Dataset Information

High-resolution optical mapping of gastric slow wave propagation.

ABSTRACT: BACKGROUND:Improved understanding of the details of gastric slow wave propagation could potentially inform new diagnosis and treatment options for stomach motility disorders. Optical mapping has been used extensively in cardiac electrophysiology. Although optical mapping has a number of advantages relative to electrical mapping, optical signals are highly sensitive to motion artifact. We recently introduced a novel cardiac optical mapping method that corrects motion artifact and enables optical mapping to be performed in beating hearts. Here, we reengineer the method as an experimental tool to map gastric slow waves. METHODS:The method was developed and tested in 12 domestic farm pigs. Stomachs were exposed by laparotomy and stained with the voltage-sensitive fluorescence dye di-4-ANEPPS through a catheter placed in the gastroepiploic artery. Fiducial markers for motion tracking were attached to the serosa. The dye was excited by 450 or 505 nm light on alternate frames of an imaging camera running at 300 Hz. Emitted fluorescence was imaged between 607 and 695 nm. The optical slow wave signal was reconstructed using a combination of motion tracking and excitation ratiometry to suppress motion artifact. Optical slow wave signals were compared with simultaneously recorded bipolar electrograms and suction electrode signals, which approximate membrane potential. KEY RESULTS:The morphology of optical slow waves was consistent with previously published microelectrode recordings and simultaneously recorded suction electrode signals. The timing of the optical slow wave signals was consistent with the bipolar electrograms. CONCLUSIONS AND INFERENCES:Optical mapping of slow wave propagation in the stomach is feasible.

SUBMITTER: Zhang H

PROVIDER: S-EPMC6724537 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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High-resolution optical mapping of gastric slow wave propagation.

Zhang Hanyu H Yu Han H Walcott Gregory P GP Paskaranandavadivel Niranchan N Cheng Leo K LK O'Grady Gregory G Rogers Jack M JM

Neurogastroenterology and motility 20180820 1

<h4>Background</h4>Improved understanding of the details of gastric slow wave propagation could potentially inform new diagnosis and treatment options for stomach motility disorders. Optical mapping has been used extensively in cardiac electrophysiology. Although optical mapping has a number of advantages relative to electrical mapping, optical signals are highly sensitive to motion artifact. We recently introduced a novel cardiac optical mapping method that corrects motion artifact and enables ...[more]

PMID: 30129082

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Project description:BackgroundGastric contractions are coordinated by slow waves, generated by interstitial cells of Cajal (ICC). Gastric surgery affects slow wave conduction, potentially contributing to postoperative gastric dysfunction. However, the impact of gastric cuts on slow waves has not been comprehensively evaluated. This study aimed to define consequences of surgical excisions on gastric slow waves by applying high-resolution (HR) electrical mapping and in silico modeling.MethodsPatients undergoing gastric stimulator implantation (n = 10) underwent full-thickness stapled excisions (25 × 15 mm, distal corpus) for histological evaluation, enabling HR mapping (256 electrodes; 36 cm(2) ) over and adjacent to excisions. A biophysically based in silico model of bidirectionally coupled ICC networks was developed and applied to investigate the underlying conduction mechanisms and importance of excision orientation.Key resultsNormal gastric slow waves propagated aborally (3.0 ± 0.2 cpm). Excisions induced complete conduction block and wavelets that rotated around blocks, then propagated rapidly circumferentially distal to the blocks (8.5 ± 1.2 vs normal 3.6 ± 0.4 mm/s; p < 0.01). This 'conduction anisotropy' homeostatically restored antegrade propagating gastric wavefronts distal to excisions. Excisions were associated with complex dysrhythmias in five patients: retrograde propagation (3/10), ectopics (3/10), functional blocks (2/10), and collisions (1/10). Simulations demonstrated conduction anisotropy emerged from bidirectional coupling within ICC layers and showed transverse incision length and orientation correlated with the degree of conduction distortion.Conclusions & inferencesOrienting incisions in the longitudinal gastric axis causes least disruption to electrical conduction and motility. However, if transverse incisions are made, a homeostatic mechanism of gastric conduction anisotropy compensates by restoring aborally propagating wavefronts. Complex dysrhythmias accompanying excisions could modify postoperative recovery in susceptible patients.

Project description:New findingsWhat is the central question of this study? This study aimed to provide the first comparison of simultaneous high-resolution mapping of anterior and posterior gastric serosa over sustained periods. What is the main finding and its importance? Episodes of spontaneous gastric slow-wave dysrhythmias increased significantly following intravenous infusion of vasopressin compared with the baseline state. A number of persistent dysrhythmias were defined, including ectopic activation, conduction block, rotor, retrograde and collision/merger of wavefronts. Slow-wave dysrhythmias could occur either simultaneously or independently on the anterior and posterior gastric serosa, and interacted depending on activation-repolarization and frequency dynamics. High-resolution 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. High-resolution mapping (8 × 16 electrodes on each serosa; 20-74 cm2 ) was performed in anaesthetized dogs. Baseline recordings (21 ± 8 min) were followed by intravenous infusion of vasopressin (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 postinfusion. All dogs demonstrated an increased prevalence of dysrhythmic events following infusion of vasopressin (17 versus 51%). Both amplitude and velocity demonstrated significant differences (baseline versus postinfusion: 3.6 versus 2.2 mV; 7.7 versus 6.5 mm s-1 ; P < 0.05 for both). Dysrhythmias occurred simultaneously or independently on the anterior and posterior serosa, and then interacted according to frequency dynamics. A number of persistent dysrhythmias were compared, including the following: ectopic activation (n = 2 animals), conduction block (n = 1), rotor (n = 2), retrograde (n = 3) and collision/merger of wavefronts (n = 2). We conclude that infusion of vasopressin induces gastric dysrhythmias, which occur across a heterogeneous range of frequencies and patterns. The results demonstrate 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 to inform interpretation of clinical dysrhythmia.

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High-resolution optical mapping of gastric slow wave propagation.

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High-resolution optical mapping of gastric slow wave propagation.

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