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The impact of surgical excisions on human gastric slow wave conduction, defined by high-resolution electrical mapping and in silico modeling.

ABSTRACT: Gastric 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.Patients 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.Normal 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.Orienting 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.

SUBMITTER: Du P

PROVIDER: S-EPMC4598186 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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The impact of surgical excisions on human gastric slow wave conduction, defined by high-resolution electrical mapping and in silico modeling.

Du P P Hameed A A Angeli T R TR Lahr C C Abell T L TL Cheng L K LK O'Grady G G

Neurogastroenterology and motility 20150806 10

<h4>Background</h4>Gastric 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.<h4>Methods</h4>Patient ...[more]

PMID: 26251163

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Project description:Background/aimsHigh-resolution extracellular mapping has improved our understanding of bioelectric slow-wave and spike-burst activity in the small intestine. The spatiotemporal correlation of electrophysiology and motility patterns is of critical interest to intestinal function but remains incompletely defined.MethodsIntestinal jejunum segments from in vivo pigs and rabbits were exteriorized, and simultaneous high-resolution extracellular recordings and video recordings were performed. Contractions were quantified with strain fields, and the frequencies and velocities of motility patterns were calculated. The amplitudes, frequencies, and velocities of slow-wave propagation patterns and spike-bursts were quantified and visualized. In addition, the duration, size and energy of spike-burst patches were quantified.ResultsSlow-wave associated spike-bursts activated periodically at 10.8 ± 4.0 cycles per minute (cpm) in pigs and 10.2 ± 3.2 cpm in rabbits, while independent spike-bursts activated at a frequency of 3.2 ± 1.8 cpm. Independent spike-bursts had higher amplitude and longer duration than slow-wave associated spike-bursts (1.4 ± 0.8 mV vs 0.1 ± 0.1 mV, P < 0.001; 1.8 ± 1.4 seconds vs 0.8 ± 0.3 seconds, P < 0.001 in pigs). Spike-bursts that activated as longitudinal or circumferential patches were associated with contractions in the respective directions. Spontaneous peristaltic contractions were elicited by independent spike-bursts and travelled slower than slow-wave velocity (3.7 ± 0.5 mm/sec vs 10.1 ± 4.7 mm/sec, P = 0.007). Cyclic peristaltic contractions were driven by slow-wave associated spike-bursts and were coupled to slow-wave velocity and frequency in rabbit (14.2 ± 2.3 mm/sec vs 11.5 ± 4.6 mm/sec, P = 0.162; 11.0 ± 0.6 cpm vs 10.8 ± 0.6 cpm, P = 0.970).ConclusionsMotility patterns were dictated by patterns of spike-burst patches. When spike-bursts were coupled to slow-waves, periodic motility patterns were observed, while when spike-bursts were not coupled to slow-waves, spontaneous aperiodic motility patterns were captured.

Project description:BackgroundElectrical status epilepticus during slow-wave sleep (ESESS) which is also known as continuous spike-wave of slow sleep (CSWSS) is type of electroencephalographic (EEG) pattern which is seen in ESESS/CSWSS/epilepsy aphasia spectrum. This EEG pattern can occur alone or with other syndromes. Its etiology is not clear, however, brain malformations, immune disorders, and genetic etiologies are suspected to contribute. We aimed to perform a systematic review of all genetic etiologies which have been reported to associate with ESESS/CSWSS/epilepsy-aphasia spectrum. We further aimed to identify the common underlying pathway which can explain it. To our knowledge, there is no available systematic review of genetic etiologies of ESESS/CSWSS/epilepsy-aphasia spectrum. MEDLINE, EMBASE, PubMed and Cochrane review database were searched, using terms specific to electrical status epilepticus during sleep or continuous spike-wave discharges during slow sleep or epilepsy-aphasia spectrum and of studies of genetic etiologies. These included monogenic mutations and copy number variations (CNVs). For each suspected dosage-sensitive gene, further studies were performed through OMIM and PubMed database.ResultsTwenty-six studies out of the 136 identified studies satisfied our inclusion criteria. I51 cases were identified among those 26 studies. 16 studies reported 11 monogenic mutations: SCN2A (N?=?6), NHE6/SLC9A6 (N?=?1), DRPLA/ ATN1 (N?=?1), Neuroserpin/SRPX2 (N?=?1), OPA3 (N?=?1), KCNQ2 (N?=?2), KCNA2 (N?=?5), GRIN2A (N?=?34), CNKSR2 (N?=?2), SLC6A1 (N?=?2) and KCNB1 (N?=?5). 10 studies reported 89 CNVs including 9 recurrent ones: Xp22.12 deletion encompassing CNKSR2 (N?=?6), 16p13 deletion encompassing GRIN2A (N?=?4), 15q11.2-13.1 duplication (N?=?15), 3q29 duplication (N?=?11), 11p13 duplication (N?=?2), 10q21.3 deletion (N?=?2), 3q25 deletion (N?=?2), 8p23.3 deletion (N?=?2) and 9p24.2 (N?=?2). 68 of the reported genetic etiologies including monogenic mutations and CNVs were detected in patients with ESESS/CSWSS/epilepsy aphasia spectrum solely. The most common underlying pathway was channelopathy (N?=?56).ConclusionsOur review suggests that genetic etiologies have a role to play in the occurrence of ESESS/CSWSS/epilepsy-aphasia spectrum. The common underlying pathway is channelopathy. Therefore we propose more genetic studies to be done for more discoveries which can pave a way for proper drug identification. We also suggest development of common cut-off value for spike-wave index to ensure common language among clinicians and researchers.

Dataset Information

The impact of surgical excisions on human gastric slow wave conduction, defined by high-resolution electrical mapping and in silico modeling.

Publications

The impact of surgical excisions on human gastric slow wave conduction, defined by high-resolution electrical mapping and in silico modeling.

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