Clonidine inhibits postprandial response of antral myoelectrical activity

Clonidine. an alpha (2)-adrenergic agonist, is known To inhibit gastric mot ility 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 i nvestigate the effect of clonidine on postprandial gastric myoelectric acti vity. The experiment was performed in eight hound dogs (14.5-22.6 kg) impla nted with three pairs of bipolar serosal electrodes with an interval of 4 c m and the most distal pair 2 cm above the pylorus, Each dog was studied twi ce on two separate days after a complete recovery from surgery. Gastric myo electrical activity was recorded for 30 min in the fasting state and 90 min after a solid test meal of 838 kcal. Two tablets of clonidine (0.4 mg) wer e given with the meal in one of the sessions. The dominant frequency and po wer of the slow waves from the most distal pair were calculated by computer ized spectral analysis. All data were expressed as mean +/- se. A significa nt postprandial increase in the dominant power of the slow wave and an incr ease in the percentages of gastric slow waves with spike bursts were observ ed in the control session, whereas the dominant frequency of gastric slow w aves showed a significant postprandial decrease after the meal. The dominan t power increased 8.24 +/- 0.5, 8.6 +/- 0.2, and 7.5 +/- 0.3 dB, respective ly, in the first, and second, and third 30-min period after the meal tall P t 0.01 vs baseline). Clonidine completely abolished the postprandial increa se in the dominant power of the gastric slow wave and significantly inhibit ed spike bursts. The dominant power only increased 2.4 +/- 1.1 dB (P > 0.05 vs baseline; Pt 0.01 vs the first postprandial period in the control sessi on), 0.6 +/- 1.5 dB (P > 0.05 vs baseline; Pt 0.05 vs the second postprandi al period in the control session) and -1.5 +/- 2.2 dB (P > 0.05 vs baseline ; Pt 0.05 vs the third postprandial period in the control session) respecti vely during the first, second, and third periods after the meal and clonidi ne. However, it did not affect the postprandial change of the dominant freq uency of gastric slow waves. No significant changes in percentage of regula r slow waves were noted with the meal or with clonidine (P > 0.05). In conc lusion, 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.