Tachygastria induced by gastric electrical stimulation is mediated via α- and β-adrenergic pathway and inhibits antral motility in dogs

Background: it is known that tachygastria is associated with gastric hypomotility and retrograde gastric electrical stimulation (RGES) delays gastric emptying and is proposed for treating obesity. The aim was to investigate the effects and mechanisms of RGES on postprandial antral contraction in dogs. Methods: Seven dogs were implanted with a gastric cannula and three pairs of gastric serosal electrodes. Antral contractions and gastric myoelectrical activity were recorded immediately after a solid meal, with or without RGES, or with GES on the corpus, or with RGES under administration of propranolol. The stimulus was composed of long pulses with a tachygastrial frequency. Results: (i) GES at the tachygastrial frequency impaired gastric myoelectrical activity and induced tachygastria (ANOVA P < 0.05). (ii) GES at the tachygastrial frequency suppressed antral contractions (ANOVA P < 0.01) and the effect was stronger with retrograde stimulation than forward stimulation (P < 0.05). (iii) GES-induced tachygastria was correlated with antral hypomotility (r = -0.60, P = 0.01). (iv) Propranolol and phentolamine abolished GES-induced tachygastria and antral hypomotility. Conclusions: Long-pulse RGES at a tachygastrial frequency suppresses postprandial antral contractions, which is attributed to an induction of tachygastria via the alpha- and beta-adrenergic pathway.