Evaluation of the effect of bupivacaine on the heart tissue in rats with glycerol-induced acute kidney injury.

AIM: This study aims to evaluate the effects of bupivacaine on acute kidney injury (AKI) through kidney function parameters and cardiac tissue damage via TRPM2, HSP70, TLR4, NF-κB, and TNF-α biomarkers.

MATERIAL AND METHOD: Male Wistar albino rats were divided into 4 groups, with seven rats in each group: Control group, AKI group (kidney damage induced by glycerol), AKI + L group (group treated with bupivacaine), and L group (group treated with bupivacaine alone). At the end of the experiment, kidney and heart tissues were collected for histological analysis, and serum samples were taken for biochemical analysis. In serum samples, urea nitrogen (BUN), creatinine (Cr), troponin t, Creatine Kinase, Creatine Kinase-MB, and total oxidant levels were measured. In histological analysis, changes in heart and kidney tissues were evaluated histopathologically and immunohistochemically through KIM-1, TNF-α, TRPM2, HSP70, NF-κB, and TLR4 parameters.

RESULTS

In the AKI group, a significant increase in blood urea nitrogen (BUN) and creatinine (CR) levels was observed when compared to the control group (p < 0.05). Notably, in the AKI + Local Anesthetic (L) group, these levels were found to be elevated compared to the AKI group. KIM-1 and TNF-α immunoreactivity in kidney tissue were both significantly elevated in the AKI group compared with the Control group, and further increased in the AKI + L group compared with the AKI group. In heart tissues, significant increases in the immunoreactivity levels of TLR4, NF-κB, TNF-α, HSP70, and TRPM2 were observed in the AKI + L group relative to the AKI group (p < 0.05). Moreover, in the AKI + L group, the extent of histopathological damage was found to be more severe compared to the AKI group (p < 0.05).

CONCLUSION

This study demonstrates that bupivacaine exacerbates acute kidney injury and leads to significant histopathological changes in kidney function and heart tissue parameters. It was observed that bupivacaine might affect cardiac conduction, impairing heart functions, and lead to changes in molecular pathways such as KIM-1, TNF- α, TRPM2, HSP70, TLR4, and NF-κB. Furthermore, the increase of oxidant levels and biomarker levels suggest that bupivacaine may induce oxidative stress and inflammation, leading to damage in both kidney and heart tissues.