significantly decreased after RSD; IVSd and LVPWd increased after RSD; the level of plasma BNP and ET-1 was significantly declined, and the expression of MMP-2, MMP-9 in cardiac was decreased after RSD; (3) The expression of TH in renal artery decreased after RSD. Conclusions RSD has preventive and therapeutic effects on post-MI heart failure, and its mechanism probably mediate through restraining renal sympathetic nervous activity and decreasing myocardial expression of MMP2, MMP-9.