The electrophysiological effects of prostacyclin (PGI2) at increasing doses (2.5, 5 and 10 ng/kg/min) were assessed in 16 patients during classical investigations of sinus node function and atrioventricular conduction and during programmed atrial and right ventricular under basal conditions and during prostacyclin perfusion. Ten patients had normal sinus node function and atrioventricular conduction under basal conditions. Stastistically significant changes were observed during PGI2 perfusion: shortening of the sinus cycle length (p 0.01), decreased intraatrial conduction time (p less than 0.05), reduced atrial functional refractory period (p less than 0.01) and reduced effective and functional refractory periods of the AV node (p less than 0.05), increased anterograde (p less than 0.01) and retrograde (p less than 0.05) Wenckebach point. The changes were dose dependent. No significant changes were observed in sinus node recovery periods of the His Purkinje system. Similar changes were recorded on 4 other patients with various conduction defects. Paired atrial stimulation induced manifestations of hyperexcitability in 5 patients. In 2 patients with normal responses under basal conditions it was possible to induce non-sustained atrial tachycardia during PGI2 administration. In 3 patients with inducible atrial tachycardia under basal conditions, it was still possible to induce the tachycardia after PGI2 but this disappeared in all but one patient with the sick sinus syndrome after the addition of propranolol. The changes in ventricular excitability were studied by a specific protocol in 16 patients. Of the 13 patients without inducible ventricular tachycardia under basal conditions, 4 developed inducible non-sustained ventricular tachycardia after PGI2. Three patients had inducible VT under basal conditions.