Diabetes mellitus is associated with changes in gastrointestinal motility. The effects of experimental diabetes, induced by streptozotocin administration to rats 3–4 weeks previously, on the nitric oxide (NO)‐mediated (nitrergic) relaxation of the duodenum have now been investigated. The non‐adrenergic, non‐cholinergic (NANC) relaxation of the isolated duodenum induced by nicotine (0.3 – 10 μm) or the nicotinic agonist, 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP; 10 μm) was inhibited by the NO synthase inhibitor, NG‐nitro‐l‐arginine (3–100 μm). This nitrergic relaxation induced by nicotine or DMPP of the duodenum from diabetic rats was substantially smaller than that of the tissue from control rats. By contrast, the relaxation of the duodenum from diabetic rats to the NO donor, nitroprusside (0.3–10 μm) was similar to that of control tissue, whereas the relaxation to ATP (0.1–3 μm) was enhanced to a small but significant degree. Incubation of duodenal tissue from control rats at 4°C for 72 h, which leads to neuronal disruption, significantly attenuated the relaxation to nicotine or DMPP whereas the relaxation induced by nitroprusside or ATP was not affected. Comparable cold‐storage did not affect the endothelium‐dependent relaxation of rat aortic rings induced by acetylcholine (0.01–2 μm). The calcium‐dependent NO synthase activity in duodenal tissue, determined by the conversion of radiolabelled l‐arginine to citrulline, was significantly reduced in cold‐stored tissue and in tissue obtained from diabetic rats. These findings in the rat duodenum indicate that a reduction in intestinal NO synthase activity is associated with an impairment of the NANC relaxation. A defect in the intestinal nitrergic innervation could thus contribute to the motility dysfunction observed in diabetes.

The ingestion of plain coffee was compared in 150 duodenal ulcer patients (DU) and 100 control subjects without digestive complaints (C). The DU and C groups were registered in accordance with their daily consumption of coffee: none, 1-100 ml, 101-300 ml, 301-500 ml, and more than 500 ml. Fifty millilitres of coffee as prepared in Brazil contain around 50 mg of a caffeine, which is 2.8 times more than in an equal volume of coffee in the United States. Patients with DU stopped drinking coffee or reduced the volume significantly after symptoms started. There was a significant change in coffee intake at all volume levels except at 1-100 ml. The main reason for the reduction of coffee ingestion was the relationship observed by the patients between the consumption of coffee and dyspeptic complaints. Our results suggest a close correlation between the ulcer-like symptoms and the amount of coffee ingested by patients with duodenal ulcer.

Antacid (AA) in a very low dose (88 mmol/day) was compared to the standard 800-mg dose of cimetidine in healing duodenal ulcers. The influence of sex, age, symptom duration at entry, night pain, smoking, coffee consumption, and alcohol on ulcer healing was studied. The antacid was given in two different schedules: group I--20 ml 1 hr after breakfast and at bedtime; group II--10 ml 1 hr after breakfast and lunch and 20 ml at bedtime. Cimetidine (group III) was given in two divided doses: 400 mg 1 hr after breakfast and 400 mg at bedtime. Endoscopic control was performed after four weeks and, if necessary, after eight weeks of treatment. The healing rate after four weeks of treatment was, respectively, for groups I, II, and III, 45.5%, 55.8%, and 69.4% (group I = group II, and group III different from groups I and II). After eight weeks of treatment the healing rate was 61.5%, 80.8%, and 88.0% for groups I, II, and III, respectively (group II = group III, and group I different from groups II and III). Except for group I, smoking did not influence healing rate. Age, sex, symptoms at entry, night pain, and coffee consumption did not influence the treatment results. The authors concluded that the very low dose of magaldrate (88 mmol/day), when administered in three divided doses (10 ml after breakfast and lunch and 20 ml at bedtime) for eight weeks was as effective as 800 mg of cimetidine (400 mg twice a day) in healing duodenal ulcer.