Prostaglandins in Patients with Pulmonary Hypertension

To the Editor: We would like to congratulate Dr. Kunimoto et al. for their excellent study on the IV application of prostaglandin E1 to patients suffering from pulmonary hypertension related to either mitral valve replacement or adult respiratory distress syndrome (ARDS) [1]. However, we would like to draw the authors' attention to a different route of prostaglandin application, which is inhaled endotracheal administration. This approach can be achieved by nebulizing prostaglandins into the inspiratory limb of the respiratory circuit. It does not matter what kind of nebulizer is used (ultrasonic nebulizer or jet nebulizer), as long as the nebulizer produces a particle size capable of reaching the alveoli (diameter 1-5 mm). This therapeutic regimen has been tested by us and others in animal models with [2,3] and without lung injury [4,5]. These results were reproducible in patients suffering from severe ARDS, no matter whether prostaglandin I2[6] or prostaglandin E1[7] was used. In all studies, the inhaled application of either prostaglandin I2 or prostaglandin E1 proved to reliably lower pulmonary artery pressure without affecting systemic hemodynamics, especially without lowering systemic vascular resistance index. The latter also holds true in patients with ARDS, and, subsequently, reduced pulmonary metabolism of prostaglandin E1, as suggested by Kunimoto et al. [1]. Further, an improvement in arterial oxygenation was achieved in patients with ARDS by improving ventilation/perfusion ratio and, thus, lowering the intrapulmonary shunting [6,7]. However, in a few cases, only a reduction in pulmonary artery pressure without any improvement in arterial oxygenation can be seen [2,8]. The reason for this phenomenon is not quite clear, yet. Walmrath et al. [9] suggested that a preexistent pulmonary fibrosis may be responsible for this phenomenon. In conclusion, the inhaled route of prostaglandin administration in cases of ARDS and/or pulmonary hypertension seems to be as effective as the IV route in terms of lowering pulmonary vascular resistance but has no negative side effects, such as increased pulmonary shunting, reduced arterial oxygenation, or systemic vasodilation. Further, the inhaled application of prostaglandins does not cause any harm to the airway, even when given over a prolonged period of time [10]. Consequently, in our opinion, the inhaled application of vasodilators such as prostaglandin E1 seems to be superior to the IV administration. Michael Booke, MD, PhD Hugo Van Aken, MD, PhD Gregor Theilmeier, MD Jorg Meyer, MD, PhD Klinik und Poliklinik fur Anasthesiologie und operative Intensivmedizin; Westfalische Wilhelms-Universitat Munster; 48129 Munster, Germany