Abstract
Experimental studies have demonstrated that general anesthetics administered during the period of synaptogenesis may induce widespread neurodegeneration, which results in permanent cognitive and behavioral deficits. What remains to be elucidated is the extent of the potential influence of the commonly used hypnotics on comorbidities including epilepsy, which may have resulted from increased neurodegeneration during synaptogenesis. This study aimed to test the hypothesis that neuropathological changes induced by anesthetics during synaptogenesis may lead to changes in the seizure threshold during adulthood. Wistar rat pups were treated with propofol, sevoflurane, or saline on the sixth postnatal day. The long-term effects of prolonged propofol and sevoflurane anesthesia on epileptogenesis were assessed using corneal kindling, pilocarpine-, and pentylenetetrazole-induced seizure models in adult animals. Body weight gain was measured throughout the experiment. No changes in the seizure threshold were observed in the three models. A significant weight gain after exposure to anesthetics during synaptogenesis was observed in the propofol group but not in the sevoflurane group. The results suggest that single prolonged exposure to sevoflurane or propofol during synaptogenesis may have no undesirable effects on epileptogenesis in adulthood.
Highlights
On a daily basis, propofol and sevoflurane are administered to millions of children who are to undergo surgical procedures [1]
This study aimed to test the hypothesis that prolonged exposure to sevoflurane and propofol during synaptogenesis may lead to changes in seizure threshold during adulthood in three experimental seizure models
Exposure of 6-day old rats to anesthetics sevoflurane and propofol did not result in a significant decrease in the number of stimulations needed to achieve grade 4 and grade
Summary
Propofol and sevoflurane are administered to millions of children who are to undergo surgical procedures [1]. Pediatric anesthesia is considered safe based on short-term observations, mounting data from animal studies have proven that general anesthetics administered in early life induce widespread apoptotic neurodegeneration in a developing brain [2,3,4,5]. One of the major concerns of the clinical and scientific community is that histological changes observed after exposure to anesthetics are associated with long-term cognitive and behavioral deficits observed in preclinical studies [3,6,7]. The majority of general anesthetics act in the central nervous system (CNS) via two mechanisms: agonism on the γ-butyric acid (GABA) receptor or antagonism on the Nmethyl-D-aspartate (NMDA) receptor [8]. Propofol and sevoflurane act via GABA agonism. Propofol (2,6 Disopropyl-phenol) is a short-acting intravenous sedative and anesthetic
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: International Journal of Environmental Research and Public Health
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
