Recovery Of Peristalsis Research Articles

One-year follow-up after laparoscopic Heller-Dor operation for esophageal achalasia.

The Heller-Dor operation has recently been proposed for the treatment of esophageal achalasia even via a laparoscopic approach. To measure the medium-term effectiveness of this new minimally invasive technique, an evaluation of pre- and postoperative symptoms, esophagogram, endoscopic findings, esophageal manometry, and pH monitoring was prospectively designed in 43 patients with primary esophageal achalasia. The mean clinical follow-up for all the patients is 12 months (range 3-43), while the mean radiological follow-up is 11 months (range 1-23). Endoscopic data 1 year after surgery are currently available for 27 patients (63%), whereas a 12-month (range 1-26) functional follow-up (including manometric and pH-monitoring studies of the esophagus) is currently available for 35 patients (81.4%). No dysphagia was reported in 38 cases (88.4%); two (4.6%) complained of occasional swallowing discomfort which regressed spontaneously; two (4.6%) had persistent dysphagia which regressed with pneumatic dilatation. One patient (2.8%) reported mild occasional dysphagia after a 1-year asymptomatic period. Preoperatively, esophagograms showed an average maximum diameter of 40.6 +/- 9.1 mm which decreased to 24.1 +/- 6.0 mm after operation. Mean lower esophageal sphincter (LES) resting and residual pressures decreased significantly from 28.6 +/- 10.7 mmHg to 8.8 +/- 4.1 mmHg and from 17.0 +/- 9.7 mmHg to 4.7 +/- 4.0 mmHg, respectively (p < 0.0001). These effects on esophageal diameter and LES function seem to persist over time. The complete absence of any peristaltic contractions recorded preoperatively in all cases remained unchanged after surgery in all but four patients. However, this rare recovery of peristalsis proved to be transient, and patients revealed a manometric impairment of their esophageal body function, but without complaining of dysphagia. Twenty-four-hour pH monitoring showed abnormal gastroesophageal reflux episodes in two (5.7%) of the 35 patients who were monitored: one was asymptomatic; the other had heartburn and endoscopically demonstrated grade II esophagitis. Laparoscopic Heller-Dor operation achieves excellent medium-term results which, together with the already-demonstrated advantages of a minimal surgical trauma and rapid convalescence, validate the use of such a minimally invasive approach to treat patients with primary achalasia of the esophagus.

Recovery of esophageal peristalsis after congenital tracheoesophageal fistula repair in an adult

Congenital tracheoesophageal fistulas are usually recognized during early life and are associated with severe esophageal dysmotilities that supposedly persist after fistula repair. We present the case of a patient with abdominal distension diagnosed to result from congenital tracheoesophageal fistula at the age of 17 years. Prior to surgery, manometry showed aperistalsis in the esophageal body that gradually improved during the 14 months of post-operative follow-up. We hypothesized that the dysmotility was due to increased gastroesophageal reflux or to intragastric distension. Therefore, we studied: (1) the correlation between motility and gastroesophageal reflux before and after surgery, and (2) the effect of isotonic gastric distension on esophageal motility. Our studies demonstrated that one year after surgery gastroesophageal acid reflux remained abnormal and that acute experimental gastric distension had no effect on esophageal motility. In summary, esophageal dysmotility in congenital tracheoesophageal fistula may return to normal after surgical repair; neither acute gastric distension nor gastroesophageal reflux are responsible for the reversible esophageal motor abnormalities.

Effects of substance P, cholecystokinin octapeptide, bombesin, and neurotensin on the peristaltic reflex of the guinea-pig ileum in the absence and in the presence of atropine.

1. Slow peristalsis (less than one peristaltic wave/min) was induced by continuous elevation of intraluminal pressure in vascularly perfused segments of the guinea-pig isolated ileum. The intraluminal pressure at the aboral side of the segment and the volume of fluid propelled by each peristaltic wave were recorded. 2. Intraarterial infusion of substance P (11.5–115 pmoles min−1), cholecystokinin octapeptide (CCK-8; 1.5–15 pmoles min−1), bombesin (1–10 pmoles min−1), and neurotensin (3.6–36 pmoles min−1) dose-dependently stimulated peristalsis, the degree of stimulation being largest with CCK-8. Histamine, a drug contracting the smooth muscle directly, did not stimulate peristalsis. 3. Atropine (1 μM in the bath and perfusion solution) caused a transient inhibition or blockade of the peristaltic reflex, followed by a partial recovery of peristalsis (“atropine-resistant peristalsis”). Atropine-resistant peristalsis was greatly stimulated by CCK-8 (6–15 pmoles min−1), only slightly stimulated by bombesin (4 pmoles min−1), and first stimulated and then inhibited by neurotensin (36 pmoles min−1). 4. Substance P (11.5–1,000 pmoles min−1) inhibited or abolished atropine-resistant peristalsis, which was probably due to desensitization of intestinal smooth muscle and/or neurones against the peptide. [d-Pro2, d-Trp7,9] substance P, an analogue of substance P with antagonistic properties (40 nmoles min−1), also inhibited atropine-resistant peristalsis. 5. Naloxone (4.6 nmoles min−1) stimulated peristalsis both in the absence and in the presence of atropine; this indicates that endogenous opioids modulate peristaltic motility. 6. It is concluded that neuropeptides stimulate peristalsis by exciting intramural cholinergic and non-cholinergic neurones. The inhibitory actions of substance P desensitization and of the substance P antagonist in the presence of atropine indicate that substance P neurones play a role in the mechanism af the atropine-resistant peristalsis.

Postoperative Recovery of Ureteral Peristalsis

The right ureters of 5 adult dogs were 1) cut open longitudinally for 1cm and sutured lengthwise, 2) cut 3-4cm lengthwise and sutured lengthwise, 3) cut 1cm and sutured transversely and 4) cut 3-4cm and sutured transversely. Electroureterograms above and below the suture were taken for 5 hours after the operation. The results can be summarised as follows: The discharges starting from the ureteropelvic junction began to pass over the suture in 30 to 100 minutes after the operation in most cases, then gradually increased and attained a nearly constant rate in 120 minutes. The earliest discharge passing over the suture occurred in the short-incision lengthwise-sutured cases in 30 to 45 minutes after the operation. Next, in 30 to 100 minutes in the long-incision lengthwise-sutured cases, and finally in 60 to 90 minutes in the short-incision transverse-sutured cases. There were only little differences among them except in the long-incision transverse-sutured cases, in which no discharge was observed for 5 hours after the operation. From the findings obtained, it has been shown that normal discharge function of the ureter was least inhibited in the short-incision lengthwisesutured cases, next least inhibited in the long-incision lengthwise-sutured cases and short-incision transverse-sutured cases in close succession, and most inhibited in the long-incision transverse-sutured cases.