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SILDENAFIL MEDIATED NEOVASCULARIZATION AND PROTECTION AGAINST MYOCARDIAL ISCHEMIA REPERFUSION INJURY IN RATS: PROBABLE ROLE OF VEGF/ ANGIOPOIETIN-1.

Koneru S, Penumathsa SV, Thirunavukkarasu M, Vidavalur R, Zhan L, Singal PK, Engelman RM, Das DK, Maulik N

Department of Surgery, Molecular Cardiology and Angiogenesis Laboratory, Farmington, CT, USA.

Sildenafil Citrate (SC), a drug for erectile dysfunction, is now emerging as a cardiopulmonary drug. Our study aimed to determine a novel role of sildenafil on cardioprotection through stimulating angiogenesis during ischemia (I) reperfusion (R) at both capillary and arteriolar levels and to examine the role of VEGF and angiopoietin-1 (Ang-1) in this mechanistic effect. Rats divided into: Control sham (CS), Sildenafil sham (SS), Control + IR (CIR) and Sildenafil + IR (SIR). Rats were given 0.7 mg/kg, i.v, SC or saline 30 min before occlusion of left anterior descending artery followed by reperfusion (R). Sildenafil treatment increased capillary and arteriolar density followed by increased blood flow (2 fold) compared to control. Treatment with sildenafil demonstrated increased VEGF and Ang-1 mRNA after early reperfusion. PCR data was validated by Western blot analysis. Significant reduction in infarct size, cardiomyocyte and endothelial apoptosis were observed in SC treated rats. Increased phosphorylation of Akt, eNOS and expression of anti-apoptotic protein Bcl(2), and thioredoxin, hemeoxygenase-1 were observed in SC treated rats. Echocardiography demonstrated increased fractional shortening and ejection fraction following 45 days of reperfusion in the treatment group. Stress testing with dobutamine infusion and echocardiogram revealed increased contractile reserve in the treatment group. Our study demonstrated for the first time a strong additional therapeutic potential of sildenafil by upregulating VEGF and Ang-1 system, probably by stimulating a cascade of events leading to neovascularization and conferring myocardial protection in in vivo I/R rat model.

Published 31 March 2008 in J Cell Mol Med.
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