Propofol effects in rodent models of traumatic brain injury: a systematic review

Abstract

Background Traumatic brain injury (TBI) causes high mortality and disability worldwide. Animal models have been developed to explore the complex processes in TBI. Propofol is used to manage head injuries during surgical intervention and mechanical ventilation in patients with TBI. Many studies have investigated the neuroprotective effect of propofol on TBI. However, other studies have shown neurotoxic effects. Objectives To review systematically the literature regarding the neuroprotective and neurotoxic effects of propofol in rodent models of TBI. Methods Data from rodents as models of TBI with propofol as one of the intervention agents, and/or comparing the neuroprotective effects of propofol with the other substances in rodent models of TBI, were obtained from PubMed, EBSCO Host, and ProQuest databases. The PRISMA 2020 statement recommendations were followed and research questions were developed based on PICOS guidelines. Data was extracted from the literature using a standardized Cochrane method. Results We analyzed data from 12 articles on physiological changes of experimental animals before and after trauma, the effects of propofol administration, and the observed neurotoxic effects. The effects of propofol administration were observed in terms of changes in traumatic lesion volume, the release of antioxidants and inflammatory factors, and the neurological function of rodent models of TBI. Conclusion Propofol has neuroprotective and neurotoxic effects via several mechanisms, and various doses have been used in research to determine its effects. The timing of administration, the dose administered, and the duration of administration contribute to determine the effect of propofol in rodent models of TBI. However, the doses that produce neuroprotective and neurotoxic effects are not yet clear and further research is needed to determine them.

Are GABAergic drugs beneficial in providing neuroprotection after traumatic brain injuries? A comprehensive literature review of preclinical studies

“…Propofol exerts its action by augmenting the activity of chloride currents through GABA A Rs and also blocks voltage-gated sodium channels ( 14 , 30 ). However, several preclinical TBI studies ( 19 , 31 – 34 ) have highlighted the inefficacy of propofol in causing neuroprotection and promoting functional recovery.…”

Oxygen saturation profile in traumatic brain injury animal model after propofol administration

“…However, its effects on brain tissue following TBI, either neuroprotective or neurotoxic, are not fully understood [11][12][13][14][15]. In addition, apart from its neuroprotective effect, propofol can also cause respiratory depression, bronchospasm, laryngospasm, and apnea [16,17]. To investigate the double effects of propofol, conducting study on its effects on cerebral hypoxia is of significant importance.…”

Comparison between premortem histopathology findings in rats with and without traumatic brain injury: prospective application in forensic medicine

“…6 TBI induces a complex cascade of immunologic or tissue inflammatory responses that mimic ischemic reperfusion injury. 7 Primary head injury and secondary head injury activate the release of cellular mediators in the form of prostaglandins, pro inflammatory cytokines, and free radicals. In secondary injuries, there are disturbances in the processes of metabolism and homeostasis of brain cell ions, intracranial hemodynamics, and cerebro-spinal fluid (CSF) compartments which begin after the trauma but are not clinically apparent immediately after the trauma.…”

“…In secondary injuries, there are disturbances in the processes of metabolism and homeostasis of brain cell ions, intracranial hemodynamics, and cerebro-spinal fluid (CSF) compartments which begin after the trauma but are not clinically apparent immediately after the trauma. 7,8 Deaths due to TBI are some of the most common cases encountered by forensic pathologists. TBI is routinely implicated in cases classified as accidents, as well as in suicides and homicides.…”