Clonidine inhibits postprandial response of antral myoelectrical activity

Clonidine, an α₂-adrenergic agonist, is known to inhibit gastric motility and delay gastric emptying in both humans and animals, but its effect on gastric myoelectric activity is unclear. The aim of this study was to investigate the effect of clonidine on postprandial gastric myoelectric activity. The experiment was performed in eight hound dogs (14.5-22.6 kg) implanted with three pairs of bipolar serosal electrodes with an interval of 4 cm and the most distal pair 2 cm above the pylorus. Each dog was studied twice on two separate days after a complete recovery from surgery. Gastric myoelectrical activity was recorded for 30 min in the fasting state and 90 rain after a solid test meal of 838 kcal. Two tablets of clonidine (0.4 mg) were given with the meal in one of the sessions. The dominant frequency and power of the slow waves from the most distal pair were calculated by computerized spectral analysis. All data were expressed as mean ± SE. A significant postprandial increase in the dominant power of the slow wave and an increase in the percentages of gastric slow waves with spike bursts were observed in the control session, whereas the dominant frequency of gastric slow waves showed a significant postprandial decrease after the meal. The dominant power increased 8.24 ± 0.5, 8.6 ± 0.2, and 7.5 ± 0.3 dB, respectively, in the first, and second, and third 30-min period after the meal (all P < 0.01 vs baseline). Clonidine completely abolished the postprandial increase in the dominant power of the gastric slow wave and significantly inhibited spike bursts. The dominant power only increased 2.4 ± 1.1 dB (P > 0.05 vs baseline; P < 0.01 vs the first postprandial period in the control session), 0.6 ± 1.5 dB (P > 0.05 vs baseline; P < 0.05 vs the second postprandial period in the control session) and - 1.5 ± 2.2 dB (P > 0.05 vs baseline; P < 0.05 vs the third postprandial period in the control session) respectively during the first, second, and third periods after the meal and clonidine. However, it did not affect the postprandial change Of the dominant frequency of gastric slow waves. No significant changes in percentage of regular slow waves were noted with the meal or with clonidine (P > 0.05). In conclusion, the postprandial response of gastric myoelectrical activity in dogs to a solid meal is featured with an increase in amplitude and spike bursts, which is inhibited by clonidine.