Selective vasodilatation by nitric oxide inhalation during sustained pulmonary hypertension following recurrent microembolism in pigs

Purpose: This study establishes a new model of sustained pulmonary hyperten sion induced by recurrent microembolism in pigs and evaluates the effects o f nitric oxide (NO) inhalation in this model. Materials and Methods: Fourteen pigs were embolized under general anesthesi a with 300-mu m microspheres intravenously three times over a period of 7 w eeks. Four pigs served as untreated controls. Hemodynamic and gas exchange measurements were performed on days 1 and 7 after the last embolization. Results: Recurrent microembolism caused sustained pulmonary hypertension (m ean pulmonary artery pressure [MPAP] 26 +/- 2 and 18 +/- 1 mm Hg on days 1 and 7, respectively) compared with the control group (MPAP 13 +/- 1 mm Hg e ach for days 1 and 7; P < .05, respectively). Right heart hypertrophy was p resent at autopsy as indicated by an increase in minimal myocyte diameter. Inhaled NO (5 and 40 parts per million [ppm]) was administered on days 1 an d 7. On both days, inhaled NO significantly reduced MPAP and pulmonary vasc ular resistance without affecting systemic hemodynamics. There were no diff erences in responses to 5 and 40 ppm inhaled NO. Conclusion: We conclude that recurrent microembolization in pigs provides a reliable model of sustained pulmonary hypertension. In this model inhaled NO is a selective pulmonary vasodilator, indicating that active vasoconstri ction significantly contributes to sustained pulmonary hypertension after r ecurrent microembolism. Copyright (C) 1999 by W.B. Saunders Company.