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Acute Cardiopulmonary Hemodynamic Effects of Brain Natriuretic Peptide in Patients With Pulmonary Arterial Hypertension*

James R. Klinger, FCCP; Jeanne Houtchens; Sejal Thaker; Nicholas S. Hill, FCCP; Harrison Farber, FCCP
Author and Funding Information

*From the Division of Pulmonary Medicine, Rhode Island Hospital, Providence RI; and the Division of Pulmonary Medicine, New England Medical Center, Boston, MA; and Boston University Medical Center, Boston, MA.

Correspondence to: James R. Klinger, MD, FCCP, Rhode Island Hospital, SWP Rm 422B, Pulmonary and Critical Care Medicine, 593 Eddy St, Providence, RI 02903; e-mail: james_klinger@brown.edu



Chest. 2005;128(6_suppl):618S-619S. doi:10.1378/chest.128.6_suppl.618S-a
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Brain natriuretic peptide (BNP) has been shown to reverse hypoxic pulmonary vasoconstriction and to blunt the development of hypoxic pulmonary hypertension in animal models, but its acute cardiopulmonary effects on adult patients with established pulmonary arterial hypertension (PAH) has not been well-studied. We compared the acute pulmonary vasodilator effect of BNP to that of inhaled nitric oxide (iNO) [5, 10, 20 ppm] and/or IV epoprostenol (4 to 12 ng/kg/min) in 13 adult patients with PAH. Each patient received two BNP infusions (a 2 μg/kg bolus followed by a 3-h infusion at 0.01 μg/kg/min) separated by a washout period of at least 6 h. One BNP infusion was preceded by a 100-mg oral dose (50-mg if the age of the patient was > 65 years) of the phosphodiesterase inhibitor sildenafil. BNP changes from baseline hemodynamic measurements are shown in Table 1 .

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