Why the study?
Does propofol infusion affect regional myocardial contractility and left ventricular afterload in an open-chested pig model?
Does propofol infusion affect regional myocardial contractility and left ventricular afterload in an open-chested pig model?
Propofol infusion dose-dependently decreases myocardial contractility, stroke volume, heart rate, and cardiac output in a pig model, with delayed recovery of contractility after cessation.
Should not yet change propofol use in humans; leaves open dose-dependent contractility effects in clinical settings.
The cardiovascular effects of propofol infusions, designed to maintain constant plasma concentrations, were examined in an open-chested pig model. Regional myocardial contractility was measured with the end-systolic pressure-length relationship (Ees) and left ventricular afterload quantified by the effective arterial elastance (Ea). The propofol plasma concentrations in this study varied between 0 and 7.73 (SEM 0.96) micrograms/mL. A significant correlation for the increasing propofol plasma concentration and a decrease in myocardial contractility (P = 0.0056) was demonstrated, and the Ea remained constant. This gave rise to a reduction in stroke volume (P = 0.002) and, combined with a decrease in the heart rate (P = 0.0001), led to a reduction in the cardiac output (P = 0.0001). When the propofol infusion was stopped, myocardial contractility did not recover in parallel with the decrease in plasma propofol concentration.
No takes yet. Share an insight, caveat, or question.
Zee et al. (1989) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: