Effects of propofol on ischemia-reperfusion and traumatic brain injury

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 ava...

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Bibliographic Details
Published in:	Journal of critical care Vol. 56; pp. 281 - 287
Main Authors:	Hausburg, Melissa A., Banton, Kaysie L., Roman, Phillip E., Salgado, Fernando, Baek, Peter, Waxman, Michael J., Tanner, Allen, Yoder, Jeffrey, Bar-Or, David
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 01-04-2020 Elsevier Limited
Subjects:	Anesthesia Anesthetics Aneurysms Animal cognition Animals Antioxidants Apoptosis Astrocyte Astrocytes - drug effects Brain - drug effects Brain - metabolism Brain Injuries, Traumatic - drug therapy Brain injury Critical care Disease Models, Animal Edema Free radicals Humans Inflammation Ischemia Lipid peroxidation Lipids Metabolism Neuron Neurotoxicity Oxidative Stress Propofol - adverse effects Propofol - therapeutic use Reperfusion Injury - drug therapy Stroke Suffering Surgery Traumatic brain injury United States > US IRI BBB PRIS AQP4 MDA Trk NTR TNF GLAST Tg t-BOOH Anesthesia IVBP TBI hCMEC/D3 EAA BDNF IL-1 PKC Inflammation GOS Astrocyte OGD Neuron ZO TJ ROS ICP TEER SOD-1 Brain injury GLT-1
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Summary:	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. •Overview of oxidative stress in TBI and cerebral ischemia-reperfusion injury•Evidence that propofol may be neuroprotective or neurotoxic to the injured brain.•Propofol is toxic to neurons but not astrocytes, a type of glial cell.•Astrocytes may protect injured neurons when exposed to propofol.
ISSN:	0883-9441 1557-8615
DOI:	10.1016/j.jcrc.2019.12.021