scholarly journals Su1312 – Abnormal Bioelectrical Slow-Wave in Patients with Gastric Submucosal Tumor, Defined by In-Vivo Laparoscopic High-Resolution Electrical Mapping

2019 ◽  
Vol 156 (6) ◽  
pp. S-538
Author(s):  
Xiaoyu Wang ◽  
Qingxiang Yu ◽  
Peng Du ◽  
Zhongqing Zheng ◽  
Tao Wang ◽  
...  
Author(s):  
Chih-Hsiang Alexander Chan ◽  
Zahra Aghababaie ◽  
Niranchan Paskaranandavadivel ◽  
Recep Avci ◽  
Leo K Cheng ◽  
...  

Gastric distension is known to affect normal slow wave activity and gastric function, but links between slow wave dysrhythmias and stomach function are poorly understood. Low­-resolution mapping is unable to capture complex spatial properties of gastric dysrhythmias, necessitating the use of high-resolution mapping techniques. Characterizing the nature of these dysrhythmias has implications in the understanding of post-prandial function and the development of new mapping devices. In this two‑phase study, we developed and implemented a protocol for measuring electrophysiological responses to gastric distension in porcine experiments. In vivo, serosal high-resolution electrical mapping (256 electrodes; 36 cm2) was performed in anaesthetized pigs (n = 11), and slow wave pattern, velocity, frequency, and amplitude were quantified before, during, and after intragastric distension. Phase I experiments (n = 6) focused on developing and refining the distension mapping methods using a surgically inserted intragastric balloon, with a variety of balloon types and distension protocols. Phase II experiments (n = 5) used barostat‑controlled 500 mL isovolumetric distension of an endoscopically introduced intragastric balloon. Dysrhythmias were consistently induced in 5 of 5 gastric distensions, using refined distension protocols. Dysrhythmias appeared 23 s (SD = 5 s) after the distension and lasted 129 s (SD = 72 s), which consisted of ectopic propagation originating from the greater curvature in the region of distension. In summary, our results suggest that distension disrupts gastric entrainment, inducing temporary ectopic slow wave propagation. These results may influence the understanding of the post‑prandial stomach and electrophysiological effects of gastric interventions.


2016 ◽  
Vol 29 (5) ◽  
pp. e13010 ◽  
Author(s):  
T. R. Angeli ◽  
P. Du ◽  
N. Paskaranandavadivel ◽  
S. Sathar ◽  
A. Hall ◽  
...  

2013 ◽  
Vol 19 (2) ◽  
pp. 179-191 ◽  
Author(s):  
Timothy R Angeli ◽  
Gregory O'Grady ◽  
Niranchan Paskaranandavadivel ◽  
Jonathan C Erickson ◽  
Peng Du ◽  
...  

2003 ◽  
Vol 124 (4) ◽  
pp. A163
Author(s):  
Wim Lammers ◽  
Luc Ver Donck ◽  
Jan A.J. Schuurkes ◽  
Betty Stephen

2012 ◽  
Vol 143 (3) ◽  
pp. 589-598.e3 ◽  
Author(s):  
Gregory O'Grady ◽  
Timothy R. Angeli ◽  
Peng Du ◽  
Chris Lahr ◽  
Wim J.E.P. Lammers ◽  
...  

2019 ◽  
Vol 317 (2) ◽  
pp. G141-G146 ◽  
Author(s):  
Tim H.-H. Wang ◽  
Timothy R. Angeli ◽  
Grant Beban ◽  
Peng Du ◽  
Francesca Bianco ◽  
...  

Postsurgical gastric dysfunction is common, but the mechanisms are varied and poorly understood. The pylorus normally acts as an electrical barrier isolating gastric and intestinal slow waves. In this report, we present an aberrant electrical conduction pathway arising between the stomach and small intestine, following pyloric excision and surgical anastomosis, as a novel disease mechanism. A patient was referred with postsurgical gastroparesis following antrectomy, gastroduodenostomy, and vagotomy for peptic ulceration. Scintigraphy confirmed markedly abnormal 4-h gastric retention. Symptoms included nausea, vomiting, postprandial distress, and reflux. Intraoperative, high-resolution electrical mapping was performed across the anastomosis immediately before revision gastrectomy, and the resected anastomosis underwent immunohistochemistry for interstitial cells of Cajal. Mapping revealed continuous, stable abnormal retrograde slow-wave propagation through the anastomosis, with slow conduction occurring at the scar (4.0 ± 0.1 cycles/min; 2.5 ± 0.6 mm/s; 0.26 ± 0.15 mV). Stable abnormal retrograde propagation continued into the gastric corpus with tachygastria (3.9 ± 0.2 cycles/min; 1.6 ± 0.5 mm/s; 0.19 ± 0.12 mV). Histology confirmed ingrowth of atypical ICC through the scar, defining an aberrant pathway enabling transanastomotic electrical conduction. In conclusion, a “gastrointestinal aberrant pathway” is presented as a novel proposed cause of postsurgical gastric dysfunction. The importance of aberrant anastomotic conduction in acute and long-term surgical recovery warrants further investigation. NEW & NOTEWORTHY High-resolution gastric electrical mapping was performed during revisional surgery in a patient with severe gastric dysfunction following antrectomy and gastroduodenostomy. The results revealed continuous propagation of slow waves from the duodenum to the stomach, through the old anastomotic scar, and resulting in retrograde-propagating tachygastria. Histology showed atypical interstitial cells of Cajal growth through the anastomotic scar. Based on these results, we propose a “gastrointestinal aberrant pathway” as a mechanism for postsurgical gastric dysfunction.


Physiology ◽  
2001 ◽  
Vol 16 (3) ◽  
pp. 138-144 ◽  
Author(s):  
Wim J. E. P. Lammers ◽  
John R. Slack

In the small intestines, the major task of the slow wave is to induce mechanical movements in the intestinal wall by generating local calcium spikes. High resolution electrical mapping reveals fundamental differences in propagation between slow waves and calcium spikes. These differences suggest that slow waves and spikes are propagated by different mechanisms through different cell networks.


2019 ◽  
Vol 156 (6) ◽  
pp. S-805
Author(s):  
Chih-Hsiang Alexander Chan ◽  
Zahra Aghababaie ◽  
Niranchan Paskaranandavadivel ◽  
Leo K. Cheng ◽  
Timothy R. Angeli

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