This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Background: Like the heart, the stomach has a pacemaker called the slow wave that regulates gastric contractions. Many diseases which produce nausea and vomiting are associated with slow wave rhythm disturbances such as tachygastria which may lead to impaired gastric motor function. Slow waves are most accurately recorded using surgically implanted electrodes, a method that is impractical for most clinical applications. The most common clinical test of slow wave function, electrogastrography (EGG), involves placement of leads on the skin overlying the stomach. However, this method produces low quality signals of uncertain reliability. We previously validated a technique involving recording slow waves using a single mucosal electrode applied to the inside of the stomach during upper endoscopy. This method provides more reliable recordings of slow wave activity, but is limited in that only a single site can be recorded for short periods of time. We have also validated several techniques which can disrupt normal slow wave cycling both using EGG and the single mucosal electrode system. A technique to measure slow waves at multiple sites concurrently over a several hour period would provide important insight into the physiology of normal gastric electrical activity and the pathophysiology of slow wave disruptions which might occur in human disease.
Specific aims : We propose a validation study of a new method to map the gastric slow wave using modified bipolar probes attached to several sites on the gastric mucosa in twelve healthy human volunteers. Fasting volunteers without gastrointestinal illness will undergo conscious sedation, then upper endoscopy will be performed to affix separate electrodes to three predetermined regions of the gastric mucosa using standard hemoclips. Slow wave signals in different gastric regions will be acquired under control conditions and during induction of acute hyperglycemia to induce slow wave uncoupling and rhythm disturbances. Parameters to be measured will include regional slow wave frequency and amplitude, direction of slow wave propagation, velocity of slow wave propagation, and percent coupling of the slow wave between each of the three recording sites. These recordings will be compared to a concurrently performed EGG to compare the fidelity of the two techniques. Significance: Findings from this investigation will provide important insight into the physiology and pathophysiology of gastric electrical activity which will provide the foundation for investigation of potentially pathogenic gastric slow wave defects in patient populations with unexplained nausea, vomiting, and conditions of gastric dysmotility such as gastroparesis.
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