Distal colitis decreases the contractility of the underlying circular smooth muscle. We examined how time after injury and lesion severity contribute to the decreased contractility and how colitis alters the calcium-handling properties of the affected muscle. Distal colitis was induced in rats by intrarectal administration of 4% acetic acid. Contractile responses to acetylcholine, increased extracellular potassium, and the G protein activator NaF were determined for circular muscle strips from sham control and colitic rats at days 1, 2, 3, 7, and 14 postenemas. Acetylcholine stimulation of tissues from day 3colitic rats was performed in a zero calcium buffer, in the presence of nifedipine, and after depletion of intracellular stores of calcium. The colitis was graded macroscopically as mild, moderate, or severe. Regardless of agonist, maximal decrease in force developed 2 to 3 days posttreatment, followed by a gradual return to control by day 14. The inhibitory effect of colitis on contractility increased with increasing severity of inflammation. Limiting extracellular calcium influx had a greater inhibitory effect on tissues from colitic rats; intracellular calcium depletion had a greater inhibitory effect on tissues from control animals. The data suggest that both lesion severity and time after injury affect the contractile response of circular smooth muscle from the inflamed distal colon. Impaired utilization of intracellular calcium may contribute to the decreased contractility.
Symptomatic esophageal epiphrenic diverticula are usually repaired with a diverticulectomy and esophagomyotomy via a left thoracotomy with substantial postoperative pain and morbidity. If a laparoscopic approach could be shown to be safe and effective, the decrease in postoperative pain and potentially shorter hospital stay would make this technique beneficial. We report three cases repaired via a transabdominal approach. The first two cases were done laparoscopically. The third case was attempted laparoscopically and completed via a midline laparotomy, demonstrating that thoracotomy is not necessary even if laparoscopy is not possible. All three patients had long-standing debilitating symptoms refractory to standard nonsurgical therapies (botulinum toxin injection, pneumatic dilation, antispasmodic medication) with abnormal esophageal motility. There was one intraoperative complication of a left pneumothorax that required neither laparotomy nor thoracostomy. An esophagram on the first postoperative day demonstrated no extravasation and good flow into the stomach. The postoperative course was uneventful for all three patients, with the laparoscopic patients discharged on the second postoperative day and the laparotomy patient discharged on the seventh postoperative day. In conclusion, laparoscopic repair of symptomatic esophageal epiphrenic diverticula is a safe and effective technique with minimal postoperative pain and morbidity. It should be considered as an alternative to the traditional transthoracic approach, and may become the standard technique.
Hypothesis: Laparoscopic Heller myotomy with anterior fundoplication will alleviate the symptoms of achalasia and result in excellent patient satisfaction. Design: Retrospective study of consecutive patients who underwent laparoscopic Heller myotomy with anterior fundoplication for achalasia between October 1995 and July 1999. A telephone survey assessed symptoms and satisfaction. Patients were asked to quantitate their symptoms on a scale of 0 to 3 (0 = none; 1, mild; 2, moderate; and 3, severe). Setting: University referral center. Patients: Twenty-four patients who underwent laparoscopic Heller myotomy with anterior fundoplication for achalasia. Main Outcome Measures: Postoperative symptoms and satisfaction. Results: Twenty-one patients (88%) were successfully contacted. Mean follow-up was 16.5 months. The lapa
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