J Neurogastroenterol Motil 2019; 25(2): 276-285  
High-resolution Mapping of Hyperglycemia-induced Gastric Slow Wave Dysrhythmias
Peng Du,1* Gregory O’Grady,1,2 Niranchan Paskaranandavadivel,1 Shou-jiang Tang,3 Thomas Abell,4 and Leo K Cheng1,5
1Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand; 2Department of Surgery, University of Auckland, Auckland, New Zealand; 3University of Mississippi Medical Center, Jackson, MS, USA; 4University of Louisville, Louisville, KY, USA; and 5Department of Surgery, Vanderbilt University, Nashville, TN, USA
Correspondence to: *Peng Du, PhD
Auckland Bioengineering Institute, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand, Tel: +64-9-373-7599, Fax: +64-9-367-7157, E-mail: peng.du@auckland.ac.nz
Received: November 13, 2018; Revised: December 27, 2018; Accepted: January 16, 2019; Published online: April 30, 2019.
© The Korean Society of Neurogastroenterology and Motility. All rights reserved.

cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background/Aims: It is now recognised that gastric dysrhythmias are best characterised by their spatial propagation pattern. Hyperglycemia is an important cause of gastric slow wave dysrhythmia, however, the spatiotemporal patterns of dysrhythmias in this context have not been investigated. This study aims to investigate the relationship between hyperglycemia and the patterns of dysrhythmias by employing high-resolution (multi-electrode) mapping simultaneously at the anterior and posterior gastric serosa.
Methods: High-resolution mapping (8 × 16 electrodes per serosal) was performed in 4 anesthetized hounds. Baseline recordings (21 ± 8 minutes) were followed by intravenous injection of glucagon (0.5 mg per dose) and further recordings (59 ± 15 minutes). Blood glucose levels were monitored manually using a glucose sensing kit at regular 5-minute intervals. Slow wave activation maps, amplitudes, velocity, anisotropic ratio, and frequency were calculated. Differences were compared between baseline and post glucagon injection.
Results: Baseline slow waves propagated symmetrically and antegrade. The blood glucose levels were increased by an average of 112% compared to the baseline by the end of the recordings. All subjects demonstrated elevated incidence of slow wave dysrhythmias following injection compared to the baseline (48 ± 23% vs 6 ± 4%, P < 0.05). Dysrhythmias arose simultaneously or independently on anterior and posterior serosa. Spatial dysrhythmias occurred before and persisted after the onset and disappearance of temporal dysrhythmias.
Conclusions: Infusion of glucagon induced gastric slow wave dysrhythmias, which occurred across a heterogeneous range of patterns and frequencies. The spatial dysrhythmias of gastric slow waves were shown to be more prevalent and persisted over a longer period of time compared to the temporal dysrhythmias.
Keywords: Electrophysiology; Gastrointestinal tract; Hyperglycemia; Interstitial cells of Cajal; Myoelectric complex, migrating


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