Bar graph represents quantitative measurement of Real Time RT‐PCR analysis between control I/R (CIR) and Cenforce 100 I/R groups following 8, 12 & 24 hrs of reperfusion: (A) VEGF mRNA; (B) Angiopoietin‐1 mRNA; (C) Angiopoietin‐2 mRNA P < 0.05 compared with CIR. Effect of Cenforce 100 on VEGF, Ang‐1 and And‐2 mRNA levels. Increased expression of VEGF (1.9‐, 2‐ and 4‐fold) and Ang‐1 (5‐, 11‐ and 23‐fold) mRNA was observed ontreatment with Cenforce 100 8, 12 and 24 hrs after reperfusion as compared to the control ( Fig.

The capillary density in the peri‐infarct area was significantly greater in the Cenforce 100‐treated group (4617 versus 3298 and 4978 versus 3449 counts/mm2) than in the CIR group following 2 & 4 day after reperfusion ( Fig. Four sections from each heart were examined. At 400 × magnification, eight non‐overlapping random fields, each selected from non‐infarcted risk area were used for CD‐31 counting.

Effect of Cenforce 100 on capillary density and arteriolar density. 3C and D ). Significant increase in the number of TUNEL‐positive cells was observed in the CIR effect was strongly inhibited by Cenforce 100 in the SIR group.Decreased cardiomyocyteapoptosis was observed in Cenforce 100‐treatedrats as compared to controls following 24 (304 versus 56) and 48 (168 versus 16) hrs of reperfusion. Effect of Cenforce 100 on cardiomyocyte and endothelial cell apoptosis.

The Cenforce 100‐treated group SIR displayed significantly elevated contractile reserve as judged from the improved dp/dtmax ( Fig. Infarct size, expressed as percent of infracted to total area at risk, was noticeably decreased to 20% in the SIR group compared to the CIR group (39%) ( Fig. As expected, cells pre‐treated with VEGF and Ang‐1 siRNA have demonstrated inhibition of Cenforce 100‐mediated tubular morphogenesis of HUVEC which was observed in corresponding control Cenforce 100‐treated cells ( Fig.

In separate experiments the cells were treated with Cenforce 100 in HUVECs which were pre‐transfected with siRNA for VEGF and Ang‐1 to demonstrate Cenforce 100‐mediated tuborogenesis involves VEGF and Ang‐1. Tubular morphogenesis by HUVECs after Cenforce 100 treatment with and without VEGF/Angiopoietin‐1 siRNA. Diastolic function was assessed in apical four chamber view, by measuring mitral peak flow velocity of the E‐wave and A‐wave in centimetres per second (cm/s) and the ratio between these two waves (E/A ratio).

The animal's paws were anchored to the electrodes on the platform to obtain electrocardiography, respiratory rate and heart rate and body temperature was maintained at 37°C throughout the procedure. The primer sets used in quantitative real‐time RT‐PCR for VEGF was forward, 5′‐CAGGAGTACCCCGATGAGATAG‐3′ reverse, 5′‐GATCT GCATAGT‐GACGTTGCTC‐3′, for Ang‐1 was forward, 5′‐GTGAGAGTGCGAC AGAGCAG‐3′ reverse 5′‐CAAGTTTTTGCAGCCACTGA‐3′ for Ang‐2 was forward, 5′‐GGCTCAGAGGTCATGAGGAG‐3′ reverse 5′‐AAACCATG‐GCACTTCTGTCC‐3′. Infarct size was reported as a percentage of the area at risk.
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