Thorac Cardiovasc Surg 2009; 56 - P144
DOI: 10.1055/s-0029-1191734

Effects of inhaled iloprost in acute pulmonary hypertension: Mechanisms beyond pure vasodilation

S Rex 1, C Missant 2, P Claus 3, R Autschbach 4, R Rossaint 5, P Wouters 6
  • 1Universitätsklinikum Aachen, Operative Intensivmedizin Erwachsene, Aachen, Germany
  • 2Catholic University Leuven, Department of Acute Medical Sciences, Centre for Experimental Anesthesiology, Emergency and Intensive Care Medicine, Leuven, Belgium
  • 3Catholic University Leuven, Department of Cardiovascular Diseases, Division of Imaging and Cardiovascular Dynamics, Leuven, Belgium
  • 4Universitätsklinikum Aachen, Klinik für Thorax-, Herz- und Gefäßchirurgie, Aachen, Germany
  • 5Universitätsklinikum Aachen, Klinik für Anästhesiologie und Klinik für Operative Intensivmedizin Erwachsene, Aachen, Germany
  • 6University Hospitals Ghent, Department of Anaesthesia, Ghent, Belgium

Objectives: Prostacyclin inhalation is increasingly used to treat acute pulmonary hypertension (PHT) and right ventricular (RV) dysfunction. Prostacyclins do not only affect vasomotor tone, but may also exert cyclic-adenosine-3′-5′-monophosphate-mediated positive inotropic effects. We studied the role of these different mechanisms in the hemodynamic effects produced by inhaled iloprost (ILO) in an experimental model of acute PHT.

Methods: Twenty-six pigs were instrumented with biventricular conductance catheters, a pulmonary artery (PA) flow probe and a high-fidelity PA-pressure catheter. The effects of 50µg inhaled ILO were studied in healthy animals and after induction of acute hypoxia-induced PHT.

Results: ILO had minimal hemodynamic effects and produced no direct effects on myocardial contractility in healthy animals. During PHT, ILO resulted in a 51% increase in cardiac output when compared with placebo (5.6±0.7 vs. 3.7±0.8l/min, P=0.0013), a selective reduction of RV-afterload (effective PA-elastance (PA-Ea): 0.6±0.3 vs. 1.2±0.5mmHg/ml; P=0.0005) and a significant increase in left ventricular (LV) end-diastolic volume (91±12 vs. 70±20ml, P=0.006). RV-contractility was reduced after ILO (slope of preload recruitable stroke work: 3.4±0.8 vs. 2.2±0.5 mW/ml; P=0.0002), while ventriculovascular coupling remained essentially preserved (ratio of RV-end-systolic elastance over PA-Ea: 0.97±0.33 vs. 1.03±0.15).

Conclusions: In acute PHT, ILO improves global hemodynamics primarily via selective pulmonary vasodilation and a restoration of LV-preload. The reduction of RV-afterload was associated with a paradoxical decrease in RV-contractility. This appears to reflect an indirect mechanism serving to maintain ventriculovascular coupling at the lowest possible energetic cost, since no evidence for a direct negative inotropic effect of ILO was found.