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Among the PDE 5 inhibitors, initially studied to highlight the zaprinast and 9 dipyridamole. In the study of Thusu and cl, the use of zaprinast combined with i NO decreasedpulmonary artery pressure and pulmonary vascular resistance and increases the actionvasodilator i NO in newborn lambs with pulmonary hypertensionexperimentally induced intrauterine ligation of the ductus arteriosus, an evidence ofsynergistic action between the two drugs. Ichinose and CL 10 ram shows that zaprinast prolonged the vasodilator effect of i NOin sheep with experimentally induced pulmonary hypertension. Hanson and CL 8 inanimal model of chronic fetal pulmonary hypertension, vascular resistance drop obtainedlung in 55 and 35% respe ctive using dipyridamole and zaprinast. 11, Buysee and cl using dipyridamole at a dose of 0. 4 mg / kg / min for 10 minutes each 12 hours for 3 doses in a term infants with congenital diaphragmatic hernia enabled thediscontinuation of i NO trailer without you and extubation of infants with one week (dipyridamoleincreased levels of c GMP in pulmonary vascular smooth muscle, allowing thevasodilation by restoration of endogenous NO). The use of dipyridamole, a blocker of PDE 5 described in humans, mitigates theincreased pulmonary artery pressure after withdrawal of i NO (inhibits degradationc GMP), however, the specific dipiridanol has no effect, while blocking the resumption ofadenosine in endothelial cells and erythrocytes 12. 13 Dukarm cl and described in newborn sheep with pulmonary hypertension, systemic hypotension with the use of dipyridamole (this systemic effect persisted for 90 minutes after stopping the infusion of dipyridamole), this pronounced effect ofdipyridamole in the systemic circulation limits its usefulness as an adjunct to i NOinhalation in PPH of the newborn. More recently he has been evaluating the role of another PDE 5 inhibitor, the sildenafi (Viagra R). A major advantage of sildenafil is the most selective activity for the bed 7. 14 pulmonary vascular and appears to be a promising agent. Their lack of vasodilationputs the systemic advantage over sildenafil in prostacyclin, dipyridamole and zaprinast. The study of Zhao and CL 15 investigated the effect of oral sildenafil in the vascular responsepulmonary hypoxia in human volunteers breathing 11% O 2. Of subtypesphosphodiesterases, PDE 5 is largely responsible for the metabolism of c GMP in the lung. Thus, inhibition of PDE 5 allows Pulm lect vasodilation with little hypotensionsystemic. These authors reported that sildenafil attenuates pulmonary hypertension inducedby hypoxia without significant effect on systemic blood pressure. Experimental study of Weimann and cl 16 showed that the use of oral sildenafil inadult sheep with induced pulmonary hypertension, caused vasodilation via selective Nitric oxide (NO) similarly to endogenous vasodilation produced by sildenafil incorpus cavernosum which requires the production of c GMP by NO produced by the nerves do notadrenergic and not cholinergic. However, in contrast to other PDE 5 inhibitors, as zaprinast, oral administration of sildenafil did not prolong the vasodilator effecti NO. A possible explanation for the difference in ability of zaprinast and sildenafil, both selective PDE 5 inhibitors, modulation of NO dependent vasodilation is thatzaprinast inhibits the phosphodiesterases that are not inhibited by sildenafil. For example, it has been reported that zaprinast inhibits PDE isoforms 1 and HCM Hcam 1 3 A, bothexpressed in the lung, whereas only high concentrations of sildenafil inhibit PDE 1. On However, only high concentrations of zaprinast inhibit PDE 9 recently described thatoccurs in the lung tissue, while sildenafil did not inhibit it. In 2001, Ichinose and 17 cl, evaluated the effect of sildenafil in mist (aerosols 10 and 30 mg) in an animal model (sheep) pulmonary hypertension. The largestauthors findings were: selective vasodilation without systemic vasodilation ca, potentiation of the vasodilator effect of i NO, without causing injury in the structuresthe lungs. 18 Experimental study of recent and classic Kleinsasser showed adverse effects ofsildenafil on oxygenation and intrapulmonary shunt fraction. Pa O 2 decreased after dose 50 and 100 mg of sildenafil in the presence of significant increase in intrapulmonary shunt andcardiac index. The fall in blood pressure occur with the higher dose significantlyused. Thus the effects of sildenafil on hemodinnica and pulmonary gas exchangeremain uncertain. The experimental study of Thebauld and cl 19 showed that sildenafil dilates theductus arteriosus, and may be an alternative adjunct to the treatment Prostaglandin E 1 as a bridge to cardiac surgery cardiac insufficiency. (We know that the patency ofductus arteriosus is critical to the survival of infants with congenital cardiac channeldependent).