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

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Abstract:

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 CO2 tension (PrCO2) 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 PCO2-gap, the difference between PrCO2 and arterial CO2 tension (PaCO2), 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 PCO2-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 (V˙O2) and augmented the increase in mixed oxygen saturation (Sv¯O2) 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.
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