This study aimed to evaluate whether serial ultrasound measurements of antral volumes are reproducible and, if so, whether they are representative of the entire gastric contents and reliably measure gastric emptying. The antral volume was measured in man after oral and intragastric administration of known amounts of 5% glucose solutions, and on two separate occasions in the same subjects, after the ingestion of a standardised solid-liquid meal (1050 kcal). Antral volume measurements were performed in both supine and upright positions; inter-and intraobserver measurement errors were also assessed. After ingestion or intragastric administration of equal amounts of liquid, antral volumes determined by ultrasound showed a wide intersubject variability. In each individual subject, however, a linear trend was found between the antral volume and amount ofingested or administered liquid. Intrasubject variability of antral volume measurements was at its minimum in fasting conditions and 300 minutes after ingestion of the solid-liquid meal. Intra-and interobserver variations and whether the patient was erect or supine did not affect measurements of antral volumes. These results support the use of real time ultrasound in determining the gastric emptying time. Results at fasting and 300 minutes after a solid-liquid meal are stable end points of measurement.

Peristaltic contractions of the distal esophageal body and lower esophageal sphincter tone were evaluated in patients affected by gastroesophageal reflux disease after either acute intravenous (8.0 mg) administration or two oral doses (5.0 mg and 10.0 mg) of cisapride and in healthy controls after a 10.0-mg oral dose of cisapride. Intravenous cisapride administration enhanced the amplitude and duration of primary peristalsis and the lower esophageal sphincter tone, which reached normal control values. Likewise, the 10.0-mg oral dose effectively enhanced the lower esophageal sphincter resting pressure in both controls and in reflux patients, whereas the amplitude and duration of primary peristalsis was improved only in controls. The 5.0-mg oral dose of cisapride proved ineffective on distal esophageal motor activity in reflux patients. To evaluate whether atropine is capable of modifying the effects of cisapride on distal esophageal motor activity, cisapride was administered intravenously before and during intravenous atropine administration. Effects of cisapride on peristaltic contractions were completely blocked by atropine, irrespective of whether atropine was administered before or after cisapride. The lower esophageal sphincter pressure response to cisapride varied according to the sequence of drug administration, showing no effect when cisapride followed atropine administration and, when this sequence was reversed, no significant atropine-induced inhibition on cisapride-stimulated lower esophageal sphincter pressure. It is suggested that cisapride enhances distal esophageal motor activity by means of a muscarinic receptor mechanism at the level of the distal esophageal body and, at least in part, via a muscarinic-independent mechanism at the level of the lower esophageal sphincter.

This study assessed the effect ofprolonged intraluminal acidification on the motor activity of the entire oesophageal body (under controlled conditions). Intraoesophageal pressures were recorded in 13 endoscopy negative subjects with gastro-oesophageal reflux disease in whom saline, HCl 0.1 N, and saline solutions were infused (15 ml/min) blindly in the oesophageal body, 6 cm distal to the upper oesophageal sphincter for three consecutive periods of 45 minutes each. These findings were compared with those of a control group. Intraoesophageal acidification caused an increase in the deglutition frequency (p<002), the occurrence of multipeaked waves (p<004) as well as a decrease of the propagating velocity (p<0.04) of the primary peristaltic contractions. Furthermore, intraoesophageal acidification determined an increase, at all levels of the oesophagus, of the duration (p<004)and, more noticeable in the proximal oesophageal body, of the amplitude (p<0.02) of primary peristaltic contraction waves. In conclusion prolonged intraoesophageal acidification can considerably affect frequency of deglutition, morphology, and propagating patterns of primary peristaltic contractions. This study shows that these effects are independent from volume distension of the oesophagus and supports the presence of acid sensitive receptors in the oesophageal mucosa.

The effect of a single oral dose of loxiglumide, a cholecystokinin antagonist, on postprandial gallbladder contraction and on gastric emptying was evaluated in humans. Following a 12-hr fasting period, two tablets of loxiglumide (400 mg each) or placebo was administered on different days, in random order and in a double-blind fashion to 10 healthy volunteers 15 min before the ingestion of a 1050-kcal standard meal. Gallbladder and antral volumes were measured by real-time ultrasonography in basal conditions and at fixed time intervals after the meal. Oral loxiglumide administration was followed by a total inhibition of the gallbladder contraction for 60 min after the end of the meal ingestion. Thereafter, up to the end of the study period, gallbladder volume was larger than that of the placebo study (at 300 min after the meal 2.7 +/- 1.6 ml after placebo and 8.2 +/- 3.5 ml after loxiglumide; P less than 0.008). No difference between placebo and loxiglumide was found in the antral volumes at any time interval (postprandial 63.5 +/- 16.5 ml after placebo and 59.4 +/- 24 ml after loxiglumide; at 300 min after the meal 20.8 +/- 13.3 ml after placebo and 18.9 +/- 9.5 ml after loxiglumide). In conclusion, a single oral dose of loxiglumide at the dose of 800 mg can inhibit postprandial gallbladder contraction without affecting gastric emptying. It would therefore appear that in man endogenous CCK, released after a solid-liquid, caloric, nutrient-balanced meal, plays a major role in the contraction of the gallbladder but does not affect gastric emptying.

SUMMARY The relationship between intraoesophageal pH value and motor activity of the lower oesophageal body ard sphincter was in-vvstigated by simultaneous evaluation of intraluminal pressure and pH in 13 patients complaining of heartburn and regurgitation. One hundred and thirty one episodes of gastro-oesophageal reflux were recorded. One hundred and eighteen (90.1%) were preceded by a swallow (one to 12 seconds), 13 reflux episodes (9.9%) were not preceded by a swallow. Gastro-oesophageal refluxes preceded by swallow were accompanied by an equal number of normal and abnormal primary peristaltic sequences and, while recording at level of the lower oesophageal sphincter, occurred during inhibition of the sphincter. Frequency of abnormal primary peristalsis increased (p<0.01) during periods of low intraluminal pH (<5 0). An increase of at least 0 5 U in intraluminal pH occurred with 45 2% of normal primary peristalsis, 29-3% of abnormal primary peristalsis, 4*3% of secondary peristalsis, 3.5% of non-peristaltic contractions. The results of this study indicate that in patients with symptoms of reflux oesophagitis, gastro-oesophagel reflux appears to be related to swallow-induced lower oesophageal sphincter inhibition and not related to abnormal motor activity of the distal oesophageal body where an increased frequency of abnormal primary peristalsis appears to occur during low intraluminal pH and primary peristalsis appears to be the most important mechanism of oesophageal clearing.

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