Abstract

Background
Sildenafil citrate at supratherapeutic levels has been reported to decrease defibrillation efficacy. However, its effects on ventricular fibrillation induction and the upper limit of vulnerability (ULV) have not been investigated. We tested the hypothesis that sildenafil citrate reduces the ventricular fibrillation threshold (VFT) and increases the ULV.
Material and Method
Twenty-one pigs (25-30 kg) were randomly assigned into 3 groups of 7 pigs each. A solution containing 100 mg (group 100) or 50 mg (group 50) sildenafil citrate or 100 cc saline (group control) was infused intravenously in each pig. A train of 10 S1s was delivered from an RV electrode, and an S2 stimulus was delivered at the peak of the T wave of the last S1 activation to determine the VFT and ULV, before and after drug administration.
Results
The 100 mg sildenafil citrate significantly (P<0.03) decreased VFT, accounting for approximately 36% by peak voltage and approximately 52% by total energy, and significantly (P<0.009) increased ULV, accounting for approximately 28% by peak voltage, and approximately 56% by total energy.
Conclusions
Supratherapeutic concentrations of sildenafil citrate significantly decreased the VFT and increased the ULV, resulting in an expansion of the VF induction window during the vulnerable period.

Keywords: Swine, Random Allocation, Sulfones - pharmacology, Purines - pharmacology, Piperazines - pharmacology, Phosphodiesterase Inhibitors - pharmacology, Ventricular Fibrillation - physiopathology, Heart Conduction System - drug effects, Electric Countershock