Abstract
Background/Aim: Local anesthetics are frequently used and often considered harmless, but they can precipitate local anesthetic systemic toxicity (LAST) when accidentally administered intravascularly or when a toxic dose is rapidly absorbed, which can result in mortality. In cases of renal function impairment, the altered pharmacokinetics of local anesthetics lead to a lowered toxicity threshold. In this study, the aim was to histopathologically investigate the increase in neurotoxicity in the central nervous system due to bupivacaine in experimental renal failure.
Methods: In the study, a total of 28 male Wistar albino rats, aged 8-10 weeks, were evenly divided into four groups: Group C (control group) received intraperitoneal 1 mL/kg saline; Group G (glycerol group) received intramuscular 10 mL/kg glycerol, Group GB (glycerol+bupivacaine group) received intramuscular 10 mL/kg glycerol followed by intraperitoneal 4 mg/kg bupivacaine; and Group B (bupivacaine group) received intraperitoneal 4 mg/kg bupivacaine. All rats were sacrificed after the experimental period. Tissue samples were preserved and stained with hematoxylin-eosin for histopathological analyses. TRPM2 and Reelin levels in brain tissue were measured using immunohistochemical methods.
Results: In the histopathological examination, Group G exhibited higher Reelin and TRPM2 levels compared to all other groups (P<0.001). In Group GB, both Reelin and TRPM2 immunoreactivity were significantly higher compared to Group B (P<0.001).
Conclusion: It can be concluded that renal dysfunction increases neurotoxicity in brain tissue associated with bupivacaine.