Biomagnetic Techniques for Assessing Gastric and Small Bowel Electrical Activity

Abstract

Recent advances in electrophysiology of the gastrointestinal tract have emphasized the need for methods of noninvasive assessment of gastric and small intestinal electrical activity (GEA and IE A). While the cutaneous electrogastrogram (EGG) may reveal the frequency dynamics of gastric electrical activity, other parameters important for characterizing the propagating electrical activity are not available from EGG recordings. Recent studies on the electroenterogram (EENG) are promising, but low-conductivity abdominal layers have complicated the identification of small intestinal electrical rhythms in cutaneous recordings. The magnetogastrogram (MGG) and magnetoenterogram (MENG) are able to characterize gastric and intestinal electrical activity noninvasively in terms of its frequency, power and characteristics of its propagation. Superconducting QUantum Interference Device (SQUID) magnetometers are used to detect the minute magnetic fields associated with electrical activity of the gastrointestinal syncytium formed by interstitial cells of Cajal and smooth muscle networks. Changes in GEA and IEA that occur in response to disease or abnormal conditions are reflected in MGG and MENG signals. Magnetic methods for assessing the electrical activity of the stomach and small bowel thus show great clinical promise. GASTROINTESTINAL ELECTRICAL ACTIVITYExtracellular electrode recordings in the stomach and small bowel exhibit spontaneous, omnipresent rhythmic variation that depends on the location of the electrode. The slow wave, also known as electrical control activity or basic electrical rhythm, is present regardless of the contractile status of the tissue and modulates the appearance of smooth muscle contractions. Recently, the interstitial cells of Cajal (ICCs) located within the gastrointestinal musculature have been implicated as the originators and propagators of the slow wave [1][2][3][4][5][6]. ICC cells are connected by gap junctions to smooth muscle cells in the longitudinal and circular muscle layers, and the electrical activity propagates passively through these layers.In the stomach, the slow wave originates at a location along the greater curvature and propagates nearly instantaneously around the circumference of the stomach. The slow wave then spreads aborally as a ring of depolarization at a velocity of about 11 mm/s in humans. The stomach's pacemaker generates a new slow wave as the previous one is terminating in the pylorus [7] at a frequency of about 3 cycles per minute (cpm).

Noninvasive assessment of the effects of glucagon on the gastric slow wave

“…While an overall decrease in the slow wave frequency might suggest bradygastria, the additional changes we observed in the PPD, with signal power shifting into both brady-and tachygastric frequency ranges, suggest that glucagon induces more complicated rhythm disturbances in the gastric syncytium that could involve uncoupling, ectopic pacemakers, conduction pathway blocks, and/or reentry loops, similar to effects observed in diseased myocardium. We have observed similar PPD effects in mechanically uncoupled gastric tissue (2,29) and in vagotomized rabbits (6).…”