Effect and Mechanism of Vagal Nerve Stimulation on Gastric Motility: A Preliminary Rodent Study

Patients with functional dyspepsia often exhibit gastrointestinal motor disorders associated with gastric myoelectrical dysrhythmia. This study investigated the effects of vagal nerve stimulation (VNS) in a rodent model of gastric slow-wave dysrhythmia induced by colorectal distention (CRD).

Male Sprague-Dawley rats were implanted with wires in the gastric body to record gastric slow waves and in the left cervical vagal nerve for stimulation. VNS was conducted over six sessions to optimize its efficacy on CRD-induced gastric dysrhythmia: control, CRD, and CRD with four different sets of parameters varying in frequency and stimulation on/off times. Both the CRD and VNS were conducted throughout the recording after the meal. Atropine was administered in two additional sessions, with or without VNS, to explore the involvement of the cholinergic pathway. The percentage of postprandial normal gastric slow waves (NSW), defined as the percentage of time during which the gastric slow wave was normal, was quantified using adaptive spectral analysis.

The study findings were 1) CRD significantly reduced the percentage of NSW from 89.2% ± 1.6% to 64.3% ± 3.5% (p < 0.001), which was mitigated by VNS at 14 Hz (83.5% ± 3.0%, p < 0.001) and 25 Hz (88.4% ± 1.7%, p < 0.001); 2) atropine slightly, but not significantly, decreased the percentage of NSW to 54.1% ± 3.2% and abolished the beneficial effects of VNS at 25 Hz on gastric slow waves (60.9% ± 3.3%, p < 0.01); and 3) CRD delayed gastric emptying, which was restored by 25 Hz VNS.

VNS using optimal parameters effectively ameliorated CRD-induced gastric dysmotility mediated through the vagal-cholinergic pathway, suggesting that VNS may hold therapeutic potential for functional gastrointestinal disorders.