Origins and patterns of spontaneous and drug-induced canine gastric myoelectrical dysrhythmia

The aim of this study was to investigate the characteristics and orientation of gastric dysrhythmia using multichannel serosal recordings in dogs. Ten dogs chronically implanted with four to eight pairs of electrodes were studied. Gastric slow waves were recorded in four sessions: postsurgical and after atropine, vasopressin, and glucagon. A total of 554.7 min of bradygastria, 201 min of tachygastria and 22.3 min of arrhythmia were observed in the recordings. The majority of bradygastria (80.5 ± 9.4%) originated in the proximal stomach (P < 0.04, vs other locations) and propagated all the way to the distal antrum. In contrast, tachygastria mainly originated in the distal antrum (80.6 ± 8.8%) (P < 0.04, vs other locations) and propagated partially or all the way to the proximal stomach. Dysrhythmia appeared intermittently with normal gastric slow waves. In all recordings, normal slow waves were present 38.0 ± 5.3% of the time, while bradygastria, tachygastria, and arrhythmia were present 35.9 ± 5.3%, 23.0 ± 1.6%, and 2.4 ± 0.5% of the time, respectively. The prevalence of dysrhythmia was highest in the distal antrum (80.4%) (P < 0.01) and lowest in the proximal part of the stomach. In conclusion, tachygastria originates from an ectopic pacemaker in the distal antrum. It may completely or partially override the normal slow waves. Bradygastria is attributed to a decrease in the frequency of the normal pacemaker in the corpus. The prevalence of gastric dysrhythmia is different in different locations of the stomach and is highest in the distal antrum.