title: Postprandial response of jejunal slow waves and mediation via cholinergic mechanism.
abstract: The postprandial characteristics of jejunal myoelectrical activity and its mediation via cholinergic nerves were investigated in this study. Four pairs of bipolar electrodes were implanted on the serosa of the proximal jejunum of nine female hound dogs (14-22 kg). In the control session, the recording of jejunal myoelectrical activity was made for 30 min in the fasting state and for 90 min after a solid meal (0.45 kg, 838 kcal). The study session followed the same protocol except that a bolus of 0.25 mg/kg atropine was injected intravenously 30 min after the meal. Computerized spectral analysis was performed to calculate the frequency, power, and percentage of 17-22 cycles/min (cpm) slow waves. A special artificial neural network program was applied to compute the spike bursts superimposed on slow waves. All data were expressed as mean +/- SE. The postprandial frequency of the jejunal slow waves was significantly increased from 18.42 +/- 0.28 cpm in the fasting state to 18.95 +/- 0.22, 19.28 +/-0.23, and 19.28 +/- 0.22 cpm during the first, second, and third 30-min periods after the meal (all P < 0.03 in comparison with the fasting state). The percentage of the slow waves superimposed 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 comparison with fasting state). Atropine abolished the postprandial increases in the frequency of slow waves and the number of spike bursts. No significant postprandial changes in the power and the percentage of 17-22 cpm slow waves were observed. In conclusion, the postprandial response of the jejunal slow waves after a solid meal presents as an increase of the frequency of slow waves 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.
authors.affiliation: Lynn Institute for Healthcare Research, Oklahoma City, Oklahoma, USA.
authors.forename: L W
authors.initials: LW
authors.lastname: Qian
authors.forename: L J
authors.initials: LJ
authors.lastname: Peters
authors.forename: J D
authors.initials: JD
authors.lastname: Chen
mesh_terms: D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002799:Cholinergic Fibers / Q000502:physiology*; D004285:Dogs; D004435:Eating / Q000502:physiology*; D004594:Electrophysiology; D005215:Fasting / Q000502:physiology; D005260:Female; D005769:Gastrointestinal Motility / Q000187:drug effects / Q000502:physiology*; D007583:Jejunum / Q000502:physiology*; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009130:Muscle, Smooth / Q000502:physiology
chemical_list: D018727:Muscarinic Antagonists; D001285:Atropine