No abstract

When exposed to cholera toxin (CT), distal ileal loops of the rabbit small intestine showed an alteration in myoelectric activity. This alteration was defined as the migrating action potential complex (MAPC). The purpose of this study was to determine, using myoelectric recording techniques, the effects of live toxigenic Escherichia coli (TEC) on motility. Live TEC, live nontoxigenic E. coli (NTEC), and culture filtrates of these organisms were studied. Live TEC and its filtrate induced MAPC activity similar to that of CT. Live TEC induced a mean of 3.8 MAPCs/h, significantly greater than induced by live NTEC. TEC filtrate induced a mean of 14.2 MAPCs/h, significantly greater than NTEC filtrate. Heating the TEC filtrate to 100 degrees C before use resulted in a significant decrease of MAPC activity. This experiment demonstrated that live TEC and its culture filtrate altered ileal myoelectric activity. The effect may have been mediated by a heat-labile enterotoxin. This study suggests that alterations in small intestinal motility may be important in the pathogenesis of TEC diarrhea.

Dysphagia and chest pain are well-described symptoms in subjects with achalasia, diffuse esophageal spasm (DES), and high-amplitude peristaltic contractions, a subset of nonspecific motor disorders (NEMD). We observed a high incidence of chest pain and dysphagia in a different NEMD subgroup characterized by prolonged peristaltic contractile duration (PPCD) and normal contractile amplitude. We compared the manometric characteristics of patients with PPCD to healthy controls and compared the clinical profile of PPCD patients to that of patients with achalasia, DES, and high-amplitude peristalsis. In 20 patients with PPCD, mean contractile duration was 7.4 +/- 0.3 sec, significantly greater than healthy controls (3.7 +/- 0.1 sec) (P less than 0.001). PPCD was associated with an 85% incidence of chest pain and 65% incidence of dysphagia. These symptoms were similar to those observed in patients with achalasia, DES, and high-amplitude peristalsis. In PPCD patients, chest pain was more frequently of long duration in comparison to achalasia and DES. PPCD was encountered more frequently than either achalasia or DES in patients referred to our laboratory. This study suggests that in symptomatic NEMD patients, abnormal duration of peristaltic contractions, rather than abnormal amplitude, may be a distinguishing manometric feature.

Invasive strains of Escherichia coli (4608-58 and TD 213 CL) altered myoelectric activity of the small intestine in New Zealand White rabbits. The altered myoelectric activity had two distinct complex patterns. The first was defined as repetitive bursts of action potentials (RBAPs) that occurred predominantly in infected ligated ileal loops. The RBAP activity is characterized by action potential discharge activity greater than 1.5 s in duration and occurring on three or more successive slow waves on the same electrode recording site. These bursts of action potentials often migrated to adjacent electrode sites. The second complex pattern, defined as the migrating action potential complex (MAPC), occurred predominantly in the uninfected small intestine orad to the ligated ileal loop. The MAPC consists of action potential discharge activity of 2.5 s or longer that propagates aborally over at least two consecutive electrode sites. These studies demonstrated an altered myoelectric pattern, the RBAP, characteristic of invasion within the infected ligated loop. The MAPC, characteristic of noninvasion, was noted in the uninfected proximal small intestine.

There is much evidence to suggest that peristaltic function is defective in esophagitis patients and that this defect may contribute to prolonged acid exposure, promoting esophageal mucosal injury. Abnormal peristalsis may also be related to the generation of reflux symptoms. We evaluated primary peristalsis and its relationship to symptoms under basal conditions and during saline and HCl perfusion in 15 symptomatic reflux patients with gross esophagitis and 15 healthy controls. In the basal state, LES pressure (15.3 vs 25.1 mm Hg) and peristaltic amplitude (74.2 vs 104.8 mm Hg) were significantly lower in subjects with gastroesophageal reflux disease (GERD) (P less than 0.05). During HCl perfusion, peristaltic amplitude and duration increased slightly, and peristaltic velocity slightly decreased similarly in both groups. There was no difference in the incidence of nonpropagated, segmental, or swallow-initiated simultaneous contractions, or change in resting intraesophageal pressure during HCl perfusion in control and GERD groups. This study identified abnormal contractile amplitude as a specific defect in the primary peristaltic wave of esophagitis patients but does not support a role for acid-induced motility changes in the generation of symptoms in GERD.