Abstract

We recently defined the sites of four colonic pacemakers that appear to generate the electric waves assumed to be responsible for the colonic motility. We hypothesized that a dysfunction of one or more of these pacemakers might interfere with the generation of electric waves and the colonic motility. This hypothesis was investigated in the current communication. The tests were performed during the repair of huge incisional hernia of 8 subjects (5 F, 3 M; mean age 42.8 +/- 3.3 SD years). Two electrodes were applied to each of the terminal ileum (TI), cecum (C), and ascending (AC), transverse (TC), descending (DC), and sigmoid (SC) colon. The electric activity of the TI and the various colonic segments was recorded using surface silver-silver chloride electrodes applied to the colon. The site of change of the wave variables between the TI and the C and between the different other colonic segments was determined by changing the position of the electrodes placed over the segments to be examined. Presumably, the sites where the wave variables changed represent the potential location of the pacemakers. We anesthetized these sites individually by injection of 2% Xylocaine, and then recorded the electric activity after 20 min in all the subjects and after 2 h in only 5 subjects. Electric waves in the form of pacesetter and action potentials were recorded from the TI and the colon. The sites of potential pacemakers could be defined at the ileocecal and cecocolonic junctions, at the mid third of the TC, and at the colosigmoid junction. Anesthetization of the cecal pole resulted in disappearance of the cecal electric waves, with persistence of the waves from the other colon segments. Anesthetization of the cecocolonic junction eliminated the electric waves of the AC and the right half of the TC, while the waves in the rest of the colon persisted. The remaining two pacemaker sites produced similar results when anesthetized. The electric waves reappeared after the anesthetic effect had waned. Thus, the colon possesses at least four pacemakers that appear to mediate the colonic motor activity. Individual pacemaker block by anesthetization effected disappearance of electric waves in the relative colonic segment, which reappeared after waning of the anesthetic effect. The disappearance of these waves upon pacemaker anesthetization supports a relationship between the pacemakers at the anesthetized site and the electric waves. The electric waves seem to be generated by these pacemakers. We suggest that colonic inertia, segmental or total, results from the dysfunction of one or more pacemakers, and that an artificial pacemaker could be applied for the treatment of such conditions. These suggestions need to be further studied.

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