Why the study?
Does propofol improve systolic and diastolic performance in isolated rabbit hearts subjected to ischaemia and reperfusion?
Does propofol improve systolic and diastolic performance in isolated rabbit hearts subjected to ischaemia and reperfusion?
In an isolated rabbit heart model, propofol reduces ischaemic and postischaemic chamber stiffness but does not protect active relaxation or systolic function.
Propofol may limit chamber stiffness in rabbit ischaemia-reperfusion; leaves open clinical translation to human diastolic protection.
Background and objective: The effect of propofol on myocardial dysfunction during ischaemia and reperfusion is controversial yet important because of its frequent use in cardiac anaesthesia. Although animal studies suggest a free radical-scavenging potential, the cardioprotective properties of propofol have not been demonstrated consistently in vivo. Previous studies focused on systolic function while diastolic function may be a more sensitive marker of ischaemic injury. The main aim was to document the effect of propofol on diastolic function in isolated, blood perfused rabbit hearts subjected to moderate global ischaemia and reperfusion. Methods: Propofol 168 μmol L−1, or the equivalent of its vehicle, Intralipid®, was administered to 34 paced parabiotic Langendorff blood-perfused isolated rabbit hearts before and after 30 min of global normothermic ischaemia. Recovery of systolic function was quantified with the maximum rate of rise of left ventricular pressure. Diastolic performance was assessed using the time constant of the decline in left ventricular pressure (τ) and chamber stiffness (VdP/dV at 12 mmHg). Results: Recovery of systolic function during reperfusion was comparable in the two groups. There was no difference in left ventricular pressure between the two groups at any time during the experiments. Chamber stiffness increased significantly during ischaemia and reperfusion in the control group (from 34 ± 9 to 54 ± 8 mmHg during ischaemia, and 43 ± 5 mmHg after 30 min reperfusion; mean ±95% confidence interval) but not in the propofol-treated group (29 ± 5, 36 ± 8 and 30 ± 8 at baseline, ischaemia and 30 min reperfusion, respectively). Conclusions: Propofol has no protective effect on active relaxation or on systolic function in the present model, but it reduces ischaemic and postischaemic chamber stiffness.
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Leather et al. (2003) studied this question.
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