Effects of dopamine and olprinone on ventricular energetics in sevoflurane-induced acute left ventricular depression in dogs.
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.
Iwade
Motoyo
M
Department of Anesthesiology, Tokyo Women's Medical University, Tokyo, Japan.
Nomura
Minoru
M
Uezono
Shoichi
S
Ashikari
Eri
E
Ozaki
Makoto
M
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*
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