title: Effects of dopamine and olprinone on ventricular energetics in sevoflurane-induced acute left ventricular depression in dogs.
abstract: OBJECTIVE
  The purpose of this study was to compare the effects of dopamine and a new phosphodiesterase (PDE)-3 inhibitor, olprinone, on hemodynamics and myocardial energetics in dogs with acute myocardial depression.
  
  
  METHODS
  Prospective, randomized, crossover study.
  
  
  METHODS
  University animal laboratory.
  
  
  METHODS
  Mongrel dogs.
  
  
  METHODS
  Eight open-chest, barbiturate-anesthetized dogs with instruments for measurement of left ventricular pressure and volume were exposed to 2 MAC (minimum alveolar concentration) of sevoflurane to induce acute myocardial depression. Each dog was randomly assigned for either infusion of dopamine (5 microg/kg/min) for 15 minutes or bolus of olprinone (10 microg/kg), followed by an infusion (0.3 microg/kg/min) for 30 minutes. Treatment was crossed over after a washout period of 90 minutes.
  
  
  RESULTS
  For analysis of ventricular energetics, ventriculoarterial coupling was assessed using the ratio of arterial elastance to end-systolic pressure-volume relation and mechanical efficiency was calculated using the ratio of external work to pressure-volume area. Measurements were performed prior to sevoflurane administration, and before and after treatment. Two MAC of sevoflurane significantly impaired ventriculoarterial coupling and mechanical efficiency. Both olprinone and dopamine improved ventriculoarterial coupling and mechanical efficiency to similar degrees, but by different mechanisms. Olprinone improved ventricular energetics at a lower energy expenditure, probably because of olprinone's vasodilating effect, which augments energy transfer from the ventricle into the systemic circulation.
  
  
  CONCLUSIONS
  Although both dopamine and olprinone improve sevoflurane-induced impairment of ventricular energetics, olprinone accomplishes this with lower ventricular energy expenditure.
authors.affiliation: Department of Anesthesiology, Tokyo Women's Medical University, Tokyo, Japan.
authors.forename: Motoyo
authors.initials: M
authors.lastname: Iwade
authors.forename: Minoru
authors.initials: M
authors.lastname: Nomura
authors.forename: Shoichi
authors.initials: S
authors.lastname: Uezono
authors.forename: Eri
authors.initials: E
authors.lastname: Ashikari
authors.forename: Makoto
authors.initials: M
authors.lastname: Ozaki
mesh_terms: D015105:3',5'-Cyclic-AMP Phosphodiesterases / Q000037:antagonists & inhibitors*; D000818:Animals; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; D004285:Dogs; D004298:Dopamine / Q000494:pharmacology*; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D006352:Heart Ventricles / Q000378:metabolism*; D007093:Imidazoles / Q000494:pharmacology*; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D011728:Pyridones / Q000494:pharmacology*; D000077149:Sevoflurane; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D007093:Imidazoles; D008738:Methyl Ethers; D010726:Phosphodiesterase Inhibitors; D011728:Pyridones; D000077149:Sevoflurane; C059498:olprinone; D015105:3',5'-Cyclic-AMP Phosphodiesterases; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; D004298:Dopamine