6 patients with severe symptomatic diabetic gastroparesis were studied in a placebo-controlled randomized manner to establish if intravenous domperidone accelerates the delayed gastric emptying of a semisolid homogenized meal. Domperidone, 10 mg intravenously, shortened the gastric emptying half-time in all of the 6 patients significantly, but not in the healthy control subjects. These results suggest that intravenous domperidone may be potentially beneficial to diabetic gastroparesis patients by improving delayed gastric emptying.

SUMMARY A new method is described which allows simultaneous measurement of gastric emptying and duodenogastric reflux and avoids transpyloric intubation. After intragastric instillation of a liquid lipid meal in six healthy volunteers the fractional gastric emptying rate was 2.9±0.3 in the upright and 2.5±0 6 SEM x1T2/min in the supine position, respectively (p>0.5). The duodenogastric reflux rate (expressed as fraction of the intraduodenal amount of duodenal marker) was 0.30 (range 0.03-081) and 0.22 (0.01-0.55) x102/min, respectively (p>0.2). Atropine (40 ,g/kg) decreased the supine gastric emptying rate to 1.1 ±02 (p<005) and increased the supine duodenogastric reflux rate to 2.74 (0.04-9.80) x 102/min (p<005). Fasting duodenogastric reflux rate was similar in the supine and upright position, 0.49 (0.04-0.89) and 0.42 (0.06-0.97) x 102/min, respectively (p>0.5). Fractional gastric emptying rate was similar in 10 volunteers and 17 patients with type I gastric ulcer (21±04 vs 1.7±0.2 SEM x 10-2/min, p>0O2). Their duodenogastric reflux rates were also similar, 0-65 (0.01-5.24) vs 1.10 (0.01-10.83)x102/min (p>05). We conclude therefore that (1) gastric emptying and both fasting and postprandial duodenogastric reflux are independent of the posture; (2) fasting and postprandial reflux are of similar magnitude; (3) atropine shows gastric emptying and increases duodenogastric reflux; and (4)

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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.

The relationship between gastric mucosal blood flow and stress lesion formation during hemorrhagic shock was studied in anesthetized dogs. Shock was induced by graded arterial bleeding. Blood flow was measured by means of the radioactive microsphere technique. Mapping of blood flow was achieved by measuring the microsphere accumulation in mucosal and muscle segments of 1–2 cm side length of the entire stomach. To produce a varying incidence of lesions the metabolic acidosis of shock was either fully corrected by intravenous sodium bicarbonate (n = 5), partially corrected (n = 4) or left uncorrected (n = 3). Mucosal lesions developed more frequently in dogs without correction than in dogs with partial correction or full correction. In 4 dogs not subjected to shock, no mucosal lesions were observed at the end of the experiments. Mucosal blood flow varied from segment to segment by a factor of up to 20, but individual segments tended to maintain their relative flow values during shock. Correction of metabolic acidosis did not significantly affect blood flow. Likewise, flow was similar in segments with and without lesions. Therefore, low regional blood flow did not predispose to the development of lesions and high flow did not prevent them. We conclude that focal mucosal ischemia alone does not lead to stress lesion formation during hemorrhagic shock.