Effects of olprinone, a new phosphodiesterase inhibitor, on gastric intramucosal acidosis and systemic inflammatory responses following hypothermic cardiopulmonary bypass

Background: Phosphodiesterase (PDE) III inhibitors have both an inotropic and a peripheral vasodilatory effect, and also inhibit the activation of macrophages. Thus a newly developed PDE III inhibitor, olprinone, could modify gastric intramucosal pH (pHi), systemic oxygen consumption, and systemic inflammatory responses in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Methods: We studied 23 patients. In 15 patients, olprinone (0.1 or 0.2 μg . kg -1 . min -1 ) was administered from the commencement of CPB until their admission to the ICU. The other 8 patients received placebo. The pHi and regional CO 2 tension (PrCO 2 ) were assessed by a capnometric air tonometry. Systemic inflammatory responses were evaluated by serum interleukin-6 (IL-6), IL-10, and leucocyte counts. Results: The pHi and PCO 2 -gap, the difference between PrCO 2 and arterial CO 2 tension (PaCO 2 ), showed a transient decrease and an increase after CPB, respectively. Although olprinone did not affect pHi, olprinone at 0.2 μg.kg -1 min -1 significantly lessened post-CPB increase in PCO 2 -gap. Olprinone at 0.2 μg.kg -1 . min -1 significantly increased IL-10 and reduced the extent of leucocytosis, while it did not affect IL-6 levels. At the same dosage, olprinone also lessened the surge in systemic oxygen uptake index (VO 2 ) and augmented the increase in mixed oxygen saturation (SvO 2 ) both of which occurred after CPB. At 0.1 μg kg -1 . min -1 , however, olprinone did not show any significant effect. Conclusion: Our results suggest that olprinone at 0.2 μg.kg -1 . min -1 suppresses gastric intramucosal acidosis and systemic inflammation following CPB.