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Eur J Cardiothorac Surg 1998;14:494-502
© 1998 Elsevier Science NL

Inhaled nitric oxide and inhaled prostaglandin E₁: effect on left ventricular contractility when used for treatment of experimental pulmonary hypertension¹

^a Department of Cardiothoracic and Vascular Surgery, Hannover Medical School, Hannover, Germany
^b Department of Anaesthesiology, Hannover Medical School, Hannover, Germany

Received 23 March 1998; accepted 22 July 1998.

Corresponding author. Thorax-, Herz- und Gefäßchirurgie, OE6210, Medizinische Hochschule Hannover, 30623 Hannover, Germany. Tel.: +49 511 5326580; fax: +49 511 5325404; e-mail: krieg@thg.mh-hannover.de

Objective: Pulmonary hypertension (PHT) is a life-threatening complication after isolated heart and lung transplantation. Recent work has shown that inhaled nitric oxide (NO) in combination with inhaled prostaglandin E₁ (PGE₁) reduce pulmonary hypertension but their influence on cardiac contractility is less well defined. Methods: This study investigated left ventricular contractility as measured by the `Preload Recruitable Stroke Work-Relation' (PRSW) in 24 anesthetized open chest pigs, 12 receiving in random order NO (50 ppm), PGE₁ (20 µg/ml) and their combination compared to 12 controls. PHT was induced by embolization with glass beads (500 µm). Prior to induction of PHT, sonomicrometric crystals were placed on the heart to measure instantaneous cardiac dimensions. Instantaneous intraventricular pressure (micro-tip catheter) and intraventricular dimensions were recorded digitally, while intraventricular volumes were calculated from the intraventricular dimensions applying the cylindric ellipsoidal volume model for the left ventricle. PRSW was calculated from the instantaneous pressure and volume data during rapid vena caval occlusion by analysis of generated pressure-volume loops. All data were analyzed by MANOVA and corrected for heart rate (level of significance #: P<0.05); PRSW-slope measures contractility, (PRSW-X-intercept did not change significantly). Results: PRSW-change±SEM (in percent of initial PRSW after induction of PHT) was -14.6%±4.4% versus 1.6%±4.4% for NO versus Control (P=0.004), -8.8%±4.6% versus 1%±3.3% (P=0.18) for PGE₁ versus Control and -5.7%±4.4% versus 2.5%±4.2% for NO+PGE₁ versus Control (P=0.33), respectively. In summary, application of NO 50 ppm significantly reduced left ventricular contractility while PGE₁ 20 µg/ml and the combination of NO and PGE₁ did not. Conclusion: If NO is not available, the sole application of nebulized PGE₁ (20 µg/ml) appears to be safe with respect to left ventricular contractility in the setting of PHT. The combination of NO and PGE₁ for the treatment of pulmonary hypertension should be considered for clinical application in situations where a combination of pulmonary hypertension and decreased left ventricular function is present.

Key Words: Left ventricular function • Nitric oxide • Prostaglandin E₁ • Inhalation of Drugs • Pulmonary hypertension