The purpose of this study was to determine some relationships between colonic myoelectric spiking activity and intraluminal propulsion when colonic peristalsis was stimulated by bisacodyl. Myoelectric recordings were obtained in 12 subjects by means of a 50 cm long Silastic tube equipped with four bipolar electrodes fixed at 10-cm intervals. The tube was introduced into the left colon by flexible sigmoidoscopy and the electrodes were located at 50, 40, 30, and 20 cm from the anal verge. A small polyethylene catheter opening at the proximal end of the Silastic tube was used for introducing the laxative into the colon. One hour recording sessions were obtained before and after bisacodyl administration (5 mL of 0.4% solution). The control tracings showed that colonic spiking activity was made of rhythmic stationary bursts that occurred at only one electrode site and of sporadic bursts that were either propagating over the whole colonic segment or nonpropagating. Administration of bisacodyl was followed by complete suppression of the rhythmic stationary activity; a considerable increase in the sporadic spiking activity, propagating as well as nonpropagating; the occurrence of abdominal cramps and urgency to defecate, both associated with the propagating sporadic spike bursts. It is concluded that colonic propulsion induced by bisacodyl may be dependent upon the production of the sporadic bursts, particularly the propagating ones, while the rhythmic stationary bursts do not seem to play a significant role in colonic transit.
A double-blind crossover study on the effects of trimebutine on large bowel function was performed in 24 consecutive patients complaining of chronic idiopathic constipation. Their stool frequency, colonic transit time, and colonic electrical activity were measured. They were divided into a group of constipated patients with "normal" transit time (less than 40 hours) (n = 12) and another group of constipated patients with "delayed" transit time (more than 40 hours) (n = 12). The patients received trimebutine (200 mg/day per os) for one month and a placebo for another month, at random, with a washout period in between. Results show that stool frequency increased (P < 0.001) in all patients as soon as they entered the study; there was no difference between trimebutine and placebo. Colonic transit time was significantly reduced (P < 0.05) with trimebutine in patients with delayed transit time (from 105 +/- 19 hours to 60 +/- 11 hours; mean +/- SE), while it did not change with placebo (from 103 +/- 17 hours to 95 +/- 10 hours). It was slightly but not significantly increased in patients with normal transit time following trimebutine therapy. Electrical activity was not influenced by trimebutine or placebo in constipated patients with normal transit time, either before or after a meal. The number of propagating bursts during the postprandial period was significantly (P < 0.05) increased in patients with delayed transit (from 2.1 +/- 0.3 bursts/hour to 3.5 +/- 0.6 bursts/hour after trimebutine); it was decreased but not significantly with placebo (from 2.6 +/- 0.8 bursts/hour to 1.6 +/- 0.6 bursts/hour) in the same group of patients. Thus, stool frequency in patients with chronic idiopathic constipation was influenced mainly by a placebo effect. Colonic transit time was reduced by trimebutine, but this was found only in patients with delayed colonic transit; myoelectric propagating bursts were increased, and this probably explains the improvement. In conclusion, trimebutine may be of value in the treatment of patients with chronic idiopathic constipation, provided that a careful pathophysiologic evaluation reveals that they have a colonic transit time that exceeds the normal range. In addition, this study provides some argument for selecting patients with functional motor disorders of the large intestine to be entered into a research protocol or to be treated not on the basis of what they complain about--the symptom--but on the basis of some kind of measurement of dysfunction--a corresponding sign.
The great variability which is known to affect colonic motility may partly be the result of changes in physiological conditions. In order to test this hypothesis, 40 subjects were sequentially put in conditions of vigilance, rest, stress, and feeding while colonic motility was monitored. The myoelectric spiking activity of the left colon was recorded with a 50-cm-long silastic tube equipped with four bipolar ring electrodes (located 10 cm apart) introduced into the left colon by flexible sigmoidoscopy. Tracings were performed while the subjects were kept awake (by conversation) for 1 hr, put at rest (quiet) for another 1 hr, submitted to a stress (by alternatively immersing and removing one hand from 2-4 degrees C cold water) for 20 min, and finally recorded for 2 hr after a 800-kcal meal. In 18 other subjects, the sequences of vigilance and rest were randomized. The results showed that colonic spiking activity was made of sporadic bursts that are known to be associated with intraluminal propulsion and of stationary bursts that probably play no role in colonic peristalsis. The duration of sporadic spiking activity was respectively 13.6 +/- 1.2 min/hr (mean +/- SEM) during the period of vigilance, 5.4 +/- 0.6 min/hr during the period of rest (P less than 0.001), 14.3 +/- 1.0 min/hr during the period of stress (NS), and 16.8 +/- 1.2 min/hr after a meal (P less than 0.05). The duration of stationary spiking activity did not change significantly throughout the four periods, respectively, 6.6 +/- 4.9, 4.4 +/- 3.7 (NS), 5.2 +/- 3.9 (NS), and 3.3 +/- 2.8 min/hr (NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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