ELECTRICAL ACTIVITY OF SMALL INTESTINAL SMOOTH MUSCLE

Intestinal slow waves occur spontaneously and continuously in most mammalian species studied, including man, regardless of the presence or absence of contractions. They originate in the longitudinal muscle. Spikes may or may not occur during slow wave depolarization. Spikes initiate contractions, the maximal frequency of which is equal to the frequency of slow waves. Slow waves seem to provide a timing mechanism which allows spiking and subsequent contractions only at regular intervals. Slow waves are conducted from longitudinal to circular muscle along interconnecting strands of muscle fibers, thereby coordinating contractions in the two layers. The frequency of intestinal slow waves is amazingly constant in any one part of the gut; it averages 11.8 cycles per minute in human duodenum and declines to 9.0 cycles per minute in lower ileum. The negative aboral frequency gradient is stepwise, with variable lengths of intestine operating at successively lower frequencies. Within each constant frequency region, slow waves seem to be conducted aborally from a pacemaker, and apparent conduction times can be measured as the lag between corresponding points on waves recorded from two sites along the gut. However, conduction may be more apparent than real. Slow waves may originate from all cells or groups of cells in the longitudinal muscle, which would then act as a long series of oscillators. Coupling of these oscillators so that the faster ones drive the slower ones would result in many of the features of slow wave activity in the intestine. Apparent conduction times may simply represent the phase lag between a driving and a driven oscillator. The well known coordination between contractions in the gastric antrum and those in the duodenal bulb can be explained by the presence of attenuated gastric slow waves a short distance into the duodenal bulb. In this region, the duodenal slow waves are superimposed on gastric waves resulting in augmentation of those duodenal waves directly after antral activity. These augmented waves are more likely to result in spikes and, therefore, contractions of the duodenal bulb than are the ordinary duodenal slow waves. Transection (with healed end to end anastomosis) or merely damage to the myenteric plexus abolishes coupling along the chain of slow wave oscillators so that aboral regions are no longer driven by higher frequency regions oral to the injury. The maximal frequency of contraction is, therefore, decreased below such an injury. Frequency of slow waves within a segment of gut with damaged myenteric plexus is even lower than it is aboral to such a segment. The myenteric plexus is apparently involved somehow in coupling of slow wave activity along the gut and in establishing the uncoupled spontaneous frequency of slow waves. Feeding has no effect on frequency of slow waves but does lead to an increased percentage of slow waves having spikes, and, therefore, a decrease in the amount of time the gut is mechanically quiescent. Analysis of electrical spiking provides a convenient means of following the effects of feeding on intestinal contractions. A number of studies on patients with a variety of disorders have been reported but no diagnostic value of electroenterography has been established, although its use at surgery to determine the extent of irreversible bowel damage may prove to be useful. © 1969.