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At least 199 records · Page 11Linked to original sources
PubMed1996

Proliferation of submesothelial mesenchymal cells during early phase of serosal thickening in the rabbit bladder is accompanied by transient keratin 18 expression.

Partial outlet obstruction of the rabbit bladder induces serosal thickening and smooth muscle (SM) hypertrophy. Within thickened serosa, submesothelial (mesenchymal) cells differentiate into SM cells after 30 days of obstruction[S. Buoro et al. Lab. Invest. 69, 589-602, 1993]. Here, we show that submesothelial cells transiently express keratin (K) 18 but not K8 soon after obstruction. We investigated a possible relationship between keratin expression and cell proliferation/differentiation in vivo and in vitro. The results of this study indicate that expression of K18 is spatiotemporally related to the pattern of cell proliferation with respect to the localization of an elastic membrane which divides the thickened serosa into an "extrinsic" and an "intrinsic" region. Moreover, K18 is not present in bladder mesenchyma during early development, indicating that its expression in the adult is not attributable to a dedifferentiation process. However, simultaneous K18, K8, and desmoplakin (DP) expression can be induced in normal and thickened serosa upon treatment with bromo-deoxyuridine. Our results indicate that K18 is a marker of proliferating mesenchymal cells in rabbit serosa, whereas the combined expression of K18, K8, and DP might be related to the hypothesized alterations in the stability of gene expression. A model is proposed in which keratin-containing submesothelial cells can act as a "transit" cell phenotype involved in both regenerating mesothelial cells and formation of SM cells.

Animals↗
PubMed1996

Effects of serosal-side acidosis on cell pH (pHi) and membrane electrical properties in gastric mucosa.

Acute gastric mucosal injury and bleeding occur in the settings of both respiratory acidosis or metabolic acidosis secondary to systemic sepsis or shock. Respiratory acidosis, however, is more predictably associated with acute injury than metabolic acidosis. We hypothesized that the gastric surface epithelial cells are more susceptible to acute increases in PCO2 than to acute decreases in HCO3-, even for the same level of extracellular acidification. To evaluate this hypothesis, we used intracellular microelectrodes to measure pHi, cell membrane potential (Vc), as well as ion conductances of the apical (Ga) and basolateral (Gb) membranes and the paracellular pathway (Gs) in gastric mucosal cells during acute changes in serosal PCO2 or HCO3-. Necturus antral mucosae were mounted in Ussing chambers, perfused on both sides by Ringer solution (40 mmHg PCO2, 18 mM HCO3-, pH 7.3). Measurements were performed before and during increases in PCO2 (80 mmHg, pH 7.0) or decreases in HCO3- (7.2 mM, pH 6.8 or 2.4 mM, pH 6.4). Both forms of acidosis acidified pHi, depolarized membrane potentials, and decreased ion conductances across apical and basolateral membranes, but not the paracellular pathways. For the same level of extracellular acidification, increases in PCO2 were more effective than acute decreases in HCO3- in acidifying pHi and eliciting disturbances in voltage-generating and ion permeability properties of the cell membranes. These findings suggest that pH-buffering mechanisms in gastric surface cells respond less effectively to high PCO2 than low HCO3.

Acidosis↗
PubMed1993

Metabolic changes in cimetidine treatment for scald injury on the peritoneo-serosal surface in far-advanced gastric cancer patients treated by intraperitoneal hyperthermic perfusion.

Since pretreatment with cimetidine results in the prevention of scald injury on the peritoneo-serosal surface caused by intraperitoneal hyperthermic perfusion (IPHP) for advanced gastric cancer, the diverse influence of IPHP on patients who were either given or not given cimetidine was studied both during and after IPHP treatment. Cimetidine 50 mg/kg was injected intravenously into 12 patients immediately prior to IPHP. There were no statistical background differences between the cimetidine and control groups (those not given cimetidine). The inflow and outflow temperatures of the hyperthermic perfusate in the control and cimetidine groups were 46.1 +/- 0.1 degree C and 44.1 +/- 0.1 degree C and 46.3 +/- 0.1 degree C and 44.2 +/- 0.04 degree C, respectively. Either the pre-IPHP hypothermia or IPHP in the control group resulted in a considerable increase in serum noradrenaline and adrenaline. The intravenous administration of cimetidine led to a stransient but moderate drop in the mean blood pressure as well as a delayed appearance of high concentrations of noradrenaline and adrenaline, induced by high concentrations of circulating histamine released with cimetidine. These results suggest that the sympathetic nervous responses were activated either by hypothermia or hyperthermia. The transient hypotension and delayed increases of both serum catecholamines were attributed to a marked increase in circulating histamine, released with the intravenous cimetidine.

Blood Pressure↗
PubMed1984

Influence of serosal hydrostatic pressure on net water and electrolyte transport across the isolated rat colonic mucosa exposed to different secretagogues.

The influence of 2 cm and 7 cm hydrostatic pressure applied upon the serosal side on net water and electrolyte transport and paracellular permeability was investigated in everted sacs of stripped rat colon mucosa exposed to different secretagogues. A 2 cm pressure abolished net fluid absorption in the presence of deoxycholic acid, bisacodyl, ethacrynic acid and rhein and reduced absorption in the tissue pretreated with cholera toxin. The paracellular permeability was increased by deoxycholic acid, bisacodyl and ethacrynic acid and diminished under the influence of rhein and cholera toxin. At a pressure of 7 cm H2O fluid movement was directed toward the mucosal side parallel to the increase of the paracellular permeability. The fluid appearing at the mucosal side was isotonic in the presence of deoxycholic acid, ethacrynic acid and rhein but hypotonic when the tissue was pretreated with cholera toxin. From the pressure-induced net water flow and the composition of the transferred fluid secretagogues acting predominantly on paracellular pathway can be distinguished from secretagogues acting on basis of other mechanisms.

Animals↗
PubMed1990

Copper transfer through the intestinal wall. Serosal release of metallothionein.

The elucidation of the molecular side of copper transport in biological systems is a promising task. In this context the transfer of ingested copper into the portal blood plasma was examined. Intralumenal addition of 200 microM copper caused the release of Cu-thionein into the venous effluent. This Cu-thionein became detectable after prior perfusion of the porcine small bowel using a modified isotonic phosphate-buffered saline (Pi/NaCl) medium. The protein was characterized by gel chromatography, luminescence, electronic absorption and immunological identification. ELISA and immunoblotting employing a murine monoclonal antibody to rat liver metallothionein-I proved to be most convenient. Using buffer-loaded sacs of porcine jejunum into which Cu2+, Zn2+ and Cd2+ were added, the release of metallothionein into the serosal fluid was successfully seen by ELISA. The observed excretion of metallothionein into the portal compartment may be a genuine metal transport system for many biochemically active metals.

Animals↗
PubMed1993

Helicobacter pylori potentiates histamine release from serosal rat mast cells in vitro.

Helicobacter pylori seems to be involved in the etiology of peptic ulcer and chronic gastritis. Histamine is fundamental in gastric secretion modulation, and some features of H. pylori-associated gastritis (edema, vasodilatation, inflammatory cell infiltration) are typical of the histamine-mediated response. This in vitro study has been undertaken as a preliminary step, in order to find a possible link between H. pylori and histamine release. H. pylori isolated from gastric biopsies has been tested as whole washed bacterium, whole formalin-killed bacterium, and crude cell wall preparation with serosal mast cells obtained by density gradient centrifugation or elutriation from peritoneal and pleural washings of male Wistar albino rats. Histamine release was assayed fluorimetrically. No significant histamine release was obtained by testing the various bacterial preparations alone with mast cells. On the contrary, whole washed cells, whole formalin-killed cells and crude cell walls from H. pylori have been found to potentiate compound 48/80 or calcium ionophore A23187-induced histamine release. Crude cell walls showed the highest activity, whereas filtered supernatants from broth cultures constantly appeared inactive. The enhancement in histamine release differed between the different strains. The present in vitro study, which shows the potentiating effect of H. pylori on histamine release, may prove interesting; however, at present, clinical implications cannot be inferred and further studies as well as in vivo demonstrations are needed.

Animals↗
PubMed1976

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. III. Exchangeability of epithelial cellular potassium.

The exchangeability of toad bladder epithelial cell potassium has been investigated. An insignificant amount of cellular potassium exchanged with mucosal medium 42K. From the rate of uptake of 42K into the cells from the serosal medium at least two cellular potassium pools were identified. The more rapidly exchanging pool contained about one-quarter to one-third of the cellular potassium and exchanged with a half-time of about 30 min. It was from this pool that potassium was lost from cells exposed to ouabain or to a potassium-free medium. In addition, when 3.5 mM rubidium replaced 3.5 mM potassium in sodium Ringer's the epithelial cells lost in 60 min about one-quarter of their cellular potassium in exchange for rubidium. Inhibition of transepithelial sodium transport by amiloride, 10(-5) mM, seemed to depress the rate of potassium uptake into the more rapidly exchanging pool without affecting total cellular potassium content. However, stimulation of transepithelial sodium transport by vasopressin appeared not to affect the rate of potassium uptake. The rate of potassium uptake into this pool seemed much less than that required for a tight 1:1 coupling between transepithelial sodium transport and potassium uptake. The remaining cellular potassium exchanged at a much slower rate and even after 19 hours of incubation only 67% of cellular potassium was labelled. If this slower exchanging potassium represents a single pool, 99% of cellular potassium would be labelled only after incubation with 42K for 56 hours.

Animals↗
PubMed1987

Computed tomographic investigation of serosal and intramural gastrointestinal pathology.

Various cases are presented demonstrating the role of computed tomography (CT) in the assessment of serosal and bowel wall pathology. Reference is made to the morphology of the lesions. Illustrative examples of tumors, secondary malignant dissemination, irradiation injury to the gut, and intramural gas associated with ulcerative colitis, are all illustrated.

Aged↗
PubMed1983

Antigen-induced release of histamine from serosal mast cells, lung, and tracheal tissue: variation with tissue and rat strain in relation to serum IgE-antibody level.

Rats of the Brown Norway (BN)2, Fischer, PVG and Sprague Dawley (SD) strains were immunized intraperitoneally with graded doses of ovalbumin (OA) together with either alum or Silica gel. At specified times after immunization, in vitro histamine release from serosal mast cells and from chopped lung and tracheal tissue was determined after challenge with OA. The development of the capacity to respond in these tests seemed to vary within strain independently for mast cells, lung, and tracheal tissue with immunization dose of antigen and nature of adjuvant. These variations were not closely correlated to observed variations in serum levels of OA-IgE antibody or ratio OA-IgE to total IgE as determined by radioimmunoassay. Furthermore, variations between strains in response capacity did not correlate to inter strain variation in median serum OA-IgE antibody level. These results do not clearly conform to the possibility that one single class of IgE mediates anaphylactic reactivity of various tissues of the rat.

Animals↗
PubMed1987

Histamine release from serosal mast cells by intermediate products of arachidonic acid metabolism.

In the present paper we report the results of experiments carried out to measure the release of histamine from isolated rat mast cells during the metabolic activation of arachidonic acid. Arachidonic acid (10(-8)-10(-4) M) and the terminal products (10(-6) M) of the arachidonic acid pathways were devoid of any significant histamine releasing properties. A substantial amount of histamine was released from rat mast cells by low concentrations of arachidonic acid during incubation with prostanoid generating systems, such as guinea-pig lung microsomes, rat serosal macrophages and polymorphonuclear cells and prostaglandin-H-synthase from calf seminal vesicles. The release of histamine was not accompanied by a leakage of lactate dehydrogenase and was blocked by D-mannitol and by lipoxygenase and cyclooxygenase pathway inhibitors. The data are consistent with the hypothesis that free radical derivatives of arachidonic acid, originating from hydroperoxy fatty acids, are generated during catalysis, causing mast cell histamine release.

Animals↗
PubMed1994

Helicobacter pylori potentiates histamine release from rat serosal mast cells induced by bile acids.

In the present study we have experimentally addressed the effects of Helicobacter pylori on the bile acid capability of histamine release. Bile acids alone were confirmed to be able to induce in vitro histamine release from rat serosal and mucosal mast cells. On the contrary, no significant histamine release was obtained when incubating any Helicobacter pylori preparations alone with mast cells. However, histamine release induced by bile acids was significantly enhanced, without any significant increase in lactate dehydrogenase activity, when whole washed or formalin-killed bacterial cells or crude cell walls were incubated with mast cells in the presence of cholic (0.3 mM), deoxycholic (0.3 mM), or lithocholic (0.3 mM) acids, chenodeoxycholylglycine (0.3 mM), and deoxycholyltaurine (3 mM). The electron microscopic features of mast cells incubated with Helicobacter pylori were consistent with an exocytotic secretion. The release of histamine induced by 0.3 mM deoxycholic acid in the presence of Helicobacter pylori was inhibited by the preincubation of the cells with dimaprit (an H2 agonist) and potentiated by the H2 antagonist, ranitidine. The current results suggest a link between human Helicobacter pylori infection and histamine release and a possible involvement of gastric mucosal mast cells in the pathogenesis of Helicobacter pylori-associated gastritis.

Animals↗
PubMed1987

Continent ileostomy simplified by musculo-serosal window. An experimental study.

Experience with pouch procedures in the quest for continence after total panproctocolectomy has been associated with significant reoperation rates, making these procedures suitable only for highly selected and motivated patients. The purpose of this study was to determine, in an acute dog model, the optimum configuration of a new continence mechanism consisting of a musculo-serosal window formed between the afferent and efferent loops of small bowel. The following geometric measures were varied: single or double window (efferent and afferent loops, respectively); percent circumference of bowel wall used for the window; and distance between pouch apex and window. Intraluminal pressure against volume infused in standard time was recorded. Four hundred seventy experiments in 47 pouches were conducted. The authors suggest that the optimal configuration for this "valve" is bowel circumference used for the window--50 to 60 percent on both the afferent and efferent loops, with a pouch-valve distance of 5 to 6 cm. It is concluded that a biologic valve obviating the need for a nipple may be possible. The geometric configuration has been defined and should be studied in a chronic animal model to determine long-term results.

Animals↗
PubMed1979

Prostaglandin thromboxane, and 12-hydroxy-5,8,10,14-eicosatetraenoic acid production by ionophore-stimulated rat serosal mast cells.

Production of several metabolites of arachidonic acid by purified rat serosal mast cells in response to stimulation with the ionophore A23187 was assessed by stable isotope dilution assay using gas chromatography-mass spectrometry. Compounds quantified were prostaglandins D2, E2, F2 alpha, 6-keto-F1 alpha, thromboxane B2, and 12-hydroxy-5,8,10,14-eicosatetraenoic acid. Mast cells incubated at 37 degrees C for 30 min without ionophore produced measurable quantities of all metabolites assayed. 4 microM A23187 resulted in substantial increased synthesis of all metabolites compared to control cells. Of the metabolites quantified, prostaglandin D2 and prostacyclin were the major products derived from arachidonic acid in ionophore-stimulated rat mast cells.

Animals↗
PubMed1986

Characterization of calcium-activated, phospholipid-dependent protein kinase from rat serosal mast cells and RBL-1 cells.

Evidence is presented that rat serosal mast cells and cells of the rat basophilic leukemia line, RBL-1, each contain a calcium-activated, phospholipid-dependent protein kinase. The enzymes are very similar in their activation requirements to the calcium-dependent enzymes termed protein kinase Cs in brain. The enzyme is selectively stimulated by diolein and phosphatidylserine and is inhibited by several local anesthetics. The Ka for Ca2+ is 1.0 X 10(-3) M and 1.5 X 10(-4) M in mast cells and RBL-1 cells, respectively. The enzyme in mast cells is rapidly activated and apparently changed in its intracellular distribution when intact mast cells are stimulated with 48/80, A-23187, and anti-IgE and 12-O-tetradecanoyl-13-acetate in combination.

Animals↗
PubMed1990

Reactivity of guinea-pig isolated trachea to methacholine, histamine and isoproterenol applied serosally versus mucosally.

Guinea-pig tracheas were perfused with recirculating modified Krebs-Henseleit solution while monitoring changes in inflow-outflow pressure difference, which is an index of trachealis muscle tone. The reactivities of the trachealis muscle to methacholine, histamine and isoproterenol applied separately to the mucosal (intraluminal, IL) or serosal (extraluminal, EL) compartments were compared, and evidence for the agonist-induced release of epithelium-derived relaxing factor (EpDRF) was sought. All agents were more potent when added to the EL compartment, but the IL/EL EC50 ratios were different: 100 for methacholine, 41 for histamine and 25 for isoproterenol. Methacholine or histamine added to the IL compartment, after the preparations were pre-contracted with the same concentration of the agonist or 30 mM KCl added EL, did not result in relaxation. Likewise, IL isoproterenol did not evoke contraction. IL KCl evoked relaxation. The results indicate that the epithelium reduces access of bronchoactive agents to the muscle, while an immediate relaxant effect of EpDRF released by agonists could not be demonstrated.

Animals↗
PubMed1983

Serosal and mucosal facilitated transport of urea in urinary bladder of of Bufo bufo: evidence for an alleged water uptake.

In Bufo bufo urinary bladder an urea facilitated transport has been localised on the luminal membrane. The transport fulfils the criteria for such a mechanism, i.e. is saturable and is inhibited by phloretin, a specific inhibitor for urea transport. Similarly to that of Bufo marinus and Rana esculenta the luminal membrane of Bufo bufo urinary bladder shows an ADH stimulated facilitated transport. Experiments wtih Amphotericin B, serosal phloretin (with and without ADH), have demonstrated the presence of a facilitated urea transport localised on basolateral membrane. Urea uptake on the isolated epithelial cells of Bufo bufo urinary bladder shows a characteristic feature, different from molecules passively transported such as glycerol yet inhibited by phloretin. Allegedly with urea, water flows in to the cells by a dragging or osmotic effect.

Amphotericin B↗
PubMed1985

Transmission of virus from serosal fluids and demonstration of antigen in neutrophils and mesothelial cells of cattle infected with bovine ephemeral fever virus.

Following intravenous injection of bovine ephemeral fever (BEF) virus 6 cattle were autopsied after clinical disease became evident. Fluid from serosal cavities with serofibrinous inflammatory changes showed large increases in neutrophil numbers. BEF virus was detected for the first time in pericardial, thoracic and abdominal fluids. Virus was also detected in synovial fluids, confirming an earlier report of transmission with a synovial fluid sample. Using a direct fluorescent antibody technique, BEF virus antigen was identified for the first time in synovial, pericardial, thoracic and abdominal fluids, in synovial membranes and epicardium. In synovial membranes and epicardium, specific fluorescence was observed in two cell types, mesothelial cells and neutrophils. In the fluids, fluorescence was restricted to neutrophils, the predominant cell type. Specific fluorescence was observed in blood smears from only one animal although blood samples collected at autopsy from all animals contained infective virus.

Animals↗