Cholinergic effects on esophageal transit and clearance.

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 contractions, 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.

Enterogastric reflux in normal subjects and patients with Bilroth II gastroenterostomy. Measurement of enterogastric reflux.

Initially, scintigraphy was established as a valid method for detecting and quantitating enterogastric reflux. A new, tubeless technique for the measurement of enterogastric reflux 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 111In bound to diethylene-triamine penta-acetic acid (250 microCi) 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 reflux indices were determined. Ten normal subjects and 13 patients with vagotomy, hemigastrectomy, and Bilroth II gastrojejunostomy were evaluated. The enterogastric reflux index in asymptomatic postsurgical patients was increased significantly to 24.6 +/- 4.7 compared with 8.2 +/- 6.0 (P less than 0.01) in normal subjects. In postsurgical patients with the syndrome of alkaline gastritis, the enterogastric reflux index was increased significantly to 86.3 +/- 7.1 (P less than 0.01) compared with asymptomatic postsurgical patients.

Esophageal scintigraphy to quantitate esophageal transit (quantitation of esophageal transit).

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.

Effects of endogenous hyperglucagonemia on lower esophageal sphincter pressure and gastric acid secretion.

Lower esophageal sphincter function and gastric acid secretion were studied in a patient with endogenous hyperglucagonemia due to a functioning islet cell carcinoma. Complete resection of the tumor resulted in a fall of the serum concentration of immunoreactive glucagon to a normal level. Pre- and postoperative resting lower esophageal sphincter pressures and lower esophageal sphincter pressure responses to administration of pentagastrin, edrophonium, and bethanechol were unchanged. After surgery, preoperative immunoreactive glucagon concentrations were reproduced by intravenous infusion or intramuscular injection of exogenous glucagon. Lower esophageal sphincter resting pressures and responses to agonists were unchanged. In contrast, glucagon administered at 36 micrograms/kg/hr, which produced a serum concentration of immunoreactive glucagon (32,000 pg/ml) much greater than observed preoperatively (1200 pg/ml), diminished resting lower esophageal sphincter pressure and sphincter responses to pentagastrin, edrophonium, and bethanechol. Similarly, pentagastrin-stimulated gastric acid secretion was unaffected by tumor resection or low-dose glucagon infusion but was decreased at a glucagon infusion rate of 36 micrograms/kg/hr. This series of observations supports the thesis that endogenous glucagon plays no physiological role in the regulation of lower esophageal sphincter pressure or gastric acid secretion.