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Propofol toxicity in the developing mouse heart mitochondria.

Matthew B Barajas1, Sarah D Brunner2, Aili Wang1

  • 1Department of Anesthesiology, Columbia University Medical Center, New York, NY, USA.

Pediatric Research
|February 17, 2022
PubMed
Summary
This summary is machine-generated.

Propofol infusion syndrome (PRIS) impairs heart mitochondria in newborns by disrupting energy production. This study reveals propofol causes mitochondrial dysfunction, explaining why children are vulnerable to PRIS.

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Area of Science:

  • Biochemistry
  • Cardiology
  • Pediatrics

Background:

  • Propofol infusion syndrome (PRIS) is a life-threatening condition linked to prolonged propofol use.
  • Cardiac complications are common in pediatric PRIS and contribute to mortality.
  • The mechanisms of propofol toxicity in developing hearts remain unclear.

Purpose of the Study:

  • To investigate the specific effects of propofol on immature cardiac mitochondria.
  • To determine if propofol induces mitochondrial defects in newborn cardiomyocytes.

Main Methods:

  • Isolated cardiac mitochondria from newborn mice were exposed to propofol or intralipid in vitro.
  • Mitochondrial respiration, membrane potential (ΔΨ), and respiratory chain complex kinetics were assessed.
  • The effects of a coenzyme Q analog (CoQ0) were evaluated.

Main Results:

  • Propofol induced a dose-dependent increase in proton leak and impaired substrate oxidation at coenzyme Q (CoQ).
  • These mitochondrial defects prevented adequate ΔΨ generation in propofol-exposed cardiomyocytes.
  • Coenzyme Q0 addition reversed propofol-induced leak and enhanced Complex II+III activity.

Conclusions:

  • Propofol uncouples immature cardiomyocyte mitochondria via CoQ-sensitive proton leak.
  • Propofol interferes with electron transport at the CoQ level, impairing mitochondrial function.
  • These findings elucidate propofol toxicity mechanisms in the developing heart, explaining pediatric vulnerability to PRIS.