Postprandial response of jejunal slow waves and mediation via cholinergic mechanism

The postprandial characteristics of jejunal myoelectrical activity and its mediation via cholinergic nerves were investigated in this study. Four pair s of bipolar electrodes were implanted on the serosa of the proximal jejunu m of nine female hound dogs (14-22 kg). In the control session, the: record ing of jejunal myoelectrical activity was made for 30 min in the fasting st ate and for 90 min after a solid meal (0.45 kg, 838 kcal). The study sessio n followed the same protocol except that a bolus of 0.25 mg/kg atropine was injected intravenously 30 min after the meal. Computerized spectral analys is was performed to calculate the frequency, power, and percentage of 17-22 cycles/min (cpm) slow waves. A special artificial neural network program w as applied to compute the spike bursts superimposed on slow waves. All data were expressed as mean +/- SE. The postprandial frequency of the jejunal s low waves was significantly increased from 18.42 +/- 0.25 cpm in the fastin g state to 18.95 +/- 0.22, 19.28 +/- 0.23, and 19.28 +/- 0.22 cpm during th e first, second, and third 30-min periods after the meal (all P < 0.03 in c omparison with the fasting state). The percentage of the slow waves superim posed with spike bursts was increased from 19.33 +/- 3.90% at fasting state to 35.16 +/- 2.76%, 32.87 +/- 4.06%, and 34.88 +/- 3.51% during the first, second, and third 30-min periods after the meal (all P < 0.03 in compariso n with fasting state). Atropine abolished the postprandial increases in the frequency of slow waves and the number of spike bursts. No significant pos tprandial changes in the power and the percentage of 17-22 cpm slow waves w ere observed. In conclusion, the postprandial response of the jejunal slow waves after a solid meal presents as an increase of the frequency of slow w aves and the number of the spike bursts which can be abolished by atropine, and the postprandial response of the jejunal slow waves is a neural reflex dominantly mediated via vagal cholinergic nerves.