Effects of propofol on ischemia-reperfusion and traumatic brain injury

Publication date: Available online 24 December 2019Source: Journal of Critical CareAuthor(s): Melissa A. Hausburg, Kaysie L. Banton, Phillip E. Roman, Fernando Salgado, Peter Baek, Michael J. Waxman, Allen Tanner, Jeffery Yoder, David Bar-OrAbstractOxidative 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. Ne...
Source: Journal of Critical Care - Category: Gastroenterology Source Type: research