The recording of intestinal electrical activity is used to study digestive motility. This activity consists of slow waves occurring at a frequency of 13–20 cycles per minute. The slow waves are sometimes superimposed with spike potentials. Different patterns of distribution of spike potentials on the slow waves have been shown to occur in physiological and pathological conditions, so that longlasting recording sessions are increasingly required. This presents the problem of analysis of large amounts of data that has not yet been resolved satisfactorily. We present herein an analogue automated system of analysis of the intestinal electrical activityin dogs. This system works in real time and provides online data recorded on a graphic recorder. A microcomputer controlled printer and tape recorder were also used. Slow waves are characterised both by the amplitude and the timing of occurrence of relative minima. The spike bursts are detected on the slow waves; their distribution on the slow waves is given, and their energy is measured. Thus, our system allows an easy analysis of long duration chronic recordings, qualitatively (distribution of the spike bursts on the slow waves) as well as quantitatively (time of occurrence of slow waves and number and energy of the spike bursts).

The mechanisms by which the intestinal interdigestive myoelectric complex (IDMEC), recurring at about 90 minute intervals in the fasted dog, is disrupted by feeding remain unknown. We investigated whether the IDMEC could be disrupted in the duodenum by perfusing a Thiry-Vella loop with glucose in the dog. An intestinal Thiry-Vella loop, measuring one half (80 to 160 cm) of the total length of the small bowel was constructed in four dogs from the jejunum, and in four other dogs from the ileum. Extracellular nichrome electrodes were sewn on the duodenum for recording the electrical activity of the intestine. After three weeks' recovery, electrical recordings were performed in the fasted dogs in order to observe whether the IDMEC persisted in the duodenum when the Thiry-Vella loops were perfused, at different days, for four hours with solutions made of either (1) NaCl 154 mM, (2) NaCl 308 mM, (3) glucose 300 mM, or (4) glucose 600 mM, at a rate of 8 ml/min. NaCl 308 mM and glucose 600 mM were also delivered at a rate of 4 ml/min. Glucose output from the Thiry-Vella loops was measured throughout the experiments over consecutive five minute intervals. Each experiment was performed three times in each dog. The results showed that perfusing the Thiry-Vella loops with NaCl 154 mM or NaCl 308 mM did not suppress the IDMEC in the duodenum whether the flow rate was 4 or 8 ml/min. On the contrary, perfusing the jejunal loops with glucose 300 mM disrupted the IDMEC in 54% of the experiments; perfusing glucose 600 mM disrupted the IDMEC in 83% of the experiments. In the ileal Thiry-Vella loop experiments, the IDMEC was disrupted in 33% of the cases with glucose 300 mM and in 66% of the cases with 600 mM. No significant difference was observed with glucose 300 mM delivered at a rate of 8 ml/min and glucose 600 mM delivered at a rate of 4 ml/min. Finally, the inhibitory effect of perfusing the Thiry-Vella loops with glucose increased as the amount of absorbed glucose increased. These results indicate that interruption of the IDMEC by feeding probably involves extraintestinal factors. These factors do not seem to be specific for any one part of the small intestine, but they seem to be activated by intestinal absorption.

It has been well established that the electrical activity of the small intestine consists, in the fasting state, in a cyclic phenomenon - the myoelectric complex - that recurs at about 90 minutes intervals in the dog. The myoelectric complex is disrupted by oral feeding whereas intravenous feeding does not change the cyclically recurring myoelectric activity. The aim of our work was to investigate whether intravenous ethanol was followed by changes in the myoelectric complex. 5 dogs were prepared with Ag AgCl electrodes sewn in the jejunum. After 15 days recovery, the electrical activity was recorded in the dogs fasted for 24 hours, after injection of 100% ethanol at doses of 2, 5 and 10 ml, the total volume of the solution being adjusted to 20 ml with saline. Controls were made with saline 154 mM. Each experiment was repeated twice. The effects of alcohol were studied on the 3 interdigestive cycles following injections of alcohol. The results showed that neither saline nor ethanol at dose of 2 ml did change the myoelectric complex with cycle was meanly of 90 +/- 3 minutes +/- SEM. On the contrary injection of ethanol at doses of 5 and 10 ml was followed by a disruption of the myoelectric complex during respectively 195 +/- 9 and 200 +/- 8 minutes. These results indicate that intravenous ethanol significantly interrupts the myoelectric complex. Therefore, ethanol cannot be considered as a usual nutriment as far as its effect on the electrical activity of the intestine is concerned.

Post-prandial intestinal motility, analysed through two electromyographic parameters, duration of inhibition of myoelectric complex (DIMC) and percentage of spike potentials (PSP), was studied after ingestion of glucids, proteins and lipids. Post-prandial intestinal motility depends on both chemical nature and caloric load of nutriments: DICM depends on those two factors but PSP only depends on nature of nutriments. Post-prandial intestinal motility also depends on route of administration of nutriments. Intra-jejunal administration versus intra-duodenal administration increases DIMC observed for glucids and proteins, diminishes DIMC observed for lipids and diminishes PSP observed for glucids and proteins. These results indicate a specificity of intestinal post-prandial motility with characteristics of nutriments. Intestinal digestion and absorption of nutriments, just as hormonal secretion in response to intestinal passage of nutriments could explain such a specificity.

Interdigestive intestinal myoelectric activity is characterized by repetitive aborally migrating complexes which are inhibited by feeding. The aim of the present work was to study the effects of different food components on the duration of inhibition of the myoelectric complex and on the number of spike potentials during this period. 4 dogs were prepared for chronic recordings with electrodes implanted on the jejunum and an alimentary cannula placed into the duodenum. Glucose, peptides and lipids were given into the cannula at doses of 7.5 and 15 kcal/kg. The results indicated that the inhibition of the myoelectric complex was longer for lipids than for glucose and even longer than for peptides. When the caloric load was increased, the duration of inhibition was also increased. As concerns the spike potentials, their number was increased after administration of glucose and of peptides, whereas it was decreased after lipids. Lastly, the increase of the caloric load did not change the number of spike potentials significantly. These results indicated that the duration of inhibition of the myoelectric complex depended on both the nature and the caloric load of the food components, whereas the number of spike potentials was determined only by the composition of food.

A method has been developed for monitoring the mechanical activities of individual longitudinal and circular muscles in a 5 millimeters long segment of intact intestine in the anesthetized dog. The longitudinal contractions were recorded by means of a new movement transducer. The circular contractions were recorded simultaneously using a water-filled intraluminal balloon A precise separation of longitudinal and circular motor activities was obtained with this method. The two muscle layers manifested motor activity most of the time, but their contractions were out of phase. Phase locking was observed only during short periods of time. The contractions were then sequential, the circular one being first.