Effect of prostaglandin I2 analogues on left ventricular diastolic function in vivo

The maximum velocity of left ventricular pressure drop worsened during the infusion of sodium nitroprusside (baseline: − 1950; sodium nitroprusside: − 1293 mm Hg/s, p < 0.05, Wilcoxon signed rank test versus vs. baseline) and adenosine (baseline: − 2015; adenosine: − 1345 mm Hg/s, p < 0.05), but remained stable during the infusion of the prostaglandins (baseline: − 1943; epoprostenol: − 1785 mm Hg/s; baseline: − 2042; iloprost: − 1923 mm Hg/s). End diastolic compliance was not altered significantly by any vasodilator. Interstitial myocardial cAMP increased during the infusion of epoprostenol (7.60 to 13.87 fmol/ml, p < 0.05) and tended to increase during the infusion of iloprost (7.56 to 11.66 fmol/ml, p = 0.21). The prostaglandin I2 analogues epoprostenol and iloprost preserved the early phase of active isovolumic relaxation, presumably mediated by myocardial cAMP, whereas sodium nitroprusside and adenosine impaired early active isovolumic relaxation. Passive relaxation and filling properties remained stable during the infusion of each applied vasodilator in the intact left ventricle in vivo.