W1234 A Comparison of Small Bowel pH Profiles in Healthy Subjects and Patients with Gastroparesis As Measured By a Non-Invasive Wireless Capsule

Abstract

Background and Aims: While intestinal motility disorders are common, the treatment options are rather limited. Electroacpuncture (EA) is known to improve gastric motility and emptying. The aim of this study was to investigate effects of EA on small intestinal motility in dogs. Methods: Six dogs were chronically implanted with 2 cannulas (one in the proximal and the other in the distal small intestine). Intestinal manometry and transit were assessed four times on 4 separate days in a randomized order: Control (saline injection), glucagon injection, glucagon plus EA, and glucagon plus EA plus naloxone. In control or glucagon session, after an overnight fast, a baseline recording of small intestinal contractions was made for a period of 30 min and then each dog was fed with a 237 ml liquid meal mixed with 100mg phenol red, and small intestinal contractions and transit were recorded simultaneously until the completion of intestinal transit (disappearance of phenol red in the chyme collected from the distal cannula). Saline or glucagon (2.87 x 10 -2 μmol/kg) was bolus injected immediately after the feeding in control or glucagon session respectively. In the EA and EA+naloxone sessions, EA was performed for a period of 15 min during Phase I of the migrating motor complex (MMC) and 30min after the meal and naloxone (1mg/kg, IV) was given 50 min before the meal. EA was delivered bilaterally at ST36 which is one of the most frequently used acupuncture points for the treatment of gastrointestinal diseases. Intestinal transit was assessed by the disappearance of phenol red and intestinal contraction was determined by the contractile index (CI: sum of the area under the curve of each contraction). Results: 1) EA induced small intestinal contractions during phase I of the (MMC) (CI: 4.4 ±0.8 at baseline vs. 8.3 ± 0.7 during EA, P =0.005); 2) in the fed state, EA significantly improved glucagon-induced small intestinal postprandial hypomotility (CI: 3.8 ± 0.4 vs. 6.1 ± 0.6, P =0.001); 3) EA significantly accelerated small intestinal transit delayed by glucagons (67.9 ± 4.3 vs. 40.2 ± 5.0 min, P =0.003); 4) there was a negative correlation between the CI and transit time (r = 0.427, = 0.039); and 5) the excitatory effect of EA was blocked by naloxone. Conclusions: EA enhances small intestinal contractions in both fasting and fed states and accelerates intestinal transit slowed by glucagon. EAmay have a therapeutic potential for treating patients with small intestinal motility disorders.