Key result
Propofol decreases myocardial function only at supratherapeutic concentrations, affecting normal and hypertrophic rabbit hearts equally.
Why the study?
Does propofol affect myocardial contractility, relaxation, and coronary flow differently in hypertrophic rabbit hearts compared to normal hearts?
Does propofol affect myocardial contractility, relaxation, and coronary flow differently in hypertrophic rabbit hearts compared to normal hearts?
Propofol only depresses myocardial function at supratherapeutic concentrations, and these effects are not exacerbated by compensated cardiac hypertrophy in a rabbit model.
Answers are grounded in this paper and cite their sources.
Propofol at therapeutic concentrations spares function in hypertrophic rabbit hearts; leaves open translation to human perioperative practice.
BACKGROUND: Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. METHODS: The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and erythrocyte-perfused heart model. In addition, to assess the myocardial and coronary effects of propofol in more severe LVH, hearts with a degree of hypertrophy greater than 140% were selected (severe LVH group, n = 7). RESULTS: The cardiac hypertrophy model induced significant left ventricular hypertrophy (136+/-21%, P < 0.05). The pressure-volume relation showed normal systolic function but an altered diastolic compliance in hypertrophic hearts. Propofol only decreased myocardial contractility and relaxation at supratherapeutic concentrations (> or = 300 microM) in SHAM and LVH groups. The decrease in myocardial performances was not significantly different in SHAM and LVH groups. Propofol induced a significant increase in coronary blood flow which was not significantly different between groups. In severe LVH group, the degree of hypertrophy reached to 157+/-23%. Similarly, the effects of concentrations of propofol were not significantly different from the SHAM group. CONCLUSIONS: Propofol only decreased myocardial function at supratherapeutic concentrations. The myocardial and coronary effects of propofol were not significantly modified in cardiac hypertrophy.
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Ouattara et al. (2001) studied Compensated Cardiac Hypertrophy (n=30). Propofol vs. Sham-operated control rabbits was evaluated on Myocardial contractility, relaxation, coronary flow and oxygen consumption. Propofol decreased myocardial function only at supratherapeutic concentrations (≥300 microM), with no significant difference in effects between normal and hypertrophic rabbit hearts.
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