Effects of propofol on ischemia-reperfusion and traumatic brain injury

Melissa A. Hausburg, Kaysie L. Banton, Phillip E. Roman, Fernando Salgado, Peter Baek, Michael J. Waxman, Allen Tanner, Jeffrey Yoder, David Bar-Or

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations

Abstract

Oxidative stress exacerbates brain damage following ischemia-reperfusion and traumatic brain injury (TBI). Management of TBI and critically ill patients commonly involves use of propofol, a sedation medication that acts as a general anesthetic with inherent antioxidant properties. Here we review available evidence from animal model systems and clinical studies that propofol protects against ischemia-reperfusion injury. However, evidence of propofol toxicity in humans exists and manifests as a rare complication, “propofol infusion syndrome” (PRIS). Evidence in animal models suggests that brain injury induces expression of the p75 neurotrophin receptor (p75NTR), which is associated with proapoptotic signaling. p75NTR-mediated apoptosis of neurons is further exacerbated by propofol's superinduction of p75NTR and concomitant inhibition of neurotrophin processing. Propofol is toxic to neurons but not astrocytes, a type of glial cell. Evidence suggests that propofol protects astrocytes from oxidative stress and stimulates astroglial-mediated protection of neurons. One may speculate that in brain injury patients under sedation/anesthesia, propofol provides brain tissue protection or aids in recovery by enhancing astrocyte function. Nevertheless, our understanding of neurologic recovery versus long-term neurological sequelae leading to neurodegeneration is poor, and it is also conceivable that propofol plays a partial as yet unrecognized role in long-term impairment of the injured brain.

Original languageEnglish (US)
Pages (from-to)281-287
Number of pages7
JournalJournal of Critical Care
Volume56
DOIs
StatePublished - Apr 2020
Externally publishedYes

Keywords

  • Anesthesia
  • Astrocyte
  • Brain injury
  • Inflammation
  • Neuron

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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