PubMed Health⌕ Search

Biomedical subjects

H Menge

Publications and source records attributed to H Menge.

At least 37 records · Page 2Linked to original sources
PubMed1987

[Aeromonas hydrophila as an autochthonous causative agent of infectious enteritis in Germany].

Aeromonas hydrophila was identified by culture technique in diarrhoeal stools and ascites in a patient of 57 years of age who suffered from known alcoholic cirrhosis and additional acute gastroenteritis. No other pathogens that would produce acute diarrhoea were found. The isolated Aeromonas hydrophila strain was characterised by the pathogenic properties known to date as pertaining to this species (formation of haemolysin and enterotoxins). Hence it is evident that Aeromonas hydrophila occurs in Germany also as an autochthonous pathogen of acute infectious enteritis.

Aeromonas↗
PubMed1987

Impaired intestinal sodium and chloride transport in the blind loop syndrome of the rat.

Self-filling blind loops of rat jejunum were used as a model for the blind loop syndrome in humans. Electrical resistance, short circuit current, and unidirectional sodium and chloride fluxes were measured using the Ussing technique. Whereas net fluxes for sodium and chloride did not differ significantly from zero in the blind loop or in the control, unidirectional fluxes of either direction were decreased and electrical resistance was increased, indicating an increase in the tightness of the intestinal wall. Measurements of alternating current impedance and micropuncture experiments revealed that this was due to an increase in epithelial resistance from 9 +/- 1 omega X cm2 (n = 15, results of both methods) to 27 +/- 4 omega X cm2 (n = 15) and in subepithelial resistance from 40 +/- 2 omega X cm2 (n = 15) to 76 +/- 7 omega X cm2 (n = 15). As the ratio of epithelial to subepithelial resistance was similar in the blind loop and in the control, lower transport rates in the blind loop are indicative of impaired epithelial transport function. Subsequently, two different transport systems were characterized. First, the 3-o-methyl-glucose-induced, phlorizin-reversible increase in short circuit current, representing glucose-coupled sodium absorption, showed a 77% decrease in maximum velocity in the blind loop and no change in Km. Second, the chloride-induced, bumetanide-reversible increase in short circuit current in tissues stimulated simultaneously by prostaglandin E1 and theophylline, representing rheogenic chloride secretion, also showed a decrease in maximum velocity (of 83%) and no change in Km. A morphometric analysis revealed that the crypt surface area increased by 100% in the blind loop, whereas the villous surface area was not significantly different between blind loops and controls. We conclude that the jejunal self-filling blind loop is characterized by impaired active ion transport processes and an increase in epithelial and subepithelial resistance.

Animals↗
PubMed1987

Comparative investigations about three different identification systems for Campylobacter pyloridis from human antrum mucosa.

Campylobacter pyloridis (C. p.) which was first isolated in 1983 in Australia by Marshall and Warren from human gastric mucosa has since been associated with chronic gastritis and ulceration of stomach and duodenum. A typical characteristic of this microorganism is very strong urease formation. Therefore, from the appearance of that enzyme in the gastric mucosa colonization with C. p. can be inferred. The investigations reported here were done to compare the cultivation of C. p. as a direct proof of the presence of this microorganism with two different enzymatic procedures to be used as a rapid indirect method for demonstration of the presence of C. p. A total of 100 patients were involved. The results show rather good agreement between all three procedures used (80%), so that, at least for epidemiological surveys, the demonstration of urease may be used as an indirect procedure for the demonstration of the presence of C. p.

Biopsy↗
PubMed1987

Adaptation of the jejunal mucosa in the experimental blind loop syndrome: changes in paracellular conductance and tight junction structure.

Self-filling blind loops of rat jejunum exhibit hyperregenerative transformation of the mucosa. We used this experimental model to characterise mechanisms, which may occur under similar conditions in man (stagnant loop syndrome). Epithelial and subepithelial resistance were measured in the Ussing-chamber by voltage divider ratio measurements after positioning a microelectrode between epithelium and subepithelial tissue layers. In the blind loop, epithelial resistance increased from 8 +/- 1 to 23 +/- 1 omega cm2 and subepithelial resistance from 39 +/- 4 to 86 +/- 8 omega cm2 as compared with control jejunum. The increase in the subepithelial resistance was paralleled anatomically by an increase in the thickness of the subepithelial tissue layers from 63 +/- 4 microns to 177 +/- 19 microns. Ultrastructural analysis of the tight junction area by freeze fracture electron microscopy revealed an increase in the total junctional 'depth' in the crypts from 243 +/- 9 nm in control jejunum to 396 +/- 17 nm in the blind loop, while the number of horizontally oriented 'strands' remained unchanged. Villus tight junctions did not differ between blind loop and control. We interpret the alterations in the self-filling blind loop as an adaptive response of the epithelium which reduces backleakage of already absorbed electrolytes across the tight junction into the intestinal lumen. This mechanism is suitable to support the intestine in maintaining body electrolyte and water contents during cellular electrolyte malabsorption.

Adaptation, Physiological↗
PubMed1987

Pathogenesis of the mucosal hyperplasia in self-filling blind loops of rat jejunum: a morphometric study in germ free animals.

Bacterial overgrowth and high intraluminal concentrations of deconjugated bile acids are thought to be responsible for mucosal hyperplasia in self-filling blind loops of rat jejunum. To investigate this hypothesis further we have assessed the three dimensional architecture of these loops created in germ free animals without or with di- or mono-association of different bacterial species. It was found that mucosal hyperplasia develops in the absence of any bacterial contamination and that bacterial association does not lead to a more pronounced mucosal proliferation. This implies that other mechanisms provoke this morphological phenomenon. Increased bulk contents in these loops or immunological events are probably the most likely explanation.

Animals↗
PubMed1987

Effect of monoclonal antibodies to enteroglucagon on ileal adaptation after proximal small bowel resection.

On the basis of circumstantial clinical and experimental evidence, it has been suggested that enteroglucagon (EG) may act as an enterotrophic factor. This study was undertaken to evaluate the effects of long term in vivo immunoneutralisation of EG, using monoclonal antibodies to EG, on the hyperplastic ileal response after small bowel resection. Nineteen rats had a 70% proximal resection. A group of 10 rats was given iv 0.5 ml of undiluted hybridoma ascites immediately after the operation and on the 7th day postoperatively. Furthermore 0.025 ml/day of the same hybridoma ascitic fluid was continuously delivered ip for 14 days via mini-osmotic pumps. The hybridoma ascites was prepared from the clone 23.6B4 synthesising a monoclonal antibody directed toward the N-terminal to central region of the glucagon molecule which showed a marked crossreaction with EG. A control group of 9 rats was given a corresponding amount of antibody-free plasmacytoma ascites (Ag 8.653) by the same technique. Seven and 14 days postoperatively there was a plasma anti-EG-antibody excess with an excess binding capacity of 84.9 glucagon eq nM and 88.5 glucagon eq nM respectively. The three dimensional architecture and the proliferative activity of the ileal remnant were evaluated two weeks postoperatively. Despite a continuous immunoneutralisation of circulating endogenous EG by monoclonal antibodies, the adaptive response of the ileal remnants was of the same magnitude as that seen in the control group. These data do not support the hypothesis that EG is a circulating enterotrophic regulatory peptide.

Adaptation, Physiological↗
PubMed1986

[Functional characterization of luminal enterocyte membranes of the small intestine mucosa using isolated brush border membranes].

Atrophy of the small intestinal mucosa is functionally characterized by a reduction in non-electrolyte transport in vivo. In order to elucidate the cellular defect being responsible for this malabsorption, we have studied the Na+-dependent D-glucose accumulation as well as the activities of aminopeptidase M and maltase in brush border membrane vesicles prepared from jejunal self-emptying blind loops and corresponding intestinal segments of sham-operated control rats. Membrane vesicles from atrophic mucosa did not show any differences in D-glucose uptake or in enzyme activities when compared with those derived from normal intestine. Thus it is unlikely that the impaired non-electrolyte absorption in the atrophic mucosa in vivo is due to a defect in cellular transport processes. It is more probable that the functional impairment is the result of the diminished absorptive surface in this pathophysiological condition.

Aminopeptidases↗