Neuropathologic damage induced by radiofrequency ablation at different temperatures

Objective: To explore the molecular mechanism of neuropathologic damage induced by radiofrequency ablation at different temperatures. Methods: This is basic research, and 36 SD rats were used to construct the neuropathological injury model. The rats were subjected to radiofrequency stimulation at different temperatures and were divided into 6 groups according to the temperature injury: 42 degrees, 47 degrees, 52 degrees, 57 degrees, 62 degrees, and 67 degrees C groups. Conduction time, conduction distance, and nerve conduction velocity were recorded after temperature injury. HE-staining was used to observe the histopathological morphology of the sciatic nerve. The expression of SCN9A, SCN3B, and NFASC protein in sciatic nerve tissue were detected by western blot. Results: With the increase in temperature, nerve conduction velocity gradually decreased, and neurons were damaged when the temperature was 67 degrees C. HE-staining showed that the degrees of degeneration of neurons in rats at 47 degrees, 52 degrees, 57 degrees, 62 degrees, and 67 degrees C were gradually increased. The expression of SCN9A, SCN3B protein in 57 degrees, 62 degrees, 67 degrees C groups were much higher than that of NC, 42 degrees, 47 degrees, 52 degrees C groups. However, the expression of NFASC protein in 57 degrees, 62 degrees, 67 degrees C groups was much lower than that of the NC, 42 degrees, 47 degrees, 52 degrees C groups. Conclusion: There was a positive correlation between temperature caused by the radiofrequency stimulation to neuropathological damage. The mechanism is closely related to the expression of SCN9A, SCN3B, and NFASC protein in nerve tissue caused by heat transfer injury.

Automated summary

This study aimed to explore the molecular mechanism of neuropathological damage induced by radiofrequency ablation at different temperatures. The results showed that with the increase in temperature, nerve conduction velocity gradually decreased, and the degree of neuronal degeneration gradually increased. Furthermore, the temperature-induced damage was closely associated with the expression of SCN9A, SCN3B, and NFASC proteins.