Objective: The severity of pulmonary hypertension is a major determinant of right ventricular dysfunction and mortality after cardiac transplantation. Serial right heart catheterizations are necessary during the waiting period to test if inhalative vasodilators might lower the pulmonary vascular resistance. A recent study at our hospital demonstrated that iloprost inhalation increases the cardiac stroke volume whereas the peripheral vascular resistance remained unchanged. We thus hypothesized that iloprost directly exerts a positive inotropic effect on human myocardium. Material & Methods: Human right atrial appendages were prepared from 22 patients undergoing elective cardiac operation. Each appendage was then divided into four trabeculae and each two trabeculae were assigned to the control or verum group, respectively. Iloprost or buffer was administered at increasing doses (1 pg/ml to 100 ng/ml, 10 min each dose) and the contractile force was recorded. The inotropic competence of trabeculae was finally proven by 10-7 M isoprenalin. Results: Iloprost did not increase the contractile force of right atrial trabeculae. Neither trabecular mass nor preoperative treatment with β-blocking agents, ACE-inhibitors, calcium channel antagonists or digitoxin counfounded the measured contractile force after iloprost administration. Discussion: We showed that iloprost is not positively inotropic on human right atrial appendages. Thus, the data from our clinical study could not be experimentally confirmed. Iloprost proved to be a useful and efficient pulmonary vasodilator during the recent years and its therapeutic application is safe and does not require an intubation. Patients with primary pulmonary hypertension frequently have been treated with iloprost in an ambulatory setting as well.