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ABSTRACT: Background
Propofol infusion syndrome (PRIS) is a potentially lethal consequence of long-term propofol administration. Children are vulnerable and cardiac involvement is often prominent and associated with mortality. We aimed to determine the mechanism of propofol toxicity in newborn mice, hypothesizing that propofol would induce discrete defects within immature cardiac mitochondria.Methods
Newborn murine cardiac mitochondria were exposed to propofol or intralipid in vitro. Non-exposed mitochondria served as controls. Mitochondrial respiration and membrane potential (ΔΨ) were measured and respiratory chain complex kinetics were determined.Results
Propofol and intralipid exerted biological activity in isolated mitochondria. Although intralipid effects were a potentia
SUBMITTER: Barajas MB
PROVIDER: S-EPMC9378757 | biostudies-literature | 2022 Nov
REPOSITORIES: biostudies-literature