Search

The effect of pirenzepine and cimetidine on healing, symptoms and relapse rate of duodenal ulcer was studied in a placebo-controlled double-blind trial. Cimetidine (1 g daily) was superior at the beginning of therapy to a low dose of pirenzepine (75 mg daily) and placebo with regard to symptoms. No significant differences in ulcer healing were found between the 3 groups of treatment. The relapse rate after treatment with pirenzepine was lower than after treatment with cimetidine.

The effect of thin and pliable gastric and transpyloric duodenal tubes on gastric emptying was studied in healthy volunteers. Gastric emptying was unaffected by both gastric and transpyloric tubes. Gastric emptying was also similar whether a milk-cream meal was instilled via a tube or was swallowed. The effect of a transpyloric tube on postprandial and fasting duodenogastric reflux was studied by using a technique that does not require a transpyloric tube in order to measure reflux. Duodenogastric reflux was similar in the fasting state and after feeding and was not affected by a transpyloric tube. In conclusion, thin and pliable gastric and transpyloric tubes do not affect gastric emptying and duodenogastric reflux in humans, and, in addition, the mode of administration of a meal does not affect gastric emptying.

Four focal foveolar hyperplasias (hyperplastic polyps) and 41 hyperplasiogenous polyps were studied by serial sections and partial graphic reconstruction. Position of mitoses and the border between foveolar epithelium and glandular epithelium were recorded. The results show that the hyperplasiogenous polyp essentially is a hyperplasia of the gastric mucosa in which the foveolar epithelium always plays a major role. The zone of mitotic activity, especially the transitional zone between proliferating and differentiated cells, is widened. The glands usually show atrophy, but also may be normal or hyperplastic. An overaging of foveolar epithelia may contribute to development of erosions frequently seen. Splitting of the muscularis mucosa seems to be a secondary phenomenon which in turn may contribute to cystic dilation of foveolae. Because of its characteristics in structure and cell proliferation the term "hyperplasiogenous polyp" seems to be justified and preferable as compared to the term "hyperplastic polyp" (WHO-nomenclature; Oota, 1977).

In order to assess whether in reflux esophagitis morphological and functional disorders persist after macroscopic healing, cimetidine was given for 6-12 weeks at a dose of 1.6 g/day to 30 patients with acid gastroesophageal reflux and esophagitis. The mucosal defects healed in 6 patients, improved in 14 patients, and remained unchanged in 10 patients. Lower esophageal sphincter pressure, acid clearance, acid perfusion test, and histological signs of mucosal inflammation were assessed before and after treatment. The histological and functional findings did not improve after healing of the mucosal defects. Therefore, endoscopic normalization in patients with reflux esophagitis is not associated with the disappearance of inflammation and abnormal motor function. The persistence of these abnormalities might explain the tendency of esophagitis to recur after symptomatic and endoscopic "healing."

A two marker technique was used to measure gastric emptying, duodenogastric reflux, and gastric volume secretion after intragastric instillation of a 300 ml liquid lipid meal in 11 dogs. The dogs either had an intact pylorus (n = 5), a Heineke -Mikulicz pyloroplasty (n = 3), or an extramucosal circular pylorectomy (n = 3). The mean gastric emptying rates in the three groups of dogs were 4.9 ml/min +/- 0.3 SEM, 5.7 +/- 0.2 (p less than 0.05), and 8.6 +/- 1.8 (p less than 0.01) respectively. The duodenogastric reflux rates were 0.7 ml/min +/- 0.2 SEM, 1.8 +/- 0.2 (p less than 0.05), and 3.2 +/- 1.0 (p less than 0.05), respectively. The gastric volume secretion did not significantly differ. Although emptying rates were higher in the dogs with surgically destroyed pylorus than in dogs with intact pylorus, the rate of disappearance of the test meal from the stomach was nearly identical in the three groups. This is due to the different degrees to-and-fro movements across the gastroduodenal junction. They amounted to 2.3 percent of the test meal +/- 1.0 SEM in dogs with intact pylorus, to 7.7 +/- 1.0 in dogs with pyloroplasty (p less than 0.05), and to 15.5 +/- 2.4 in dogs with pylorectomy (p less than 0.01). It is concluded that pyloroplasty and pylorectomy increase both gastric emptying and duodenogastric reflux rate. Simple assessment of the disappearance of a test meal from the stomach without measurement of to-and-fro movements cannot detect this effect on emptying rate. The pylorus keeps to-and-fro movements across the gastroduodenal junction at a low level.

The effect of pirenzepine and cimetidine on healing, symptoms, and relapse rate of duodenal ulcer was studied in a placebo controlled double blind trial. With regard to symptoms, cimetidine (1 g daily) was superior at the beginning of therapy to a low dose of pirenzepine (75 mg daily) and to placebo. No significant differences in ulcer healing were found between the 3 treatment groups. The relapse rate after treatment with pirenzepine was lower than after treatment with cimetidine.

The effect of cisapride, a new gastrokinetic drug, on gastric emptying and duodenogastric reflux of bile salts was tested in healthy volunteers in a placebo-controlled double-blind randomized cross-over trial. Twenty subjects were treated with either 10 mg of cisapride, tid orally or with matching placebo tablets for 1 wk. On test days, the subjects were studied using a marker technique with gastric intubation in the fasting state and after feeding a mixed liquid meal. Cisapride did not affect gastric secretion and gastric emptying. There was a tendency to lower reflux rates after cisapride treatment both fasting (0.63 +/- 0.14 versus 0.38 mumol/min +/- 0.05 SEM) and after feeding (2.60 +/- 0.61 versus 1.88 mumol/min +/- 0.33 SEM). This was due to a decrease of high placebo reflux rates: the reduction of reflux rate achieved by cisapride was significantly correlated to the height of the placebo reflux rate (p less than 0.001). A similar relationship was found for gastric bile salt concentration (p less than 0.001). It is concluded that cisapride reduces high bile salt reflux. Therapeutic trials with this drug in diseases where high bile reflux is believed to play a pathogenic role are of interest.

Bile acids have experimentally been found to damage the gastric mucosa and, thus, may be involved in stress lesion pathogenesis. We therefore measured intragastric bile acid concentrations in 26 critically ill, artificially ventilated patients. The control group consisted of eight healthy volunteers, whose treatment was similar to that of the patients with respect to bed rest, enteral feeding, and administration of H2-blockers. Gastric contents were aspirated via a gastric tube every hour for 24 h. Patients had higher intragastric bile acid concentrations than healthy controls, whether fasting [median 1.3 mmol/L (range 0.7-2.5) versus 0.3 (0.2-0.5) (p less than 0.05)] or fed via a gastric tube [1.3 (0.4-4.0) versus 0.4 (0.2-0.7) (p less than 0.05)]. Physiotherapy, nursing, and drugs (opiates, benzodiazepines, dopamine, pirenzepine, and metoclopramide) had no detectable influence on intragastric bile acid concentrations and pH in patients. We conclude that patients at risk to develop stress lesions have largely increased gastric bile acid concentrations that probably are due to increased duodenogastric reflux. This might be relevant for stress lesion pathogenesis.

Acid and pepsinogen secretion were studied in the isolated luminally perfused mouse stomach. Stimulation was obtained with bethanechol 10(-5)M. Pirenzepine blocked the effect of bethanechol in a dose dependent manner. The minimal blocking dose was 10(-5)M. Atropine 10(-6)M blocked secretion to a similar extent as pirenzepine 10(-5)M. Addition of tetrodotoxin did not change the response to bethanechol or to bethanechol together with pirenzepine. It is concluded that acid and pepsinogen secretion stimulated by bethanechol are inhibited by atropine and pirenzepine. There is at present no evidence that bethanechol stimulation or antimuscarinic inhibition act via intramural nerves.

Predictors of duodenal ulcer healing and relapse were examined in a population known to have a high healing incidence. Two double-blind prospective studies were performed in 134 patients over 4 wk and in 66 patients over 1 yr, respectively. Short-term treatment consisted either of cimetidine 1 g/day, pirenzepine 75 mg/day, or placebo. In a multiple stepwise linear regression analysis the following factors proved to increase healing incidence in decreasing order of importance: female sex, moderate alcohol consumption, abstinence from smoking, young age, and cimetidine treatment. The following factors had no influence on duodenal ulcer healing: number and total area of peptic lesions, concomitant disease, relatives with duodenal ulcer, duration of duodenal ulcer disease, and status as a migrant worker. In the long-term study, treatment consisted either of cimetidine 400 mg at bedtime, pirenzepine 30 mg at bedtime, or placebo. Cimetidine prevented ulcer relapse. Smoking favored duodenal ulcer relapse in the placebo group, but not in the cimetidine and pirenzepine group. For all the other factors no statistically significant effect was found. It is concluded that in a population with high spontaneous healing incidence (a) factors other than drug treatment such as sex, alcohol intake, smoking, and age are at least as important predictors of the outcome of short-term treatment as the drug treatment itself; (b) moderate alcohol intake might favor ulcer healing; (c) the unfavorable effect of smoking on ulcer relapse is overcome by low-dose, long-term, antisecretory treatment.

The effect of a transpyloric tube on duodenogastric reflux and on gastric emptying was studied in dogs with either an intact pylorus, a Heineke-Mikulicz pyloroplasty, or an extramucosal circular pylorectomy. In fasting dogs, duodenogastric reflux was 10 times smaller than after feeding a liquid lipid meal. A transpyloric tube increased the reflux rate in fasting, but not in fed dogs, while pylorectomy increased reflux rate and intragastric accumulation of a duodenal marker in fed, but not in fasting dogs. It is concluded, therefore, that in the dog (1) methods to measure duodenogastric reflux should not involve the necessity to position a transpyloric tube and (2) the pylorus and adjacent structures are involved in keeping duodenogastric reflux at a low level.

In humans duodenogastric reflux and gastric emptying were measured simultaneously by a two-marker technique that avoids transpyloric intubation. The duodenal marker consisted of 99mTc-labeled Hepatobida and was infused intravenously at a constant rate. Hepatobida was cleared almost exclusively by the liver and entered the duodenum at a constant rate via the bile. The gastric marker consisted of 51CrCl2 and was used to measure total intragastric volume by the double-sampling technique. Duodenogastric reflux occurred both after meals and under fasting conditions. Reflux rate was on the average 13 times smaller than emptying rate. It was higher with a lipid than with a protein meal and was independent of the rate of gastric emptying. The gastric concentration and total amount of duodenal contents were higher after lipid than protein meals. Since gastric emptying of a protein meal was faster than emptying of a lipid meal, the increased gastric concentration and accumulation of duodenal contents after lipid meals are due to a slowed gastric clearing and increased reflux of duodenal contents. Under fasting conditions, the reflux was lower and the gastric concentration of duodenal contents was higher than with both types of meals. Hence regurgitated duodenal contents may cause more damage to the gastric mucosa under fasting conditions than postprandially.

Conventional gastric analysis by continuous aspiration and a marker technique that allows the stomach to retain its volume were compared with respect to the measured rates of gastric secretion and bile salt reflux in 10 fasting subjects. In marker technique studies, the stomach contained 35.7 +/- 3.3 ml (mean +/- SEM) and emptied at a rate of 4.1% +/- 0.4% per minute. Secretion rates of volume and acid were similar in studies using continuous aspiration and in marker technique studies. In contrast, the bile salt reflux rate was significantly higher when continuous aspiration was performed (0.89 +/- 0.11 vs. 0.38 +/- 0.06 mumol/min, p less than 0.01). Gastric bile salt concentrations were also higher (765 +/- 48 vs. 366 +/- 67 mumol/L, p less than 0.01). This may be due to changes in the gastroduodenal pressure gradient induced by evacuating the stomach. It is concluded that measurements of bile salt reflux are influenced by the method of collecting gastric juice.

Duodenogastric reflux of a perfused marker and bile salt reflux, as well as emptying of fasting gastric contents and gastric secretion, were measured simultaneously in six healthy volunteers. Each of the subjects was studied three times in randomized order during intravenous administration of either saline or atropine (40 micrograms/kg/4 hr) or cerulein (360 ng/kg/4 hr). Fractional gastric emptying rate was inhibited from 4.57%/min +/- 0.50 SE to 0.70 +/- 0.15 by atropine (P less than 0.001) and to 1.80 +/- 0.29 by cerulein (P less than 0.005). Atropine increased reflux of duodenally perfused phenol red from 0.95 +/- 0.28 to 26.09 +/- 4.98% (P less than 0.005) without affecting bile salt reflux (0.44 +/- 0.07 vs 0.51 +/- 0.17 mumol/min). In contrast, cerulein did not significantly affect duodenogastric marker reflux (2.23 +/- 0.82%) but increased bile salt reflux to 0.94 +/- 0.16 mumol/min (P less than 0.05). It is concluded that reflux of duodenal contents and reflux of bile salts do not necessarily parallel each other. This may produce considerable confusion by apparently contradictory results in studies on duodenogastric reflux.

The effect of cisapride, a new gastrokinetic drug, on gastroduodenal motility was tested in six healthy volunteers. In order to obtain a model for slowed gastric emptying, dopamine was infused at a rate of 8 micrograms/kg/min. Dopamine significantly slowed the fractional emptying rate of fasting gastric contents from 5.14 +/- 0.37 to 1.45 +/- 0.67 %/min. Injection of either 10 mg of cisapride or 10 mg of metoclopramide restored emptying rate to normal (5.87 +/- 0.56 and 5.62 +/- 0.61 %/min, respectively). When cisapride was given without dopamine background, emptying was only moderately enhanced. Reflux of bile salts was not significantly affected by either cisapride or dopamine alone. When given on a dopamine background, however, both metoclopramide and cisapride decreased bile salt reflux below control values without any active treatment. It is concluded that emptying of fasting gastric contents can be speeded by cisapride, particularly when emptying is slowed by dopamine. A clear effect on bile salt reflux cannot be demonstrated.

The question was examined as to whether or not lower esophageal sphincter pressure (LESP) rises in response to increases in intragastric pressure. Pressure profiles of the lower esophageal sphincter (LES) were recorded with low compliance rapid pull-through manometry, in 9 healthy volunteers without hiatal hernia. Fundic pressure was increased by inflating the stomach with air. Air insufflation was stopped when gastric distension became painful (at 8.4 mm Hg +/- 0.7 SEM). No subject had nausea. Mean resting LESP was 24.6 mm Hg +/- 2.2 SEM. There was a negative linear relationship between fundic pressure and LESP: LESP decreased by 1.10 +/- 0.15 SEM per 1 mm Hg fundic pressure rise. On the average, the sum of fundic pressure and LESP remained constant. Thus, there is not only a lack of reflex contraction of LES in response to fundic pressure rise, but actually a weakening of the LES by fundic distension. This mechanism might facilitate belching following swallowing of air.

Duodenogastric reflux, gastric emptying, and gastric secretion were measured simultaneously by a double-marker technique after instillation of a liquid lipid meal (300 ml Intralipid) or a protein meal (300 ml Bactopeptone) in five trained mongrel dogs. A lipid meal was emptied slower and elicited less volume secretion than a protein meal. Duodenogastric reflux rate and intragastric accumulation of duodenal contents were similar with both meals. Intravenous infusion of atropine slowed gastric emptying and inhibited gastric volume secretion only in the case of protein meal. Atropine increased duodenogastric reflux rate and gastric accumulation of duodenal contents with both protein and lipid meals. The percentage of duodenal contents inside the stomach increased continuously during gastric emptying; it did not exceed 20% with both meals given alone and 40% with both meals given together with atropine. It is concluded that duodenogastric reflux and gastric accumulation of duodenal contents are common phenomena during gastric digestion of a meal. The degree of such accumulation does not depend on the type of meal. Intragastric accumulation of duodenal contents is increased when duodenogastric reflux rate is stimulated and when gastric emptying rate is inhibited simultaneously.

Two hundred eighty-nine patients with various chest symptoms were studied by interview for the presence and type of symptoms, and by long-term esophageal pH monitoring for acid reflux. One hundred eighty of the patients also had upper gastrointestinal endoscopy. There was significant correlation between the results of all three methods. pH monitoring was more sensitive (92.9% vs. 81.0%) and specific (41.3% vs. 23.9%), and classified more patients correctly (55.6% vs. 37.2%), than an interview by an experienced gastroenterologist when esophageal erosions were regarded as "gold standard" for pathologic reflux. Of all patients, 31.5% had unclear symptoms and therefore could not be diagnosed by interview alone. Forty nine percent of these had pathologic reflux on pH monitoring. Among the patients, 72.3% who had symptoms typical of reflux disease also had a pathologic result at pH monitoring. It is concluded that most patients with unambiguous symptoms of esophageal reflux can correctly be diagnosed by interview, but that esophageal pH monitoring has a role in the management of patients with less characteristic chest symptoms.

The effect of cigarette smoking on gastroesophageal reflux and the effect of the pH electrode on salivary secretion and swallowing frequency were studied in 30 healthy volunteers (15 habitual smokers, 15 non-smokers) and in 10 smoking patients with proven gastroesophageal reflux disease. Twenty-four-hour pH profiles were measured while the subjects were ambulatory using a combined glass electrode connected to a portable recorder. In 8 of the smoking volunteers, swallowing frequency and salivary secretion were measured, both when smoking and when not. Smokers had more reflux episodes than nonsmokers [median per hour 2.8 (range 0.4-7.1) for the upright body position and 0.5 (range 0.0-1.7) for the supine body position vs. 1.4 (range 0.0-2.1) upright and 0.0 (range 0.0-0.7) supine, p less than 0.01], but the total time of exposure of the esophageal mucosa to acid was affected neither by the status of being a smoker nor by actual smoking. Nasopharyngeal intubation with the pH electrode did not affect the swallowing frequency, but it increased salivary secretion two-to threefold for a period of 4 h. Six hours after introduction of the pH electrode and later, salivary flow was similar to baseline. It is concluded that smoking and nasopharyngeal intubation does not adversely affect the results of 24-h pH-metry.

A two-marker technique was used to determine gastric emptying rate and postprandial duodenogastric reflux rate without transpyloric intubation. The fractional gastric emptying rate in five dogs with normal pylorus was 3.0 +/- 0.3 (SE) X 10(-2)/min. In three dogs with circular pylorectomy, it was 5.8 +/- 0.8 X 10(-2)/min (P less than 0.01). The duodenogastric reflux rates were 0.72 +/- 0.23 (SE) ml/min and 3.21 +/- 0.97 ml/min. (P less than 0.05). The percentage of the test meal that by to-and-fro movements across the pylorus was emptied more than once was 2.3 +/- 1.0 (SE) in normal dogs and 15.5 +/- 2.4 after pylorectomy (P less than 0.005). Because the higher emptying rate was accompanied by more to-and-fro movements, the amount of the meal remaining in the stomach, and thus net gastric emptying, was similar in both groups. It is concluded that pylorectomy increases both reflux rate and emptying rate. This effect on emptying can only be detected by a method that includes the measurement of to-and-fro movements across the pylorus. The pylorus thus appears to prevent postprandial duodenogastric reflux and to slow gastric emptying.

A two-marker technique avoiding transpyloric intubation was used to measure the volume of gastric secretion, the rate of gastric emptying and the degree of postprandial duodenogastric reflux in 8 dogs, 5 without and 3 with Heineke-Mikulicz pyloroplasties. The stomach emptied after a liquid fatty meal at an overall rate of 4.9 ml/min +/- 0.2 s.e.m. in animals with a normal pylorus and 5.7 +/- 0.2 ml/min in those with pyloroplasties (P less than 0.05). Though mean fractional emptying rates were similar, the fractional emptying rate was greater in animals with pyloroplasties than in those without in the first 10 and in the last 20 minutes. The rate of duodenogastric reflux was likewise greater in animals with pyloroplasties than in those without (1.8 +/- 0.2 ml/min and 0.7 +/- 0.2 ml/min respectively, P less than 0.05). The rates of gastric secretion did not differ materially (2.2 +/- 0.3 ml/min and 2.1 +/- 0.2 ml/min), but a greater proportion of the gastric contents was emptied more than once in animals with pyloroplasties than in those without (7.7 +/- 1.5 per cent and 2.3 +/- 1.0 per cent, P less than 0.05).

The effect of oral ranitidine 150 mg on the acid and pepsin response to sham feeding or pentagastrin was examined in healthy volunteers in a double-blind randomized trial. Gastric juice was collected up to 255 min after ingestion of the drug. In placebo treated subjects, basal acid secretion rate and the secretion rate following sham feeding and injection of 6 micrograms kg-1 of pentagastrin were 5.3 +/- 2.0 S.E.M., 12.3 +/- 3.2, and 24.4 +/- 5.4 mmol h-1, respectively. The corresponding values in ranitidine treated subjects were 0.1 +/- 0.1, 0.5 +/- 0.2, and 3.4 +/- 1.2, respectively. The reduction of acid secretion in all three instances is statistically significant (p less than 0.025, p less than 0.05, and p less than 0.05, respectively). Basal, sham feeding stimulated, and pentagastrin stimulated pepsin secretion rates in the placebo treated group were 38.4 +/- 7.0 S.E.M., 68.6 +/- 13.2, and 39.2 +/- 8.0 mg h-1, respectively. In the ranitidine treated group, the values were 5.0 +/- 3.4, 13.2 +/- 5.6, and 19.6 +/- 6.0, respectively. The reduction of pepsin secretion during basal state and following sham feeding is statistically significant (p less than 0.005 and p less than 0.01). Thus, oral ranitidine inhibits the acid and pepsin response to sham feeding in man. Its inhibitory effect on the acid response to pentagastrin lasts for at least 4 h.

Orally or intravenously administered beta 2-adrenergic drugs have been found to inhibit esophageal motor function. Since inhalation of these drugs results in less systemic side effects, the present double-blind study was designed to investigate the influence of inhalation of the beta 2-adrenergic agonist albuterol (salbutamol) on esophageal motor function and gastroesophageal reflux in ten healthy volunteers. Esophageal motor function was recorded using a pneumohydraulically perfused multilumen manometry tube. Twenty-four-hour pH profiles were measured while the volunteers were ambulatory using a combined glass electrode connected to a portable recorder. Inhalation decreased neither lower esophageal sphincter pressure nor esophageal peristaltic amplitudes. Gastroesophageal reflux was similar on both occasions during inhalation of albuterol (3.1% [range, 1.0% to 25.5%] median upright time, with esophageal pH less than 4; and 0.1% [range, 0.0% to 10.7%] supine time) and during placebo treatment (3.6% [range, 1.6% to 19.8%] upright and 0.0% [range, 0.0% to 2.5%] supine time). Our data support the study of inhalation of beta 2-adrenergic drugs in asthmatic patients with accompanying gastroesophageal reflux.

Twenty original papers that reported on the effect of wheat bran on large bowel function were analysed. Bran increased the stool weight and decreased the transit time in each study in healthy controls and in patients with the irritable bowel syndrome, with diverticula, and with chronic constipation. Statistical evaluation of the data showed, however, that constipated patients had lower stool output and slower transit whether or not they had taken bran, and they responded less well to bran treatment than controls. From these data it is concluded that bran can be expected to be only partially effective in restoring normal stool weight and transit time in patients who are constipated.

In 3935 patients who underwent upper fiberpanendoscopy in two Zurich hospitals the coincidence of different active peptide lesions has been investigated. There was an association of reflux esophagitis and duodenal ulcer in old age: in patients with reflux esophagitis aged over 60 years, duodenal ulcer was found twice as often as in elderly patients without esophagitis. No association of reflux esophagitis and gastric ulcer or of gastric ulcer and duodenal ulcer was observed.

Experimentally, the gastric and the duodenal mucosa can both be damaged by acute exposure to small intestinal juice. Though chronic exposure to bile causes mucosal erythema and hyperplasia, the gastric mucosal barrier is not damaged. Duodenogastric reflux is relevant in the pathogenesis of postoperative bilious vomiting and probably of "alkaline" reflux esophagitis. The exact mechanism of mucosal damage has not been established. Duodenogastric reflux is likely to be irrelevant in the pathogenesis of (microscopic) gastritis, of gastric ulcer, and of reflux esophagitis without previous gastric surgery.

Long-term esophageal pH-metry has become the preferred test to quantify acid gastroesophageal reflux, but its accuracy in separating physiologic from pathological reflux is not well defined. To establish optimal thresholds of 24-h pH-metry, we studied 45 patients with clinically proven gastroesophageal reflux disease and 42 healthy volunteers. Twenty-four-hour esophageal pH was measured while the subject was ambulatory, using a combined glass electrode connected to a portable recorder. Percentage of time with esophageal pH less than 4, the number and mean duration of reflux episodes, the number of episodes lasting longer than 5 min, and the duration of the longest episode were calculated for periods of upright and supine body position, respectively. Discriminant analysis and receiver-operating-characteristic analysis were used to define optimal thresholds. A maximum of sensitivity (93.3%) and specificity (92.9%) was obtained using receiver-operating-characteristic analysis with the following criteria. Only percentage of time with esophageal pH less than 4 is considered. A subject is classified as "normal" if both values for the upright and supine body position are below the thresholds, otherwise the subject is classified as "pathological." The thresholds are 10.5% of time with esophageal pH less than 4 for the upright position and 6.0% for the supine position. Within the limits of this retrospective study, it is concluded that rather simple criteria yield a high diagnostic accuracy in the evaluation of long-term esophageal pH-metry. Nevertheless, a prospective and independent confirmation of these criteria is needed.

The effect of cigarette smoking on gastric emptying, gastric secretion, and bile salt reflux was measured in 19 healthy habitual cigarette smokers (greater than or equal to 20 cigarettes per day) and 18 nonsmokers. They were studied both in the fasting state and after being fed a mixed liquid meal. Ten of the smokers were studied twice, when smoking and when not, in randomized order. Smokers had lower basal gastric secretion rates than nonsmokers irrespective of actually smoking or not. In smokers, bile salt reflux and postprandial gastric bile salt concentration were higher than in nonsmokers even when not actually smoking (p less than 0.01). Smoking during the experiment slowed gastric emptying, and increased bile salt reflux rate and gastric bile salt concentration (p less than 0.01). It is concluded that cigarette smoking has both chronic and acute effects on gastric function, and that bile salt reflux may contribute to the increased incidence, and lower healing rate, of gastric ulcers in smokers.