• Melissa A Hausburg, Kaysie L Banton, Phillip E Roman, Fernando Salgado, Peter Baek, Michael J Waxman, Allen Tanner, Jeffrey Yoder, and David Bar-Or.
• Trauma Research Department, Swedish Medical Center, 501 E Hampden, Englewood, CO 80113, USA; Trauma Research Department, St. Anthony Hospital, 11600 W 2nd Pl, Lakewood, CO 80228, USA; Trauma Research Department, Medical City Plano, 3901 W 15th St, Plano, TX 75075, USA; Trauma Research Department, Penrose Hospital, 2222 N Nevada Ave, Colorado Springs, CO 80907, USA; Trauma Research Department, Research Medical Center, 2316 E Meyer Blvd, Kansas City, MO 64132, USA; Trauma Research Department, Wesley Medical Center, 550 N Hillside St, Wichita, KS 67214, USA.
• J Crit Care. 2020 Apr 1; 56: 281-287.

AbstractOxidative 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.Copyright © 2020 Elsevier Inc. All rights reserved.

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