Biomedical subjects
Publications and source records attributed to F Halter.
We present a simple method for gastroscopy in the anesthetized rat using an implanted gastric cannula, a standard rigid arthroscope, and a newly designed valve system. The method allows high-quality endoscopy and photo documentation, large-size biopsies, electrocoagulation and fluid collection. Repeated gastroscopy in the same animal is easy and well tolerated.
The value of combined CT and ERCP for studying the pancreas has been assessed in a retrospective study. CT and ERCP used singly provided a correct diagnosis in 74 and 63% respectively; the combination of these methods increased diagnostic accuracy to 86%. ERCP is employed after CT and is indicated if the pancreas appears normal, if there is suspicion of chronic pancreatitis or neoplasia, for elucidating focal masses or if there is obstructive jaundice, without its cause being visible on CT.
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In adult rats topical application of 16,16-dm PGE2 (PGE) every 8 h for three weeks led to a dose-dependent increase of the height of the gastric and duodenal mucosa, especially pronounced in the antrum (+115% with the high dose). In the gastric corpus this resulted from an enlargement of the lamina propria and the epithelial cell mass, the latter mainly from a hyperplasia of the surface and foveolar mucous cells. In contrast, the number of parietal cells was not affected. These findings were corroborated by the observation that an increase of antral mucosal height was also induced by a similar parenteral PGE treatment regimen (dosage 25 micrograms/kg). Both longterm intragastric and intraperitoneal PGE treatment led to an increase in DNA synthesis within the mucosa of the gastric antrum and corpus by 19 to 74%. In a third study 25 or 100 micrograms/kg of PGE applied every 8 h intragastrically to 10 suckling rats from the 7th to 11th postnatal day resulted in a dose-dependent increase in the length of the villi and the disaccharidase activities (30-630%). These studies suggest that 16,16-dm PGE2 exhibits a trophic effect on both the stomach and the small bowel.
As shown in a previous study, intragastric administration of 16,16-dimethyl prostaglandin E2 (PGE, 100 micrograms/kg t.i.d.) for three weeks induces growth of the gastric mucosa. The present experiments were designed to study the time course of histological changes after intragastric PGE and to test whether a similar effect could be observed after parenteral administration. Significant thickening of the corpus, but not the antral mucosa was observed after 3 days of intragastric treatment with PGE (100 micrograms/kg t.i.d.), whereas after three weeks the effect was more marked in the antrum than in the corpus. At a dose of 25 micrograms/kg t.i.d., intraperitoneal PGE increased the height of antral mucosa to a similar degree as seen after intragastric treatment. DNA synthesis as assessed by autoradiography after administration of 3H-thymidine at the end of the three week PGE treatment was increased both in the gastric corpus and antrum. Preliminary studies in suckling rats provide evidence that intragastric administration of PGE (100 micrograms/kg t.i.d.) from day 7 to 11 accelerates maturation of the gastric mucosa. It is concluded that thickening of gastric mucosa can be induced by both local and systemic administration of PGE and is due, at least in part, to increased proliferation of gastric mucosal cells.
A case of severe pseudomembranous and ulcerative colitis is described in a 58-year-old patient with rheumatoid arthritis receiving sodium aurothiomalate. Watery diarrhea occurred after the fourth injection (total amount 130 mg). Several months elapsed prior to full recovery after discontinuation of gold administration.
Motor effects of cholecystokinin octapeptide (CCK-OP) on rat antrum, pylorus, and duodenum have been studied in vitro under standard conditions. Intraluminal pressure changes were simultaneously measured at the three locations using a perfusion manometric system with a novel intraluminal pressure-sensor device. This device comprised an acrylic cast of the rat gastroduodenal tract containing the perfusion catheters that reached the surface of the cast with their outlets in the antrum, pylorus, and duodenum. A selective and sensitive intraluminal local pressure measurement was achieved with this pressure sensor due to its shape. CCK-OP increased base-line pressure in the antrum, pylorus, and duodenum; frequencies of phasic contractions in the antrum and pylorus; and amplitudes in the duodenum. The peptide also decreased contraction amplitudes in the antrum and pylorus and frequency of phasic contractions in the duodenum. It is concluded that the novel intraluminal pressure sensor is a useful tool for measuring local pressure changes in the gastroduodenal tract of the rat. In this experimental model, effects of CCK-OP on antral, pyloric, and duodenal base-line pressure are comparable with those observed in isolated muscle strips and in the intact organ of humans, dogs, and opossums. A different behavior, however, was observed in the force of antral and frequency of duodenal phasic contractions.
The mechanism of action of cholecystokinin octapeptide (CCK-OP) on tonic and phasic contraction of antral, pyloric, and duodenal smooth muscles was studied with a novel perfusion manometric system in isolated esophagogastroduodenal preparations of the rat. CCK-OP increased baseline pressure at each site, frequencies of phasic contractions in the antrum and pylorus, and amplitudes in the duodenum. It decreased antral and pyloric amplitudes and frequency of duodenal phasic contractions. CCK-OP action on tonic contraction was tetradotoxin (TTX) susceptible and its action on phasic contractions was TTX resistant. Phentolamine, phenoxybenzamine, propranolol, catecholamine depletion of preparations by reserpine-tetrabenazine, and the block of catecholamine synthesis at different levels significantly inhibited CCK-OP-induced tonic contraction, whereas atropine had no influence. Adrenergic and cholinergic neural actions on phasic contractions altered the level of amplitudes and frequencies on which CCK-OP action occurred. It is concluded that CCK-OP action on tonic contraction of the rat gastroduodenal junction is mediated by a neural noncholinergic pathway, whereas its effect on muscles responsible for phasic contractions is a direct one.
In a 37-year-old patient with Ménétrier's disease, 51Cr-albumin and alpha 1-antitrypsin (alpha 1-AT) output was measured simultaneously in gastric juice and feces. While the 51Cr-albumin studies demonstrated a threefold increase in gastrointestinal protein loss, alpha 1-AT was found in normal quantities in gastric juice and feces. The histamine H2 antagonist, ranitidine, led to a marked reduction in gastric protein loss, as evidenced by decreased 51Cr activity in the stomach. Studies of protein loss in the gastric juice during pentagastrin stimulation (6 micrograms/kg/h) showed that the 51Cr-albumin output paralleled the volume secreted, whereas alpha 1-AT decreased with lower pH values, not being detectable below pH 3. This probably results from peptic degradation of alpha 1-AT at low pH. We conclude that fecal alpha 1-AT determination cannot be used for the assessment of protein-losing gastropathy in patients who are not achlorhydric.
We performed acid secretory and histomorphometric studies in rats treated intragastrically with a regimen of 100 micrograms/kg or 5 micrograms/kg of 16,16-dimethyl prostaglandin E2, or of saline every 8 h for 21 days. All animals given the high-dose treatment developed a macroscopically visible enlargement of the ridge at the corpus-forestomach border, due to an increase in connective tissue and epithelial cell layer. Mucosal thickness was significantly increased in all parts of the stomach, the duodenum, and the proximal colon, but most markedly in the gastric antrum (+115%), where it was accompanied by a higher mitotic rate and hyperplasia of surface and foveolar mucous cells. Within the oxyntic area (corpus), high-dose prostaglandin treatment led to an increase in the number of surface and foveolar mucous cells and chief cells. In contrast, both the number of parietal cells and maximal acid output were not influenced. It is unlikely that the hyperplasia of gastric mucosa is mediated by gastrin since gastrin has no trophic effects on the rat antrum and disproportionally increases the parietal cell number of the oxyntic gastric glands.
Observations made during intragastric titration studies performed with antacids that have an identical neutralizing capacity but differ in their chemical compositions suggested that aluminum hydroxide loses a large portion of its neutralizing capacity when applied postprandially. To further elucidate the mechanism involved in-vitro studies were performed whereby the reactivity of magnesium hydroxide, aluminum hydroxide, and calcium carbonate was estimated either in aliquots of 10 ml of water or 10 ml of 5% oxo solution. The effectively available neutralizing capacity of the respective antacids was measured for the pH range of 1 to 5. The results revealed that magnesium hydroxide as well as calcium carbonate can fully react with acid whereby their theoretically available neutralizing capacity is fully available for the pH of 1 to 4.5, this in water as well as in 5% oxo solution. In contrast, aluminum hydroxide loses a large proportion of the theoretically available neutralizing capacity already in water but especially in oxo solution in a pH dependent manner. The loss far exceeds that calculated when one takes into account the pKa dependent hydrolysis of aluminum hydroxide. This loss of reactivity increased from 20% at pH 1 in a near linear fashion up to above 80% at pH 3.5. A food induced decrease of aluminum hydroxide solubility as well as stabilisation of the macromolecular aluminum hydroxide complexes through anions and organic acids are likely to be responsible for this loss of reactivity.
Thirty-eight patients with erosive-ulcerative reflux esophagitis were treated in an open trial with the histamine-H2-receptor antagonist ranitidine (150 mg twice daily). At endoscopy after 6 weeks there was evidence of complete healing of all epithelial defects in 20 of 38 patients (53%). Continuation of treatment for another 6 weeks in 13 patients was followed by healing in 6 additional patients as judged by endoscopy. Although the symptoms of the group as a whole improved significantly during treatment, there was no correlation between the degree of symptomatic improvement and healing of esophagitis. Also, the healing rate did not depend on age, sex, smoking and drinking habits or on the severity of esophagitis. It is concluded that medical treatment of reflux esophagitis with ranitidine is promising, even in severe cases previously considered candidates for surgery.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In order to estimate their in-vivo reactivity two antacids of equal theoretical neutralizing capacity (approximately 3.9 mol/l at pH 3.5) but of different chemical composition were employed as intragastric titrant (pH 3.5) following a liquid protein meal (oxo) in two groups of five volunteers each. The two antacids chosen (alucol and Camalox) contain different amounts of aluminium hydroxide, magnesium hydroxide and Camalox in addition contains calcium carbonate. The intragastric consumption of these two antacids was much higher than their respective theoretically available neutralizing capacity (Alucol 3.9 times, Camalox 2.4 times). In-vitro studies demonstrated that interaction with oxo reduced the neutralizing capacity of the two antacids at pH 3.5 from 3.9 mol/l to 1.7 mol/l (Alucol) and 2.5 mol/l (Camalox). This potency loss was related to the aluminium hydroxide content of the two antacids. This study indicates that the neutralizing capacity of antacids is not predictable from their reactivity in aqueous solution and is markedly reduced by protein-containing foods.
In view of the conflicting results on whether pentagastrin sensitivity is genuinely increased in duodenal ulcer (DU) patients, the pentagastrin-gastric acid relationship was restudied in 17 normal subjects and 15 DU patients. In a reproducibility study performed on nine healthy subjects the mean pentagastrin responses obtained on 2 different study days, using a step technique (range, 0.025-6.4 micrograms kg-1h-1), were congruent at each of the five measuring points. Analysis of variance revealed no significant overall differences. However, ED50 values showed a large within- and between-subject variation and failed to correlate significantly, this because a plateau response was not regularly obtained with the top dose. Consequently, ED50 values in normal subjects and DU patients showed a large scatter and were not significantly different, although the potency ratio calculated from the linear parts of the respective dose-response curves was significantly different (2.6; 95% confidence limits, 1.8-3.9). This study thus supplies further evidence that the parietal cell of DU patients has a higher sensitivity to pentagastrin and demonstrates that the reliability of individual ED50 estimations obtained in pentagastrin dose-response studied should not be overrated.