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Background: The treatment of gastroparesis remains unsatisfactory despite prokinetic and anti-emetic drugs. Gastric electrical stimulation has been proposed as a therapeutic option. We have assessed the effect of gastric electrical stimulation on symptoms, medical treatment, body weight and gastric emptying in patients with intractable symptomatic gastroparesis in a non-placebo-controlled study. Methods: In this multicenter study, 38 highly symptomatic patients with drug-refractory gastroparesis were enrolled. Patients first received temporary electrical stimulation using percutaneous electrodes. The 33 responders to temporary stimulation then underwent surgical implantation of a permanent stimulator. Severity of vomiting and nausea was assessed before and after stimulation. Patients were reassessed 3, 6, and 12 months after permanent implantation. Results: With stimulation, 35/38 patients (97%) experienced >80% reduction in vomiting and nausea. This effect persisted throughout the observation period (2.9–15.6 months, 341 patient-months). Gastric emptying did not initially change, but improved in most patients at 12 months. At 1 year, the average weight gain was 5.5% and 9/14 patients initially receiving enteral or parenteral nutrition were able to discontinue it. Conclusion: Electrical stimulation of the stomach has an immediate and potent anti-emetic effect. It offers a safe and effective alternative for patients with intractable symptomatic gastroparesis.

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Gastric bleeding and the formation of gastrointestinal ulcers and erosions are the most adverse reactions in patients subjected to therapy with non-steroidal antiin¯ammatory drugs (NSAIDs) such as aspirin (ASA). 1 As shown in numerous studies, ASA damages the gastric mucosa due to the inhibition of protective prostaglandins and direct action on this mucosa. This results in enhancement in acid back-diffusion and microvascular injury accompanied by the activation of neutrophils that lead to excessive release of oxygen radicals. 2 Recent work in animal models revealed that administration of NSAIDs such as indometacin or ASA caused the release of reactive oxygen metabolites and enhanced the lipid peroxidation, but the importance of these intermediates in ASA-induced injury of human gastric mucosa has been little studied. 3 It is known that under physiological conditions in biological systems, approximately 95% of molecular oxygen undergoes controlled reduction through the addition of four electrons in the mitochondrial cytochrome oxidase system to form water. The remaining molecular SUMMARY Background: The roles of active oxygen metabolites and anti-oxidative defenses in aspirin (ASA)-induced gastric damage have been little studied. Aim: We determined the effects of aspirin (400 mg b.d.) with or without vitamin C (480 mg b.d.) for 3 days on gastric mucosa in human volunteers. Methods: Gastric injury was assessed endoscopically; gastric blood¯ow, reactive oxygen release (quanti®ed by chemiluminescence), lipid peroxidation, myeloperoxidase, superoxide dismutase and glutathione peroxidase activity and intragastric vitamin C content were measured. Expression of superoxide dismutase and glutathione peroxidase mRNAs was assayed semi-quantitatively. Results: ASA produced erosions, a marked increase in chemiluminescence, lipid peroxidation, and myeloper-

SUMMARY Epidermal growth factor (EGF) is localised in man to salivary and Brunner's glands. It is present in large concentrations in saliva and duodenal contents but the mechanisms of its release have been little studied. This study carried out on four groups of healthy subjects was designed to determine the distribution and the release of immunoreactive EGF (IR-EGF) in salivary, gastric, duodenal, and pancreatic secretions. Under basal conditions, the concentrations of IR-EGF in salivary, gastric, duodenal and pancreatic secretions were; 2.7 (0.4), 0.42 (0.12), 21 (5) and 8.5 (1.2) ng/ml, respectively. Chewing of Parafilm* significantly increased salivary but not gastric or duodenal EGF output while atropinisation led to the reduction in basal salivary and duodenal EGF output without affecting the increment in EGF release induced by chewing. Cigarette smoking caused a marked reduction in basal salivary and duodenal EGF output. Infusion of pentagastrin increased salivary and duodenal EGF output and this was blocked by the addition of somatostatin. Injection of secretin lead to an increase in pancreatic output of EGF. We conclude that in man the major sources of EGF are salivary glands, duodenum, and pancreas and that the release of EGF remains under neurohormonal control.Epidermal growth factor (EGF) originally isolated by Cohen' from the mouse submaxillary glands is a 53 amino acid peptide structurally resembling urogastrone, another peptide isolated from urine.' Urogastrone was discovered after the observation that the extracts of urine from pregnant women had beneficial effect on healing of chronic ulcers in MannWilliamson dogs.3Studies on animals showed that EGF, like urogastrone, displays many kinds of biological effects including stimulation of proliferation and differentiation of epithelial and non-epithelial tissues"4, stimulation of DNA synthesis4 through increasing ornithine decarboxylase activity,' protection of the gastroduodenal mucosa against various irritants, enhancement of healing of chronic gastroduodenal ulceration`and inhibition of gastric acid secretion." Epidermal growth factor has been reported to be Address for correspondenIcice: Prof D)r S J Konturek. Institute of lPhysiology.31-531 Kr,tkow ul. Grzegorzecka 16. Poilnd.

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The gastropathy associated with the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin is a common side effect of this class of drugs, but the precise mechanisms by which they cause mucosal damage have not been fully explained. During continued use of an injurious substance, such as aspirin, the extent of gastric mucosal damage decreases and this phenomenon is named gastric adaptation. To assess the extent of mucosal damage by aspirin and subsequent adaptation the effects of 14 days of continuous, oral administration of aspirin (2 g per day) to eight healthy male volunteers was studied. To estimate the rate of mucosal damage, gastroscopy was performed before (day 0) and at days 3, 7, 14 of aspirin treatment. Gastric microbleeding and gastric mucosal blood flow were measured using laser Doppler flowmeter and mucosal biopsy specimens were taken for the estimation of tissue DNA synthesis and RNA and DNA concentration. In addition, the activation of neutrophils in peripheral blood was assessed by measuring their ability to associate with platelets. Aspirin induced acute damage mainly in gastric corpus, reaching at day 3 about 3.5 on the endoscopic Lanza score but lessened to about 15 at day 14 pointing to the occurrence of gastric adaptation. Mucosal blood flow increased at day 3 by about 50% in the gastric corpus and by 88% in the antrum. The in vitro DNA synthesis and RNA concentration, an index of mucosal growth, were reduced at day 3 but then increased to reach about 150% of initial value at the end of aspirin treatment. The gastric microbleeding rate rose from about 0-38 mi/day at day 0 to about 7-7 mi/day at day 3 but then decreased significantly to virtually normal values at the end of the study. The neutrophil/platelet adherence showed significant increase during aspirin treatment. It is concluded that the treatment with aspirin in humans induces gastric adaptation to this agent, which entails the increase in mucosal blood flow, the rise in neutrophil activation, and the enhancement in mucosal growth.