Inhaled epoprostenol

Aerosolized epoprostenol may provide an alternative to inhaled nitric oxide as a selective pulmonary vasodilator.

Despite its potential toxicity the use of inhaled nitric oxide has been advocated because it only exerts vasodilatory properties in ventilated lung regions and allows selective reduction of pulmonary artery pressure concomitant with improved arterial oxygenation. Owing to its rapid inactivation, it does not have any deleterious effects on systemic hemodynamics. Given the nearly identical pharmacodynamic profile of nitric oxide and epoprostenol, the latter has been administered as an aerosol. Indeed, inhaled epoprostenol also allows reduction of pulmonary artery pressure and an increase in arterial PO2 with almost no effect on systemic hemodynamics. The efficacy is virtually identical with that of inhaled nitric oxide ( Schee^eQ,§Dd,Rad§rm§Ch®I,199Z). The doses of nebulized substance required to obtain this effect range from 1 to 100 ng/kg/min; the individual dosage largely depends on the patient, the underlying pathology, and the type of nebulizer used. Dosages only represent the amount of drug nebulized; because of variable droplet size and unknown drug distribution in the airways, it is not known how much of the drug reaches the alveoli.

Aerosolization of epoprostenol may result in a dose-dependent spillover of the drug into the systemic circulation. This spillover mimics the systemic effects of the intravenous application, including improved splanchnic perfusion and oxygenation ( Scheeren jnd R§.d.®rm§c.h§L199Z).

Aerosolized epoprostenol will probably remain an experimental approach unless nebulizers for continuous long-term use become available.

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