Neurogastroenterology and motility · 2025
Acute Cervical Vagus Nerve Stimulation Modulates Gastric Slow Waves in the Distal Rat Stomach.
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Athavale Omkar N, Avci Recep, Clark Alys R, Cheng Leo K, Du Peng
Аннотация
BACKGROUND: Gastric motility is coordinated by bioelectrical events, named slow waves, which propagate across the stomach. Gastric dysrhythmias are associated with disorders of gut-brain interaction. Electrical cervical vagus nerve stimulation (cVNS) affects gastric contractions, but associated changes in gastric slow waves have not been quantified.
METHODS: Three cVNS protocols (low: 0.30 ms, 0.25 mA, 1 Hz; medium: 0.50 ms, 0.50 mA, 5 Hz; high: 1.00 ms, 1.00 mA, 10 Hz) were administered to six rats. Gastric slow waves were concurrently recorded from the serosa of the antrum and distal corpus using flexible electrode arrays. Slow wave amplitude and frequency (mean ± standard deviation) were analyzed with a mixed linear effects model.
KEY RESULTS: cVNS had no effect on mean slow wave amplitude (p ≥ 0.2208). Slow wave frequency decreased during the high stimulation protocol compared to sham (3.93 ± 0.90 cpm to 3.49 ± 0.54 cpm, p = 0.0374, antrum; 3.94 ± 1.04 cpm to 3.15 ± 0.53 cpm, p < 0.0001, distal corpus) but returned to sham levels after a recovery period (p = 0.9190, antrum; p = 0.9995, distal corpus). Ectopic activation of gastric slow waves occurred during cVNS, resulting in a transient effect on gastric slow wave frequency and propagation but not amplitude.
CONCLUSIONS & INFERENCES: Slow wave activity was modified by acute medium and high cVNS stimulation protocols with changes in propagation patterns and mean frequency. Therefore, modified slow wave activity could affect gastric motility function during acute cVNS.
METHODS: Three cVNS protocols (low: 0.30 ms, 0.25 mA, 1 Hz; medium: 0.50 ms, 0.50 mA, 5 Hz; high: 1.00 ms, 1.00 mA, 10 Hz) were administered to six rats. Gastric slow waves were concurrently recorded from the serosa of the antrum and distal corpus using flexible electrode arrays. Slow wave amplitude and frequency (mean ± standard deviation) were analyzed with a mixed linear effects model.
KEY RESULTS: cVNS had no effect on mean slow wave amplitude (p ≥ 0.2208). Slow wave frequency decreased during the high stimulation protocol compared to sham (3.93 ± 0.90 cpm to 3.49 ± 0.54 cpm, p = 0.0374, antrum; 3.94 ± 1.04 cpm to 3.15 ± 0.53 cpm, p < 0.0001, distal corpus) but returned to sham levels after a recovery period (p = 0.9190, antrum; p = 0.9995, distal corpus). Ectopic activation of gastric slow waves occurred during cVNS, resulting in a transient effect on gastric slow wave frequency and propagation but not amplitude.
CONCLUSIONS & INFERENCES: Slow wave activity was modified by acute medium and high cVNS stimulation protocols with changes in propagation patterns and mean frequency. Therefore, modified slow wave activity could affect gastric motility function during acute cVNS.