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pubmed-article:11956051pubmed:abstractTextPersistent pulmonary hypertension secondary to meconium aspiration syndrome is an important cause of morbidity and mortality in the neonatal population. We investigated the use of the phosphodiesterase-5 inhibitor sildenafil, in its intravenous form, as a pulmonary vasodilator in a model of meconium aspiration syndrome. Pulmonary hypertension was induced in 18 piglets, by endotracheal instillation of human meconium, 6 piglets subsequently received an infusion of intravenous sildenafil for 2 hours, 6 received inhaled nitric oxide for 2 hours, and 6 control animals received no additional intervention. Meconium aspiration increased pulmonary vascular resistance by 70%, and increased oxygenation index by over 100%. Pulmonary vascular resistance remained elevated for the remainder of the study period in control animals. Inhaled nitric oxide reduced the pulmonary vascular resistance by 40% after 2 hours of treatment; intravenous sildenafil completely reversed the increase in pulmonary vascular resistance within 1 hour of commencing the infusion. Neither agent had an effect on systemic hemodynamics. Sildenafil also increased cardiac output by 30%, but while doing so did not adversely influence oxygenation. Intravenous sildenafil is a selective and highly effective pulmonary vasodilator, which is at least as effective as inhaled nitric oxide, in this model of neonatal persistent pulmonary hypertension.lld:pubmed
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pubmed-article:11956051pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:11956051pubmed:articleTitleIntravenous sildenafil lowers pulmonary vascular resistance in a model of neonatal pulmonary hypertension.lld:pubmed
pubmed-article:11956051pubmed:affiliationDepartment of Cardiac Intensive Care, Great Ormond Street Hospital, London, United Kingdom. shekel@cryptic.rch.unimelb.edu.aulld:pubmed
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