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In 28 controls and 142 patients subjected to a variety of antiulcer procedures, the enterogastric reflux (EGR) was quantitated by 99mTc-HIDA scintigraphy and expressed as the EGR index on 229 different occasions. The EGR index was calculated according to two different formulas: one based on the maximal radioactivity over the gastric area as a percentage value of the total abdominal activity (EGR-Im) and the other based on the relative maximal radioactivity over the gastric area as a percentage value of the relative hepatobiliary activity (EGR-It). There was a significant positive correlation of values between the two methods (P less than 0.0001). In patients with an EGR-Im greater than 20% or EGR-It greater than 57% and postgastric surgery symptoms some of the symptoms were attributed to EGR, an antireflux procedure is expected to relieve those symptoms. Sixteen of these patients underwent Roux-en-Y gastrectomy and their preoperative symptoms were relieved.

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

Plasma gastrin concentrations and gastric acid output were measured during graded balloon distention of the gastric fundus and body in 20 patients with duodenal ulcer. Acid output rose stepwise with increasing distention volumes but plasma gastrin remained unchanged. During intragastric neutralization in 5 of these subjects, fundic distention did not elicit a significant rise in plasma gastrin, whereas the acid response was similar to that observed in the control study when the gastric contents were acid. In 8 of the 20 patients, proximal gastric vagotomy profoundly suppressed the acid response to fundic distention. Basal plasma gastrin concentrations were elevated after vagotomy, but were unchanged during graded fundic distention. The results suggest that neural reflex activation of the oxyntic glands is the main mechanism by which fundic distention stimulates acid secretion in man. The failure of fundic distention to release gastrin does not, however, completely rule out the existence of an oxyntopyloric distention reflex for gastrin release in man. Fundic distention in man seems to both stimulate acid secretion and induce an inhibitory mechanism acting on acid secretion. This inhibitory mechanism may, purely speculatively, also mask the effect of an oxyntopyloric reflex for gastrin release. The present study and earlier work suggest that in man distention of the stomach is a poor stimulus for release of gastrin, regardless of whether the pyloric or the oxyntic gland area, or both, are distended.

This is a report of 21 patients presenting with epigastric pain, bilious vomiting, upper gastrointestinal bleeding, iron-deficiency anemia, and weight loss, who had undergone Billroth II gastrectomy from 3 to 35 yr earlier. Eighteen of 21 patients were found to have significant enterogastric reflux indices varying from 60% to 95% demonstrated by 99mTc HIDA scintigraphy. Thirteen patients had diversion antireflux surgery in the form of a Roux-en-Y procedure, and 1 patient had a Henley loop jejunal interposition. Postoperative 99mTc HIDA scintigraphic studies showed the enterogastric reflux indices to have decreased significantly to a range of 2%-26% (p less than 0.00001). There was marked improvement of symptoms, including correction of anemia and weight gain in those patients who had been anemic or who had sustained earlier weight loss. The enterogastric reflux indices of 10 asymptomatic control patients after Billroth II gastrectomy ranged from 4% to 45%. 99mTc HIDA scintigraphy is useful in evaluating patients before and after bile diversion surgery, and demonstrates the quantitative decrease in enterogastric reflux after such surgery.

In order to identify the mechanisms responsible for the inhibition of gastric secretion observed during acidification of the duodenal bulb, dogs were prepared with a gastric fistula (GF), Heidenhain pouch (HP), and pancreatic fistula. The duodenal bulb (5 cm) was separated from the stomach by a mucosal septum at the pyloric end and was brought to the surface in a mucocutaneous fistula distally. After the first series of experiments were completed, the dogs were reoperated and the duodenal bulb was completely separated from the stomach. The experiments were then repeated. Perfusion of the innervated duodenal bulb with 8 mEq of HC1 per hr resulted in 50% inhibition of pentagastrin (2 μg per kg-hr) -induced acid secretion from the GF and slight stimulation of pancreatic volume, bicarbonate, and protein output. Acid and pepsin secretion from the HP were unchanged by acidification of the bulb. A small dose of synthetic secretin (0.2 U per kg-hr) increased pancreatic secretion more than did bulbar acidification but did not inhibit acid secretion. A larger dose of secretin (1.6 U per kg-hr) caused 50% inhibition of acid secretion from both the GF and HP. Following the surgical separation of the duodenal bulb from the pylorus, acidification of the bulb failed to inhibit gastric secretion from the GF as well as from the HP. We interpret these results as evidence for the existence of a neural reflex, triggered by acid in the duodenal bulb, and inhibiting gastric secretion. Earlier studies by several groups have shown that acidification of the bulb inhibited HP secretion, thus indicating a hormonal mechanism. We cannot explain the failure to find evidence of such a mechanism in this study.