, Volume 29, Issue 9, pp 1574-1583
Date: 08 Aug 2003

The prostaglandins epoprostenol and iloprost increase left ventricular contractility in vivo

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The principal effects of prostaglandin I2 are vasodilation and inhibition of platelet aggregation induced by a rise in the intracellular second messenger cAMP. In the heart a rise in intracellular myocardial cAMP increases contractility. We examined whether prostaglandin I2 increases left ventricular contractility in vivo. The effects of epoprostenol and iloprost on left ventricular contractility were assessed in vivo and compared to the effects of adenosine and sodium nitroprusside, which exerts vasodilatory properties independently of cAMP.

Design and setting

Prospective, randomized, cross-over in a university laboratory.


Eleven pigs (25.9±2.8 kg, balanced anesthesia).


Each animal was exposed to intravenous sodium nitroprusside, adenosine, and epoprostenol in randomized order. Iloprost was administered at the end due to its longer half-life. The dose was titrated to achieve a 25% reduction in diastolic aortic pressure.

Measurements and results

Left ventricular contractility was assessed before, during, and after each intervention by determination of the endsystolic elastance with the conductance method. While there was no change in endsystolic elastance upon the infusion of adenosine and sodium nitroprusside; endsystolic elastance increased in the case of epoprostenol (57%) and iloprost (71%) .


Left ventricular contractility is increased in vivo by epoprostenol and iloprost but not by adenosine or sodium nitroprusside at equipotent hypotensive dose. A contribution of sympathetic reflex activation of cardiac nerves on the increase in left ventricular contractility cannot be completely ruled out.

The study was supported by a research grant (Reg-No. 79 FöFoLe), Medical Faculty of the Ludwig Maximilian University of Munich.
An editorial regarding this article can be found in the same issue (http://dx.doi.org/10.1007/s00134-003-1834-8)