Background: High-resolution (HR) mapping enables mechanistic insights into gastric slow wave dysrhythmias and is now achieving clinical translation. However, previous studies have focused mainly on dysrhythmias occurring on the anterior gastric wall. The present study simultaneously mapped the anterior and posterior gastric serosa during episodes of dysrhythmias induced by vasopressin to aid understanding of dysrhythmia initiation, maintenance and termination. Methods: HR mapping (8×16 electrodes on each serosa; 20–74 cm2) was performed in anesthetized subjects. Baseline recordings (21 ± 8 min) were followed by intravenous vasopressin infusion (0.1-0.5 IU ml−1 at 60–190 ml h−1) and further recordings (22 ± 13 min). Slow wave activation maps, amplitudes, velocity, interval, and frequency were calculated, and differences compared between baseline and post-infusion. Results: All subjects demonstrated and increased prevalence of dysrhythmic events following infusion of vasopressin (17% vs 51%).Both amplitude and velocity demonstrated significant differences (baseline vs. post-infusion: 3.6 vs. 2.2 mV; 7.7 vs. 6.5 mm s−1; P < 0.05 for both). Dysrhythmias occurred simultaneously or independently on anterior and posterior serosa, and then interacted according to frequency dynamics. A number of persistent dysrhythmias were compared, including: ectopic activation (n = 2 subjects), conduction block (n = 1), rotor (n = 2), retrograde (n = 3), collision/merge of wavefronts (n = 2). Conclusions: Infusion of vasopressin induces gastric dysrhythmias, which occurred across a heterogeneous range of frequencies and patterns. The results demonstrated that different classes of gastric dysrhythmias may arise simultaneously or independently in one or both surfaces of the serosa, then interact according to their relative frequencies. These results will help inform clinical dysrhythmia interpretations.
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