Conclusion: These preliminary results indicate that the eligible weak steady DC EFs applied on the surface of infracted myocardium induces angiogenesis and possibly collateral circulation in infracted myocardium, thereby protecting the myocardium. AS-163 KMUP-3 Attenuates Ventricular Remodeling after Myocardial Infarction through eNOS Enhancement and Restoration of MMP-9/TIMP-1 Balance. Chung-Pin Liu 1 , Jwu-Lai Yeh 2 , Bin-Nan Wu 2 , Chee-Yin Chai 2 , Ing-Jun Chen 2 , Wen-Ter Lai 2 . 1 Yuan’s General hospital, Kaohsiung, Taiwan; 2 Kaohsiung Medical University, Kaohsiung, Taiwan. Background: Previously, 7-[2-[4-(4-Nitrobenzene)piperazinyl]ethyl]- 1,3-dimethylxanthine (KMUP-3) has been shown to induce aortic smooth muscle relaxation through KATP channel opening and endo- thelial nitric oxide synthase (eNOS) enhancement. We further investi- gate the cardioprotective effect of KMUP-3 in myocardial infarction (MI) rats. Methods: Wistar rats were randomized into three groups: MI (n = 10), MI + KUMP-3 group (n = 10), and sham group (n = 10). MI was induced by ligation of the left anterior descending coronary artery. After recovery, MI + KMUP-3 group received KMUP-3 (0.3 mg·kg- 1·day-1) infusion for 4 weeks, while MI and sham group received vehicle only. To further confirm the eNOS-dependent activity, KMUP-3 was applied in the culture of transforming growth factor- (TGF-)-stimulated human cardiac fibroblasts (HCFs). Results: KMUP-3 treatment attenuated cardiac hypertrophy with reduced infarction size after MI and improved cardiac output subse- quently. The fibrotic area was reduced by KMUP-3 both in central, peri- and non-infarction area. KMUP-3 enhanced eNOS and tissue inhibitor of metalloproteinase-1 (TIMP-1) expression, with reduction of matrix metalloproteinase-9 (MMP-9) expression in MI rats. In HCFs, the ability of KMUP-3 in reducing MMP-9 and enhancing TIMP-1 expression was blocked by pretreatment with eNOS inhibitor N-nitro-L-arginine methyl ester (L-NAME). Figure 1. Effects of KMUP-3 on left ventricular remodeling (n = 10 per group). (A) Representative echocardiography obtained from each group. Fractional shortening (B) and left ventricular dimension at end of diastole (C) and systole (D) respectively. *P  0.05 versus sham group; # P  0.05 versus MI group. MI, myocardial infarction. Figure 2. Effects of KMUP-3 on myocardial infarction size. (A) Representative images of 2,3,5-triphenyltetrazolium chloride staining. (B Results of quantification of percent of infracted area (n = 10). # P  0.05 versus MI group. MI, myocardial infarction. Figure 3. Effects of KMUP-3 on cardiac fibrosis after MI. (A) Fibrosis stained blue by Masson trichrome in rat hearts. Original magnification, 200. (B) Fibrosis as percentage in the central- infarct area (n = 10). (C) Fibrosis as percentage in the peri-infarct area (n = 10). (D) Fibrosis as percentage in the non-infarct area (n = 10). The size of the bar is 100 um. *P  0.05 versus sham group; # P  0.05 versus MI group. MI, myocardial infarction. Figure 4. Effects of KMUP-3 on levels of MMP-9 (A), TIMP-1 (B) and eNOS (C) protein expression in rat hearts, determined by Western blot analysis and densitometry (n = 9-10). *P  0.05 versus sham group; # P  0.05 versus MI group. eNOS, endothelial nitric oxide synthase; MI, myocardial infarction; MMP-9, matrix metalloproteinase-9; tissue inhibitor of metalloproteinases-1, TIMP-1. 50A The American Journal of Cardiology APRIL 27–29, 2011 ANGIOPLASTY SUMMIT ABSTRACTS/Poster P O S T E R A B S T R A C T S Wednesday, April 27 - Friday April 29, 2011 (Poster Abstract Zone)