Abdominal ultrasound activates afferent vagus nerve fibers and induces anti-inflammatory effects.

Summary

In LPS-endotoxemic mice, abdominal ultrasound reduced plasma TNF-α and activated vagal afferents, evidenced by increased cervical vagus nerve activity and c-Fos in the NTS; effects were blunted by subdiaphragmatic vagotomy or afferent blockade. Intraperitoneal lidocaine abolished vagal activation, confirming engagement of abdominal sensory afferents. These data provide direct mechanistic support that ultrasound modulates systemic inflammation via vagal afferent pathways.

Key Findings

• Abdominal ultrasound significantly reduced plasma TNF-α in LPS-induced endotoxemia.
• Anti-inflammatory effects were attenuated by subdiaphragmatic vagotomy or afferent vagal blockade.
• Cervical vagus nerve activity increased during ultrasound; activation was abolished by intraperitoneal lidocaine.
• Ultrasound induced c-Fos expression in the nucleus tractus solitarius, indicating central activation via vagal afferents.

Clinical Implications

Abdominal ultrasound could be developed as a bedside, noninvasive neuromodulation to attenuate cytokinemia in systemic inflammation and sepsis; parameter optimization and safety profiling in humans are needed before trials.

Limitations

• Murine LPS endotoxemia model may not fully recapitulate human sepsis pathophysiology.
• Ultrasound parameters and dose–response require systematic optimization and translational validation.

Future Directions

Define ultrasound dosing parameters and safety in large animals and early-phase human studies; test clinical efficacy in systemic inflammation/sepsis and explore synergy with bioelectronic vagus nerve stimulation.