摘要:

Retrospective analysis was carried out among 252 patients with esophageal achalasia (135 women, 117 men, mean age 41 years) who, in the years 1961– 1992, underwent 333 Starck procedures. Mean period of follow-up was 11.5 years (range 6 months to 32 years). Evaluation of the procedure was based upon the analysis of actual symptoms and radiological and endoscopic examinations in a group of 247 patients (98%). 22 patients died; all except 1 of diseases unrelated to the esophagus. The data concerning the effectiveness of therapy refer to the remaining 225 patients. The first Starck procedure gave permanent and sufficient relief of symptoms in 140 patients (62.2%). Of the remaining patients, 62 persons underwent subsequent Starck procedures, the effectiveness of which was 64.9%. The total percentage of favorable results of the procedure was 84.4%. There was no fatal complication of the Starck procedure. One perforation of the esophagus, one aspiration pneumonia and 2 cases of incarceration of the Starck apparatus were observed. There was no case of esophageal cancer in the whole group. These results confirm that the Starck procedure is a safe and effective treatment for esophageal achalasi

ISSN:0012-2823    

DOI:10.1159/000201364

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

A retrospective non-controlled inventory study was done in order to assess the dental status, with specific attention paid to the incisor teeth, in patients with reflux oesophagitis. A questionnaire was sent to 293 consecutive patients in whom reflux oesophagitis was diagnosed endoscopically. A complete dental prosthesis was present in 46.8% of the patients, the remainder had a complete set of teeth or a partial dental prosthesis. Damage in the upper incisors was present in 32.5% of the cases, in the lower incisors in 7.8%, and in both in 26.9%. In the remainder no damage was present. No complaints were significantly associated with the presence or absence of dental damage. There was, however, a significant association between duration of complaints and presence of damage in the upper incisors. Although it is not certain that all cases of damage actually are the result of gastro-oesophageal reflux, and the data presented possibly overestimate the true prevalence, dental erosions as a complication of gastro-oesophageal reflux are likely to occur in a large number of patients.

ISSN:0012-2823    

DOI:10.1159/000201365

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

This prospective study was designed to validate a novel biopsy urease test as well as a simplified 13C-urea breath test for the detection of Helicobacter pylori. In addition, the hypothesis was tested that both the reaction velocity of the urease test and the 13CO2 excess of the urea breath test may allow a prediction of the severity of gastritis. Seventy dyspeptic patients with unknown H. pylori status were included. The H pylori status was assessed by means of culture and histology after Warthin and Starry stain. One antral and one body biopsy specimen were separately analyzed by the novel biopsy urease test (HUT). Also, a 13C-urea breath test using 75 mg 13C-labelled urea and orange juice as test meal was performed in all patients. Forty-seven patients (67%) were H. pylori positive as judged from histology and culture. In 46 patients, H. pylori infection was also detected by the novel biopsy urease test and by the urea breath test as well (sensitivity 97.9%). False-positive results were not observed by either method (specificity 100%). Both the reaction velocity of the urease test and the 13CO2 excess of the breath test significantly correlated with H. pylori density and grade and activity of gastritis. The determination coefficients, however, indicated that both methods allow a reliable prediction of the severity of gastritis only in about 40-50% of the patients. In conclusion, the novel biopsy urease test and the simplified 13C-urea breath test proved to be highly accurate in diagnosing H. pylori infection. Despite a significant correlation, neither the reaction velocity of the urease test nor the 13CO2 excess of the breath test are clinically useful for the prediction of the severity of gastritis.

ISSN:0012-2823    

DOI:10.1159/000201366

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

We have previously shown that in highly enriched rat gastric parietal cells the intestinal peptide hormones oxyntomodulin and glucagon-like peptide-2 (GLP-2) compete for receptor-binding with glucagon-like peptide-1 (GLP-1), a potent cAMP-dependent stimulus of H+ production in vitro. It is, however, unknown whether oxyntomodulin and GLP-2 elicit a biological response by interacting with the GLP-1 receptor. Therefore, we used enriched rat parietal cells to investigate the effects of both hormones on the production of cAMP and H+ ([14C]aminopyrine accumulation). Both parameters were stimulated by oxyntomodulin in a concentration-dependent manner. EC50 values were 6.2-10-8 and 2.5·10-7M oxyntomodulin for stimulation of H+ and cAMP production, respectively. The maximally effective concentrations for stimulation of [14C]aminopyrine accumulation and cAMP production were l·10-6 and 1 · 10-5M oxyntomodulin, respectively. At these concentrations oxyntomodulin was nearly as effective as 10-4Mhistamine and equally effective as 10-8 MGLP-1 (7-36)NH2. In the enriched parietal cell preparation there was no immunocytochemical evidence of contaminating D cells. Accordingly, the responses to oxyntomodulin and GLP-1 (7-36)NH2 were not augmented by incubating the cells in the presence of a polyclonal anti-somatostatin antibody. [14C]Aminopyrine accumulation in response to oxyntomodulin was inhibited by the GLP-1 (7-36)NH2 receptor antagonist, exendin (9-39)NH2, but not by the H2-receptor antagonist, ranitidine. Oxyntomodulin and carbachol acted additively to stimulate [14C]aminopyrine accumulation. GLP-2 (10-7 to 10-5M) was without effect on basal H+ and cAMP production; however, at 10-5M GLP-2 markedly inhibited oxyntomodulin-stimulated [14C]aminopy-rine accumulation. It is concluded that, by interacting with parietal cell receptors for GLP-1 (7-36)NH2, oxyntomodulin, but not GLP-2, directly stimulates H+ production by activating the adenylate cycla

ISSN:0012-2823    

DOI:10.1159/000201367

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

The poorly differentiated human gastric carcinoma cell line MKN-45 possesses histamine H2 receptors which are homologously desensitized by histamine. In order to clone the cDNA of a receptor kinase specific for H2 receptors, we performed RT-PCR at a low annealing temperature using oligo-DNA primers bearing the conserved sequences of the kinase domain of the G protein-coupled receptor kinase (GRK) family. However, we were able to isolate only cDNAs for β-adrenergic receptor kinase 1 (βARK1) and GRK6. Interestingly, treatment of MKN-45 cells with βARK1 antisense phosphorothioate oligo-DNA (PON) resulted in significant loss of desensitization of H2 receptors by histamine, whereas GRK6 antisense PON had no effect. Thus, βARK1 appears to be involved in the homologous desensitization of H2 receptors in MKN-45 ce

ISSN:0012-2823    

DOI:10.1159/000201368

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

We studied the chronic effect of ammonia, which is one of the pathogenic factors of Helicobacter pylori in gastroduodenal diseases, on the healing of acetic acid-induced gastric ulcers in rats with special reference to the collagen metabolism. Rats were given either tap water or 0.1 or 0.02% ammonia solution before and after ulcer induction. We measured the ulcer index, hydroxy-proline concentrations and type III collagen/total hydroxyproline ratios in the ulcer base. Epithelialization was achieved 4 weeks later under the influence of ammonia. Nevertheless, ammonia treatment significantly increased the collagen deposition in the ulcer base compared with the nonammonia treatment group, 4 weeks after ulcer induction. In the nonammonia treatment group, the type III collagen/total hydroxyproline ratio decreased 3 weeks after ulcer induction. On the contrary, in the groups treated with ammonia throughout the experiment, type III collagen/total hydroxyproline ratio remained high until 4 weeks after ulcer induction. In conclusion, intragastric ammonia delayed the ulcer healing process in its early phase, but did not affect the achievement of re-epithelialization. However, it disturbed the collagen metabolism in the ulcer base. Excessive deposition of collagen and an abnormally high proportion of its immature type may be unfavorable for ulcer healing. These findings may explain in part why H. pylori-màuccå ulcer is so difficult to trea

ISSN:0012-2823    

DOI:10.1159/000201369

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Endoscopical measurement of gastric mucosal blood flow seems to provide substantial advantages for noninvasive and repetitive scrutiny, especially in small animals. We employed a quartz probe 0.5 mm in diameter which was inserted into the gastric lumen through the forceps channel (0.8 mm in diameter) of the endoscope. Gastric mucosal blood flow determined with this probe in combination with laser Doppler velocimetry were sufficiently consistent and reproducible in the corpus as long as the tissue-to-probe distance was positioned in gentle contact with the gastric mucosa perpendicularly. Topical application of endothelin-1 produced a significant long-lasting decline in gastric mucosal blood flow, although laparotomy per se resulted in a slight decrease of the blood flow. Endoscopic measurement of gastric mucosal blood flow seems simple and reproducible with high potential for chronic studies.

ISSN:0012-2823    

DOI:10.1159/000201370

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Treatment with small doses of topical capsaicin protects the gastric mucosa from the damage by strong irritants but functional ablation of sensory nerves by pretreatment with larger dose of parenteral capsaicin augments the formation of gastric lesions via unknown mechanism. This study was designed to determine the role of gastric acid secretion, mucosal blood flow (GBF) and prostaglandins (PG) generation in the gastroprotection induced by small doses of topical or parenteral capsaicin in rats with intact or capsaicin-deactivated sensory nerves. Gastric lesions were produced in rats with intact sensory nerves (series A) or capsaicin-deactivated nerves (series B) using intragastric (i.g.) application of 100% ethanol, acidified aspirin (ASA) or water immersion and restraint stress (WRS). Pretreatment with i.g. capsaicin (0.12-1.0 mg/kg) in rats with intact sensory nerves (series A) reduced dose-dependently the mucosal damage caused by ethanol, ASA or WRS, the dose inhibiting the lesion area by 50% (ID5o) being 0.3, 0.5 and 0.7 mg/kg, respectively. This protection was accompanied by a significant rise in gastric mucosal blood flow (GBF). Parenteral application of capsaicin (1.2-10 mg/kg s.c.) that in intact rats dose-dependently increased GBF, also dose-dependently reduced gastric damage induced by ASA or WRS (but not by ethanol), the ID50 being 5 and 3 mg/kg, respectively. The reduction by i.g. capsaicin of ethanol- or WRS-induced mucosal lesions was accompanied by a rise in GBF and this effect was reversed by indomethacin at a dose that suppressed endogenous PG biosynthesis by about 90%, indicating that PG are involved in the protective activities of topical capsaicin. Furthermore, topical and to a lesser extent parenteral capsaicin given to rats with intact or deactivated sensory nerves inhibited gastric acid and pepsin outputs, suggesting that this inhibition could contribute to the capsaicin-induced gastroprotection against acid-dependent mucosal lesions (ASA or WRS). Capsaicin deactiva-tion of sensory nerves aggravated mucosal lesions induced by all three ulcerogens and this effect was accompanied by a marked decrease in GBF. In such capsaicin-deactivated rats, topical capsaicin also reduced ethanol-, ASA- or WRS-induced lesions, while parenteral capsaicin was effective only in the protection against the damage induced by acidified ASA and WRS but not by ethanol. The protection against WRS lesions and accompanying rise in GBF by parenteral capsaicin were also reversed by the pretreatment with indomethacin applied in a dose suppressing the generation of PG. We conclude that capsaicin is capable of protecting gastric mucosa in rats with both intact and capsaicin-deactivated rats and that this protective activity depends, at least in part, upon its hyperemic and antisecretory effects that may be mediated, at least in part, by endogenous release of PG.

ISSN:0012-2823    

DOI:10.1159/000201371

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Helicobacter pylori (Hp) is considered as the major pathogen in Hp-associated gastritis but the mechanism of its action has not been fully explained. We investigated both the damaging and protective effects of intragastric (i.g.) application of ammonia (NH4OH) and ammonium ion (NH4CI), the major products of Hp-derived urease, on the rat stomach with intact and capsaicin-deactivated sensory nerves or suppressed prostaglandin (PG) and nitric oxide (NO) synthesis. NH4OH given i.g. resulted in a concentration-dependent mucosal damage starting at 30 mM and reaching maximum at 250 mM (pH 11), the extent of damage being similar to that obtained with 100% ethanol. NaOH solution (1 mM) at pH 11 given i.g. did not affect mucosal integrity. The damage caused by NH4OH was accompanied by the fall in gastric blood flow (GBF) reaching at 250 mM NH4OH about 30% of the vehicle control value. The NH4OH-induced gastric damage was augmented by capsaicin-induced deactivation of sensory nerves, the suppression of nitric oxide (NO) synthase with L-NAME or the decrease of i.g. acidity by ranitidine. The pre-treatment with scavengers of reactive oxidants significantly reduced the area of NH4OH-induced gastric lesions. When the mucosa was first exposed to a low 15-mM concentration of NH4OH and then insulted with large 250 mM NH4OH or with 100% ethanol, the lesion area was markedly reduced as compared to that obtained with 250 mM NH4OH or 100% ethanol alone. This adaptive protection by ‘mild’ concentration of NH4OH against strong irritants (250 mM NH4OH or 100% ethanol) was reversed, in part, by pretreatment with L-NAME and indomethacin. NH4C1 (60-500 mM) given i.g. alone failed to affect the mucosal integrity but when applied before 100% ethanol it produced a concentration-dependent fall in the mucosal damage by these irritants. We conclude that; (1) ammonia at higher concentrations damages the gastric mucosa, while ammonium ion exerts the protective activity; (2) the ammonia-induced gastric damage may involve the formation of reactive oxidants; (3) ammonia at lower concentration acts like a mild irritant via the activation of sensory nerves, NO-arginine pathway and

ISSN:0012-2823    

DOI:10.1159/000201372

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Two-hundred Wistar rats were allocated to 4 groups. The groups, 3 representing our acute pancreatitis model induced by intrabiliary injection of a trypsin/enterokinase mixture, were studied as follows: (A) no treatment; (B) given a daily 30-ml enema with 20 mg/kg rifaximin; (C) given a daily 30-ml enema with 20 mg/kg rifaximin plus lactitol 0.5 g/kg, and (D) given a daily 30-ml enema with warm saline. A further group of healthy rats was given an intrabiliary injection of 0.15 ml saline. Sacrifices were made after 6,12,24,48 and 72 h of observation. Serial blood samples were drawn to measure pancreatic enzymes and endotoxin. At sacrifice, ascites, lymph nodes, pancreas, spleen, portal vein blood, arterial blood and bile were obtained for bacteriological culture. Both enema treatments brought about a significant improvement in survival. Enema treatments did not affect the serum level of pancreatic enzymes. A time-course increase in endotoxin level was observed in untreated rats. However, significantly decreased levels were observed after both enema treatments. Overall, ascites was the sample most frequently infected. Lymph nodes contiguous to the gut were found to be infected more frequently than those close to major vessels. The histological pancreatic damage was of a significantly lesser degree in both enema treatment groups. Virtually all severe necrotico-hemorrhagic pancreatic lesions were associated with bacterial infection. These data suggest that bacterial translocation plays a relevant role in the outcome of experimental necrotizing pancreatitis. Intra-abdominal spread and lymphatics seem to be the pathways most likely involved in such processes. Colonic cleansing by non-absorbable antibiotics and lactitol seems to exert a beneficial effect on the supervening infection of experimental necrotizing pancreatitis.

ISSN:0012-2823    

DOI:10.1159/000201373

出版商:S. Karger AG    

年代:1996

数据来源: Karger