Year-end Sale % OFF 
Abstract
The general anesthetic propofol protects the adult heart against ischemia and reperfusion injury; however, its efficacy has not been investigated in the immature heart. This work, for the first time, investigates the cardioprotective efficacy of propofol at clinically relevant concentrations in the immature heart. Langendorff perfused rabbit hearts (7–12 days old) were exposed to 30 minutes' global normothermic ischemia followed by 40 minutes' reperfusion. Left ventricular developed pressure (LVDP) and coronary flow were monitored throughout. Lactate release into coronary effluent was measured during reperfusion. Microscopic examinations of the myocardium were monitored at the end of reperfusion. Hearts were perfused with different propofol concentrations (1, 2, 4, and 10 μg/mL) or with cyclosporine A, prior to ischemic arrest and for 20 minutes during reperfusion. Propofol at 4 and 10 μg/mL caused a significant depression in LVDP prior to ischemia. Propofol at 2 μg/mL conferred significant and maximal protection with no protection at 10 μg/mL. This protection was associated with improved recovery in coronary flow, reduced lactate release, and preservation of cardiomyocyte ultrastructure. The efficacy of propofol at 2 μg/mL was similar to the effect of cyclosporine A. In conclusion, propofol at a clinically relevant concentration is cardioprotective in the immature heart.
Highlights
Generation of reactive oxygen species and Ca2+ overload are key triggers of ischemia and reperfusion (I/R) injury of the heart and it is generally agreed that their effect is due to opening of the mitochondrial permeability transition pore (MPTP) [1, 2]
This study tested the hypothesis that propofol at a clinically relevant dose would enhance the functional recovery of the isolated immature heart following an ischemic insult
Our study showed that propofol at 10 μg/mL showed significant negative inotropic changes before ischemia and more importantly, it did not have protective effect against I/R injury, which was confirmed by functional recovery and in histopathological examination
Summary
Generation of reactive oxygen species and Ca2+ overload are key triggers of ischemia and reperfusion (I/R) injury of the heart and it is generally agreed that their effect is due to opening of the mitochondrial permeability transition pore (MPTP) [1, 2]. Further evidence in support of a role for MPTP comes from work showing that inhibition of MPTP opening (e.g., with cyclosporine A (CsA)) is cardioprotective in vitro [1, 3, 4] and in vivo [5]. Its cardioprotective properties have clinical relevance as shown in work involving a pig model of cardiopulmonary bypass and intermittent antegrade warm blood cardioplegic arrest [19]. These beneficial effects of propofol have not been shown in immature rabbit hearts
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
