Characteristics of myoelectrical activities along the small intestine and their responses to test meals of different glycemic index in rats

The purpose of this study was to characterize intestinal myoelectrical activity along the small intestine and investigate its responses to test meals with different glycemic index at different locations. Sixteen rats were implanted with electrodes in the serosal surface of the duodenum, jejunum, and ileum. Intestinal myoelectrical activities were recorded from these electrodes for 30 min in the fasting state and 3 h after four kinds of meals with different glycemic index, together with the assessment of blood glucose. The results were as follows: 1) in the fasting state, the percentage of normal intestinal slow waves (%NISW) showed no difference; however, the dominant frequency (DF), power (DP), and percentage of spike activity superimposed on the intestinal slow wave (NS/M) were progressively decreased along the entire small intestine; 2) regular solid meal and Ensure solicited no changes in any parameters of intestinal myoelectrical activity; whereas glucose and glucose + glucagon significantly altered the %NISW, DF, DP, and NS/M, and the effects on the proximal intestine were opposite to those in the distal intestine; and 3) postprandial blood glucose level was significantly correlated with %NISW along the entire small intestine. We found that that, in addition to the well-known frequency gradient, there is also a gradual decrease in the DP and spikes along the small intestine in the fasting state. Glucose and hyperglycemic meals inhibit myoelectrical activities in the proximal small intestine but result in enhanced but more dysrhythmic intestinal myoelectrical activities. There is a significant negative correlation between the normality of intestinal slow waves and blood glucose.

Effects and mechanisms of gastrointestinal electrical stimulation on slow waves: a systematic canine study

The aims of this study were to determine optimal pacing parameters of electrical stimulation on different gut segments and to investigate effects and possible mechanisms of gastrointestinal electrical stimulation on gut slow waves. Twelve female hound-mix dogs were used in this study. A total of six pairs of electrodes were implanted on the stomach, duodenum, and ascending colon. Bilateral truncal vagotomy was performed in six of the dogs. One experiment was designed to study the effects of the pacing frequency on the entrainment of gut slow waves. Another experiment was designed to study the modulatory effects of the vagal and sympathetic pathways on gastrointestinal pacing. The frequency of slow waves was 4.88 ± 0.23 cpm (range, 4–6 cpm) in the stomach and 19.68 ± 0.31 cpm (range, 18–22 cpm) in the duodenum. There were no consistent or dominant frequencies of the slow waves in the colon. The optimal parameters to entrain slow waves were: frequency of 1.1 intrinsic frequency (IF; 10% higher than IF) and pulse width of 150–450 ms (mean, 320.0 ± 85.4 ms) for the stomach, and 1.1 IF and 10–20 ms for the small intestine. Electrical stimulation was not able to alter colon slow waves. The maximum entrainable frequency was 1.27 IF in the stomach and 1.21 IF in the duodenum. Gastrointestinal pacing was not blocked by vagotomy nor the application of an α- or β-adrenergic receptor antagonist; whereas the induction of gastric dysrhythmia with electrical stimulation was completely blocked by the application of the α- or β-adrenergic receptor antagonist. Gastrointestinal pacing is achievable in the stomach and small intestine but not the colon, and the maximal entrainable frequency of the gastric and small intestinal slow waves is about 20% higher than the IF. The entrainment of slow waves with gastrointestinal pacing is not modulated by the vagal or sympathetic pathways, suggesting a purely peripheral or muscle effect.

The effect of cholecystokinin peptides on ovine duodeno-jejunal slow waves with and without pretreatment with proglumide

Cholecystokinin exerts a composite influence on gastrointestinal motility but little is known about its effect on small-intestinal slow waves. Thus, six rams were implanted with four bipolar serosal electrodes onto the duodeno-jejunal wall. In the course of chronic experiments the myoelectric activity was continuously recorded in the non-fasted animals. After recording of the full normal migrating myoelectric complex (MMC), 0.15 M NaCl or CCK peptides were injected intravenously during various phases of the next MMC cycle. Five mℓ of saline was injected over 30 s during phases 1, 2a, or 2b of the MMC. Cerulein was administered at doses of 1 (over 30 s), 10 (over 30 or 60 s), or 100 ng/kg (over 30, 60, 120 or 300 s) and cholecystokinin octapeptide (CCK-OP) at doses 20 times higher. CCK peptides were applied during early or late phase 1 of the MMC and during phases 2a and 2b of the MMC. In the course of additional experiments, saline and hormone administration was directly preceded by infusion of proglumide, an unspecific CCK receptor antagonist, at a dose of 10 mg/kg. The myoelectric recordings were continued until the arrival of a subsequent regular phase 3 of theMMC.In the duodenal bulb, slow waves were occasionally observed. In the duodenum the slow-wave frequency oscillated between 20 and 24 cpm and in the jejunum between 19 and 22 cpm before or after CCK peptides and proglumide. In the duodenum the slow-wave amplitude increased significantly after all doses of cerulein injected during phase 2b of the MMC. After administration of CCK-OP changes in duodenal slow-wave amplitude were not significant but exhibited a tendency similar to those after cerulein. In the jejunum, injection of cerulein and CCK-OP during phase 2 of the MMC increased the slow-wave amplitude significantly and the duration of these changes was longer than in the duodenum. After infusion of proglumide, administration of cerulein at the low dose over 30 s and at the high dose over 300 s in the course of late phase 1 and phases 2a and 2b of the MMC, significantly increased the duodenal slow-wave amplitude. Cerulein injection during phase 2b of the MMC at the high dose over 30 and 60 s, preceded by proglumide infusion, significantly inhibited the duodenal slow-wave amplitude. In the jejunum these changes were even more pronounced and their duration was much longer. It is concluded that CCK peptides affect slow-wave amplitude in the duodeno-jejunum in non-fasted sheep. This effect is stronger in the jejunum and is altered but not abolished by pretreatment with proglumide. Cerulein evokes more pronounced alterations in the slow-wave amplitude than CCK-OP in conscious sheep.

In vitro analysis of rat intestinal wall movements at rest and during propagated contraction: a new method

Intestinal wall motions are not easily studied and are frequently deduced from manometric and electromyographic measurements. This study aimed to establish a method of wall movement analysis based on an automatic technique of image processing. Segments of rat jejunum were fixed in an organ bath under isometric conditions. A real-time edge-detection algorithm was used to find the contours of the intestine using video imaging. After the measurement, a mapping of intestinal wall movements was performed based on diameter variations. In the 260 experiments without stimulation, intestinal wall activity was always detected. Propagated activity was found in 40% of the experiments and periodic wall motion in 60%, with 0.5-Hz activity found more frequently (41%) than 0.24-Hz activity (19%). These cyclic activities, related to intestinal slow waves, had their amplitude decreased by acetylcholine and were modified by vapreotide. Analysis of a propagated wave after cholinergic stimulation showed that it is characterized by an increase of the diameter of the intestine followed by a decrease. Moreover, this methodology allows analysis of the initiation of a propagated wave.