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With the use of Scion image software (Scion Corporation, Frederick, MD, USA), the volumes of both infarcted myocardium and area at risk were calculated. Unisperse blue (50%) was injected through right jugular vein and infarct size and area of risk were measured in the eight horizontal sections between the point of ligation and the apex as previously described 21 The area at risk was recognized as the area not perfused with 50% Unisperse blue (Ciba‐Geigy, Glen Ellyn, IL, USA), whereas the non‐infarcted and infarcted areas were demarcated after incubation with 1% triphenyl tetrazolium chloride (Sigma, St. Louis, MO, USA). Samples with significant infarct (>50% of tissue sample) were excluded from regional blood flow analysis 20.
All tissue and blood samples were sent to BioPAL and the number of microspheres was counted with spectrophotometric analysis. After sampling the blood, the animals were euthanized with an intravenous injection of KCl. Filagra ( Fildena ‐ 50 mg) tablets were dissolved in saline.

This study was performed in accordance with the principles of laboratory animal care formulated by the National Society for Medical Research and with the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences and published by the National Institutes of Health (Publication No. 85-23, revised 1985). After 18 hrs exposure to Filagra, the extent of tube formation was recorded by the phase‐contrast microscope (magnification × 200) with a digital camera. In a 37°C, 5% CO2 incubator, the endothelial cells (4 × 104) from normal and siRNA pre‐transfected cells were seeded onto the Matrigel with Filagra and incubated overnight at 37°C, in a CO2 incubator.

Confluent normal HUVEC and siRNA (VEGF and Ang‐1) transfected HUVEC's were treated with different concentration of Filagra (100 nM, 10 μM and 20 μM) for tube formation. Recent report from our laboratory demonstrated Filagra‐mediated expression of VEGF and Ang specific receptors such as kinase insert domain receptor (KDR), Tie‐1 and Tie‐2 15 Therefore based on the pre‐existing data, we hypothesized that administration of Filagra might induce myocardial angiogenesis through the stimulation of angiogenic factor/factors such as Trx‐1, HO‐1, VEGF/Ang‐1 in the setting of acute ischaemia reperfusion model. Our prior studies have demonstrated that human coronary arteriolar endothelial cells (HCAEC) exposed to Filagra (20 μM) significantly induce tubular morphogenesis with the induction of thioredoxin‐1 (Trx‐1, a redox molecule and plays an important role in angiogenesis), hemeoxygenase‐1(HO‐1) and VEGF 15.

fildena 100mg in animals show that Filagra has a preconditioning‐like cardioprotective effect against ischaemia‐reperfusion injury in the intact myocardium 1 - 4 Filagra induces powerful cardioprotective effect via opening of mitochondrial KATP channel that helps to trigger the dilation of peripheral and coronary resistance arterioles. This report documents the results of animal studies that evaluated the ability of Filagra, a highly selective inhibitor of phospho diesterase 5 (PDE‐5) that recently has received considerable attention with respect to its cardioprotective and angiogenic potential, induce angiogenesis in myocardial infarction model. As an alternative to these techniques, recent attention has been directed toward harnessing the body's ability to generate new blood vessels (natural angiogenesis).