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Initially, scintigraphy was established as a valid method for detecting and quantitating enterogastric reflux. A new, tubeless technique for the measurement of enterogastric re flux was developed. 99mTc bound to [(2,6 dimethylphenylcarbamoylmethyl) iminodiacetic acid] (5 mCi) was administered intravenously to visualize the liver and biliary tract. One hour later, a standard liquid meal labeled with 111 In bound to diethylene-triamine penta-acetic acid (250 μCi) was given. The 99mTc and 111In activities were recorded simultaneously for 1-min periods at 15-min intervals for 2 hr over liver, gallbladder, and gastric areas of interest. Enterogastric re flux indices were determined. Ten normal subjects and 13 patients with vagotomy, hemigastrectomy, and Bilroth II gastrojejunostomy were evaluated. The enterogastric reftux index in asymptomatic postsurgical patients was increased significantly to 24.6 ± 4.7 compared with 8.2 ± 6.0 (P

Colonic transit scintigraphy was developed to quantitatively evaluate colonic transit. Using this technique the progression of a radiolabeled marker from cecal instillation to defecation was studied in 7 normal male volunteers. An 8-ml bolus containing 50 μCi of indium 111-diethylene triamine pentaacetic acid was instilled into the cecum via a 2-mm tube, which was passed orally, and serial scintigrams were obtained over 48 h. By 48 h, 70.7% ± 9.1% (mean ± SEM) of the instilled activity had been defecated. The cecum and ascending colon emptied rapidly, with a half-emptying time of 87.6 ± 27.0 min. Geometric center analysis showed an initial logarithmic progression of activity in the proximal colon and a linear progression distally. This study suggests that the transverse colon, not the cecum and ascending colon, may be the primary site for fecal storage. Colonic transit scintigraphy is a safe, physiologic, and quantitative method for evaluating the colonic transit of fecal material and may provide a useful tool for evaluating normal and abnormal large intestinal physiology.

Plasma and "equivalent" albumin loss in the feces were quantitated before and during ingestion of 40% ethanol using 51Cr-labeled albumin. Five subjects were studied in each classification of normal gastric mucosa, superficial gastritis, and chronic atrophic gastritis. During the control period, plasma albumin loss was minimal and similar in all three groups. Exposure to ethanol resulted in a greater output of plasma albumin in the feces of all subjects. This loss was statistically significant in subjects with superficial gastritis (P less that 0.01) and chronic atrophic gastritis (P less than 0.005). Two subjects from each group underwent gastric clearance studies of 51Cr-labeled albumin. Increased gastric clearance of plasma was observed in all 6 subjects during ethanol ingestion; the increase was highly significant in subjects with atrophic gastritis (P less than 0.001). We conclude that ethanol ingestion can cause increased loss of plasma protein in the feces, which may be of clinical significance in subjects with atrophic gastritis.

To evaluate the gastroesophageal (GE) scintiscan, a technique which detects andquantitates GE reflux, 30 patients with heartburn and a positive acid-reflux test and 20 normal control subjects were studied. Conventional diagnostic tests including barium esophagography, fluoroscopy, esophagogastroscopy, esophageal biopsy, acid perfusion testing, and esophageal manometry were performed on each patient with GE reflux. None of these techniques was sufficiently sensitive in detecting GE reflux. In contrast, GE reflux was visualized by scintiscanning in 27 out of 30 (90%) of patients. The GE reflux index was significantly greater in reflux patients, 11.7 ± 1.8%, compared to controls 2.7 ± 0.3%. These studies suggest that GE scintiscanning can detect GE reflux accurately, rapidly, noninvasively, and with greater sensitivity than other diagnostic techniques. In addition, it can be employed to quantitate GE reflux.

A patient is described in whom gastric stasis and vomiting of 28-yr duration were successfully treated with behavior therapy. Failure of conventional medical treatment in the face of continued vomiting led to consideration for surgery. The need for surgery was obviated by the successful application of exposure and response prevention, which resulted in a complete elimination of vomiting. Changes were produced, not only in the overt behavioral manifestation (vomiting) but in gastrointestinal motility as well. Although there was a lag, gastric emptying returned to normal. The improvements were maintained at over 1-yr follow-up study.

Modern manometric and scintigraphic techniques were employed in an effort to determine the relationships between esophageal contractions and esophageal transit and clearance. The effects of direct cholinergic stimulation with bethanechol and blockade with atropine were evaluated in a total of 20 normal subjects and 13 patients with symptomatic gastroesophageal reflux. Bethanechol increased the amplitudes of deglutition-induced and distention-induced esophageal contractions, but diminished their propagation velocities. Both esophageal transit and clearance were decreased in patients with reflux, but both were improved after bethanechol. Atropine sulfate decreased the amplitudes of contraction, accelerated their propagation velocities, and delayed esophageal transit and clearance. Both transit and clearance were diminished significantly when reflux patients were compared with normal subjects. The amplitudes of esophageal contraction were significantly lower in patients with reflux than in normal subjects. Neither bethanechol nor atropine affected the incidence of deglutition-induced esophageal contractions. These studies suggest that the efficiency of esophageal emptying may be determined by the amplitudes of esophageal contractions.

None of the tests employed currently to investigate esophageal transit is quantitative. The purpose of this study was to evaluate normal subjects and patients with a variety of esophageal disorders using a scintigraphic technique to quantitate esophageal transit. After oral administration of a bolus of water labeled with 99mTc-sulfur colloid, isotopic count rates were measured over the esophagus employing a gamma-camera on line to a digital computer. Esophageal transit was expressed as the percent emptying for each of the first 15-sec after the initial swallow and for 15-sec intervals after serial swallows. Sixty-two subjects were studied, including: normal volunteers; patients with motor disorders of the esophagus such as achalasia, diffuse esophageal spasm, and scleroderma; and patients with symptomatic gastroesophageal reflux both with and without esophageal motor dysfunction on manometic testing. Esophageal transit was decreased significantly after single and multiple swallows in patients with motor disorders of the esophagus. In addition, esophageal transit was abnormal in patients with reflux disease accompanied by abnormal motor function. In contrast, esophageal transit was normal after a single swallow, but incomplete after serial swallows in patients with reflux associated with normal esophageal motor function on manometry. We conclude that esophageal scintigraphy may be used to evaluate esophageal transit.

The role of cholinergic mechanisms in the control of gallbladder emptying has not been defined. In this report a scintigraphic technique using 2,6-dimethylphenylcarbamoylmethyl iminodiacetic acid labeled with technetium 99m to visualize the gallbladder and its emptying and diethylenetriamine pentaacetic acid labeled with indium 111 to visualize the stomach and its emptying was used to study 43 normal subjects and 18 patients with vagotomies. Direct cholinergic stimulation with bethanechol induced significant gallbladder emptying. Cholinergic blockade with atropine sulfate decreased the gallbladder emptying responses to a liquid meal, a solid meal, and the infusion of cholecystokinin-octapeptide. In patients with vagotomies, gallbladder emptying was decreased despite accelerated gastric emptying of an ingested liquid meal. The gallbladder emptying response to cholecystokinin-octapeptide was augmented in patients who had undergone vagotomy. These studies suggest that cholinergic receptors may be important in the regulation of human gallbladder emptying.

To correlate lower esophageal sphincter (LES) pressure and gastroesophageal (GE) reflux, esophageal manometry and GE scintiscanning have been used to study 40 consecutive patients. Serial scintiscanning was performed as the GE pressure gradient was increased in increments. Reflux was calculated from the ratio of esophageal to gastric radioactivity. The relationship between GE reflux and LES pressure was inverse (r = -0.60, P

The effects of morphine and the opiate antagonist naloxone on human colonic transit were investigated. In a crossover, double-blind fashion, two groups of 6 normal volunteers were studied using colonic transit scintigraphy during the administration of a test drug or control. The test drugs were morphine (0.1 mg/kg every 6 h s.c.) or naloxone (0.8 mg every 6 h s.c.); control was saline (1 ml every 6 h s.c.). Morphine significantly delayed transit in the cecum and ascending colon (p less than 0.05), slowed the progression of the geometric center (p less than 0.01), and decreased the number of bowel movements per 48 h (p less than 0.005). Naloxone accelerated transit in the transverse colon and rectosigmoid colon (p less than 0.05) and accelerated the progression of the geometric center (p less than 0.05), but had no effect on the number of bowel movements per 48 h (p greater than 0.05). These results suggest that narcotic analgesics may cause constipation in part by slowing colonic transit in the proximal colon and by inhibiting defecation. Acceleration of transit by naloxone suggests that endogenous opiate peptides may play an inhibitory role in the regulation of human colonic transit.