title: Effect of phosphodiesterase III inhibitor on contractility, afterload, and vascular capacitance during right heart bypass preparation.
abstract: OBJECTIVE
  Phosphodiesterase III inhibitors, which have both positive inotropic and vasodilatory effects, occasionally cause hypotension due to afterload reduction and possibly due to preload reduction caused by the increase in vascular capacitance.
  
  
  METHODS
  Six open-chest adult mongrel dogs were used to compare the effects on left ventricular contractility, afterload, and vascular capacitance of the phosphodiesterase III inhibitor, olprinone, with those of dobutamine using a right-heart-bypass model. Contractility and afterload were evaluated by the left ventricular pressure-volume relations with the use of a conductance catheter to derive the end-systolic elastance (Ees) and the effective arterial elastance (Ea). Vascular capacitance change was evaluated by reservoir volume change under a constant bypass flow (80 ml/kg per minute).
  
  
  RESULTS
  Ees increased significantly both with dobutamine (7.6 +/- 2.8 to 14.3 +/- 4.8 mmHg/ml, p < 0.05) and with olprinone (7.6 +/- 2.9 to 11.5 +/- 4.2 mmHg/ml, p < 0.05). Ea did not change with dobutamine (14.4 +/- 3.5 to 14.5 +/- 3.6 mmHg/ml, p = 0.9), whereas it decreased with olprinone (14.0 +/- 4.1 to 11.4 +/- 3.8 mmHg/ml, p = 0.093). Reservoir volume increased after the infusion of dobutamine (-94.0 +/- 39.8 ml), and decreased after the infusion of olprinone (-114.0 +/- 62.3 ml). The difference was statistically significant (p = 0.007). The reservoir volume change indicated that vascular capacitance decreased with dobutamine, and increased with olprinone.
  
  
  CONCLUSIONS
  Pre- and afterload reduction of olprinone combined with the positive inotropic effect are useful in treating congestive heart failure and managing low cardiac output syndrome after cardiac surgery.
authors.affiliation: Department of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Tanoue
authors.forename: S
authors.initials: S
authors.lastname: Morita
authors.forename: I
authors.initials: I
authors.lastname: Nagano
authors.forename: Y
authors.initials: Y
authors.lastname: Ochiai
authors.forename: R
authors.initials: R
authors.lastname: Tominaga
authors.forename: Y
authors.initials: Y
authors.lastname: Kawachi
authors.forename: H
authors.initials: H
authors.lastname: Yasui
mesh_terms: D015105:3',5'-Cyclic-AMP Phosphodiesterases / Q000037:antagonists & inhibitors*; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; D004280:Dobutamine / Q000494:pharmacology*; D004285:Dogs; D018610:Heart Bypass, Right; D007093:Imidazoles / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects*; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D011728:Pyridones / Q000494:pharmacology*; D018924:Vascular Capacitance / Q000187:drug effects*; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure
chemical_list: D002316:Cardiotonic Agents; D007093:Imidazoles; D010726:Phosphodiesterase Inhibitors; D011728:Pyridones; D004280:Dobutamine; C059498:olprinone; D015105:3',5'-Cyclic-AMP Phosphodiesterases; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3