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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.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Leptin, a protein product of obese gene expressed primarily by adipocytes, provides feedback information on the size of energy stores to central OB receptors controlling the food intake, energy expenditure and body weight homeostasis. It has recently been detected in the rat stomach, especially after cholecystokinin (CCK) administration and in human stomach infected with Helicobacter pylori, but its role in gastric secretory functions in humans has not been revealed. This study was designed to determine the involvement of leptin in the control of basal, CCK- and meal-induced gastric H[sup +] secretion and plasma gastrin and CCK levels in humans before and after an eradication of H. pylori. Methods: Two groups (A and B) of subjects were used; group A (n = 7), for comparison of the effects of CCK and leptin on basal gastric H[sup +] and plasma hormone (leptin, gastrin and CCK) levels, and group B (n = 6), for studies on the involvement of leptin in gastric secretory and plasma hormonal responses to vagal stimulation and gastric peptone meal before and after H. pylori eradication. Results: In H. pylori -positive subjects, CCK (12-200 pmol kg[sup -1] h[sup -1]) given i.v. caused a dose-dependent increase of gastric H[sup +] accompanied by a dose-dependent rise in plasma CCK and leptin levels. In contrast, leptin administered i.v. in graded doses (5-80 pmol kg[sup -1] h[sup -1]) resulted in a gradual inhibition of basal gastric H[sup +]secretion and in adose-dependent increment in plasma leptin accompanied by an increase in plasma gastrin without alteration of plasma CCK level. Following eradication of H. pylori by 1- weektriple therapy in group B patients, the infusion of CCK produceda significantly smaller increase in gastric H[sup +] secretion and significantly smaller rise in plasma leptin as compared to those before the eradication. Cephalic phase stimulation of gastric secretion induced by modified sham-feeding in group B H. pylori positive subjects increased gastric H[sup +] secretion to about 40% of pentagastrin maximum without affecting plasma leptin, gastrin, or CCK level, while gastric peptone meal resulted in the increase in gastric H[sup +] response reaching about 70% of pentagastrin maximum accompanied by a marked rise in plasma leptin, gastrin and CCK. The treatment with a standard dose of leptin (20 pmol kg[sup -1] h[sup -1]) failed to affect sham-feeding-induced gastric H[sup +] secretion but reduced significantly the peptone meal-stimulated H[sup +] secretion, while raising plasma gastrin in response to this meal. Plasma CCK under basal conditions and after sham-feeding was not affected, but plasma CCK response to gastric meal was significantly reduced by leptin infusion. Eradication of H. pylori did not affect basal or sham-feeding-induced H[sup +] secretion but resulted in a significant fall in gastric mealinduced H[sup +] and plasma leptin, gastrin and CCK levels. Conclusions: 1) The gastric meal and CCK enhance the release of leptin in H. pylori-positive patients and this leptin is capable of inhibiting basal and meal stimulated gastric H[sup +] secretion, while raising plasma gastrin and reducing the plasma CCK levels, and 2) the eradication of H. pylori reduces the postprandial gastric H[sup +] and plasma gastrin responses as well as the release of leptin in response to CCK and meal. [ABSTRACT FROM AUTHOR]

Background: Ultrasound-guided biopsies of abdominal organs are not without risks for the patients; in particular, hemorrhagic complications may occur. Thus, over the last few years, automatic biopsy guns have been developed to facilitate the biopsy process. Methods: The aim of our retrospective study was to examine the quality of specimens and the complication rate of ultrasound-guided biopsies of abdominal organs carried out in our institution using the automatic Autovac biopsy system during a period of 1.5 years. Of the total number of 321 biopsies, 290 were performed with the 1.2-mm Autovac needle, and in 31 cases the 0.95-mm needle was used. Among the 321 biopsies there were 211 of the liver parenchyma (66%), 47 of a liver tumor (14%), 38 of the pancreas (12%), 15 of the kidney parenchyma (5%), and 10 of a retroperitoneal tumor (3%). Results: In 310 of the 321 biopsies it was possible to obtain sufficient diagnostically usable material for the pathologist (96.6%). In the other 11 cases the material obtained did not enable proper histologic diagnosis (3.4%). Two of these 11 biopsies were carried out with the 0.95-mm needle, and the other 9 with the 1.2-mm needle.Twenty-four hours after the biopsy each patient underwent routine ultrasound examination to exclude a possible bleeding. In eight cases an afterbleeding occurred (total hemorrhagic rate, 2.5%), four times without clinical consequences. The other four bleeding complications were more serious (1.2% of all taps), and all occurred after liver biopsies in patients with a history of liver complaints and abnormal clotting variables. There were no fatalities among our biopsies (mortality rate, 0%). Conclusion: The automatic Autovac biopsy system is suitable and relatively safe for obtaining sufficient histopathologic material from intra-abdominal organs. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM PUBLISHER]

The postprandial contractions of the gall bladder result from the interaction of neurohormonal factors but their relative contribution is unknown. This study was designed to determine the role of cholecystokinin (CCK) in gall bladder contractions using a highly selective and potent CCK-receptor antagonist, CR-1505 (loxiglumide) in healthy men either infused with exogenous CCK in graded doses (1.56-50 pmol/kg/h) or subjected to modified sham feeding (MSF) and ordinary feeding tests. The gall bladder volume measured by real time ultrasonography showed dose dependent decrease in the gall bladder volume in 10 subjects when CCK8 was infused iv in graded doses reaching about 15% at 1.56 pmol/kg/h and 91% at 50 pmol/kg/h. Close correlation between the decrease in gall bladder volume and the dosage of CCK or the increments in plasma CCK-bioactivity was observed. After pretreatment with loxiglumide, CCK resulted in similar increments in plasma CCK-bioactivity but failed to affect the gall bladder volume at CCK doses up to 6.25 pmol/kg/h and caused only 53% reduction at 50 pmol/kg/h. Modified sham feeding and real feeding reduced the volume of gall bladder by 20% and 70%, respectively and loxiglumide decreased these values to 15% and 30%, respectively. This study provides evidence that loxiglumide is highly potent and selective CCK antagonist and that endogenous CCK plays an important role both in the postprandial contractions of gall bladder. [ABSTRACT FROM PUBLISHER]

Postprandial pancreatic secretion results from the interaction of neural and hormonal factors but their contribution to the net postprandial secretion is unknown. Recent description of highly specific and potent cholecystokinin (CCK) receptor antagonists allows the determination of the physiological role of CCK in the postprandial pancreatic secretion. In six dogs with chronic pancreatic fistulae, the blockade of CCK receptors by non-peptidal agent (L-364,718) caused little change in basal pancreatic secretion, but decreased significantly (p less than 0.05) by about 60% the pancreatic protein response to meat feeding and virtually abolished the pancreatic responses to CCK-8 and bombesin. The pancreatic protein responses to pentagastrin, reaching about 37% of CCK maximum, was also significantly reduced but this effect was less pronounced than that observed in tests with CCK-8 or bombesin stimulation. In contrast, cholinergically stimulated pancreatic secretion, reaching about 40% of CCK maximum, was unaffected by L-364,718. Cholecystokinin antagonism also failed to affect the postprandial and bombesin induced increments in plasma CCK and gastrin concentrations, but significantly reduced the PP responses to CCK-8 bombesin and meat feeding possibly as a result of the removal of the CCK mediated release of PP. We conclude that CCK plays a crucial role in the mediation of the postprandial and bombesin induced pancreatic secretion and in the PP release. [ABSTRACT FROM PUBLISHER]

Gastric alkaline secretion was determined in ranitidine treated healthy subjects and duodenal ulcer (DU) patients using gastric perfusion aspiration system and back titration of gastric perfusate to original pH 6.0. Basal alkaline secretion showed periodic fluctuations reaching peaks at phase III of the migrating motor complex (MMC) in the stomach. Mean basal alkaline secretion in healthy normals and DU patients averaged 1120 +/- 124 and 880 +/- 72 mumol/h, respectively and no correlation was found between basal and maximally stimulated gastric acid and alkaline secretion. Modified sham feeding in normal subjects and in DU patients increased this secretion to the peaks of about 28 and 36% of the maximal alkaline response to intragastric application of 16,16 dimethyl-PGE2 in these subjects. Vagotomy did not affect significantly basal alkaline secretion but prevented the rise in alkaline secretion induced by modified sham feeding. Atropine (5-20 micrograms/kg) decreased dose dependently basal, and prevented the modified sham feeding induced alkaline secretion, while pirenzepine (5-20 micrograms/kg) had little influence on basal, and did not affect the modified sham feeding induced, alkaline secretion. This study shows that basal gastric alkaline secretion fluctuates in phase with gastric motor activity, and is similar in normal and DU patients. Vagal stimulation strongly increases alkaline secretion, the effect being abolished by vagotomy and atropine, but not by pirenzepine, suggesting the involvement of M2 rather than M1 subtypes of muscarinic receptors in this stimulation. [ABSTRACT FROM PUBLISHER]