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PubMed1987

Characterization of the basolateral membrane conductance of Necturus urinary bladder.

Necturus urinary bladders stripped of serosal muscle and connective tissue were impaled through their basolateral membranes with microelectrodes in experiments that permitted rapid changes in the ion composition of the serosal solution. The transepithelial electrical properties exhibited a marked seasonal variation that could be attributed to variations in the conductance of the shunt pathway, apical membrane selectivity, and basolateral Na+ transport. In contrast, the passive electrical properties of the basolateral membrane remained constant throughout the year. The apparent transference numbers (Ti) of the basolateral membrane for K+ and Cl- were determined from the effect on the basolateral membrane equivalent electromotive force of a sudden increase in the serosal K+ concentration from 2.5 to 50 mM/liter or a decrease in the Cl- concentration from 101 to 10 mM/liter. TK and TCl were 0.71 +/- 0.05 and 0.04 +/- 0.01, respectively. The basolateral K+ conductance could be blocked by Ba2+ (0.5 mM), Cs+ (10 mM), or Rb+ (10 mM), but was unaffected by 3,4-diaminopyridine (100 microM), decamethonium (100 microM), or tetraethylammonium (10 mM). We conclude that a highly selective K+ conductance dominates the electrical properties of the basolateral membrane and that this conductance is different from those found in nerve and muscle membranes.

4-Aminopyridine↗
PubMed1987

Interaction between the basolateral K+ and apical Na+ conductances in Necturus urinary bladder.

Experimental modulation of the apical membrane Na+ conductance or basolateral membrane Na+-K+ pump activity has been shown to result in parallel changes in the basolateral K+ conductance in a number of epithelia. To determine whether modulation of the basolateral K+ conductance would result in parallel changes in apical Na+ conductance and basolateral pump activity, Necturus urinary bladders stripped of serosal muscle and connective tissue were impaled through their basolateral membranes with microelectrodes in experiments that allowed rapid serosal solution changes. Exposure of the basolateral membrane to the K+ channel blockers Ba2+ (0.5 mM/liter), Cs+ (10 mM/liter), or Rb+ (10 mM/liter) increased the basolateral resistance (Rb) by greater than 75% in each case. The increases in Rb were accompanied simultaneously by significant increases in apical resistance (Ra) of greater than 20% and decreases in transepithelial Na+ transport. The increases in Ra, measured as slope resistances, cannot be attributed to nonlinearity of the I-V relationship of the apical membrane, since the measured cell membrane potentials with the K+ channel blockers present were not significantly different from those resulting from increasing serosal K+, a maneuver that did not affect Ra. Thus, blocking the K+ conductance causes a reduction in net Na+ transport by reducing K+ exit from the cell and simultaneously reducing Na+ entry into the cell. Close correlations between the calculated short-circuit current and the apical and basolateral conductances were preserved after the basolateral K+ conductance pathways had been blocked. Thus, the interaction between the basolateral and apical conductances revealed by blocking the basolateral K+ channels is part of a network of feedback relationships that normally serves to maintain cellular homeostasis during changes in the rate of transepithelial Na+ transport.

Amiloride↗
PubMed1990

Water, proton, and urea transport in toad bladder endosomes that contain the vasopressin-sensitive water channel.

Vasopressin (VP) increases the water permeability of the toad urinary bladder epithelium by inducing the cycling of vesicles containing water channels to and from the apical membrane of granular cells. In this study, we have measured several functional characteristics of the endosomal vesicles that participate in this biological response to hormonal stimulation. The water, proton, and urea permeabilities of endosomes labeled in the intact bladder with fluorescent fluid-phase markers were measured. The diameter of isolated endosomes labeled with horse-radish peroxidase was 90-120 nm. Osmotic water permeability (Pf) was measured by a stopped-flow fluorescence quenching assay (Shi, L.-B., and A. S. Verkman. 1989. J. Gen. Physiol. 94:1101-1115). The number of endosomes formed when bladders were labeled in the absence of a transepithelial osmotic gradient increased with serosal [VP] (0-50 mU/ml), and endosome Pf was very high and constant (0.08-0.10 cm/s, 18 degrees C). When bladders were labeled in the presence of serosal-to-mucosal osmotic gradient, the number of functional water channels per endosome decreased (at [VP] = 0.5 mU/ml, Pf = 0.09 cm/s, 0 osmotic gradient; Pf = 0.02 cm/s, 180 mosmol gradient). Passive proton permeability was measured from the rate of pH decrease in voltage-clamped endosomes in response to a 1 pH unit gradient (pHin = 7.5, pHout = 6.5). The proton permeability coefficient (PH) was 0.051 cm/s at 18 degrees C in endosomes containing the VP-sensitive water channel; PH was not different from that measured in vesicles not containing water channels. Measurement of urea transport by the fluorescence quenching assay gave a urea reflection coefficient of 0.97 and a permeability coefficient of less than 10(-6) cm/s. These results demonstrate: (a) VP-induced endosomes from toad urinary bladder have extremely high Pf. (b) In states of submaximal bladder Pf, the density of functional water channels in endosomes in constant in the absence of an osmotic gradient, but decreases in the presence of a serosal-to-mucosal gradient, suggesting that the gradient has a direct effect on the efficiency of packaging of water channels into endosomes. (c) The VP-sensitive water channel does not have a high proton permeability. (d) Endosomes that cycle the water channel do not contain urea transporters. These results establish a labeling procedure in which greater than 85% of labeled vesicles from toad urinary bladder are endosomes that contain the VP-sensitive water channel in a functional form.

Animals↗
PubMed1990

Regulation of the formation and water permeability of endosomes from toad bladder granular cells.

Osmotic water permeability (Pf) in toad bladder is regulated by the vasopressin (VP)-dependent movement of vesicles containing water channels between the cytoplasm and apical membrane of granular cells. Apical endosomes formed in the presence of serosal VP have the highest Pf of any biological or artificial membrane (Shi and Verkman. 1989. J. Gen. Physiol. 94:1101-1115). We examine here: (a) the influence of protein kinase A and C effectors on transepithelial Pf (Pfte) in intact bladders and on the number and Pf of labeled endosomes, and (b) whether endosome Pf can be modified physically or biochemically. In paired hemibladder studies, Pfte induced by maximal serosal VP (50 mU/ml, 0.03 cm/s) was not different than that induced by 8-Br-cAMP (1 mM), forskolin (50 microM), VP + 8-Br-cAMP, or VP + forskolin. Pf was measured in endosomes labeled in intact bladders with carboxyfluorescein by a stopped-flow, fluorescence-quenching assay using an isolated microsomal suspension; the number and Pf (0.08-0.11 cm/s, 18 degrees C) of labeled endosomes was not different in bladders treated with VP, forskolin, and 8-Br-cAMP. Protein kinase C activation by 1 microM mucosal phorbol myristate acetate (PMA) induced submaximal bladder Pfte (0.015 cm/s) and endosome Pf (0.022 cm/s) in the absence of VP, but had little effect on maximal Pfte and endosome Pf induced by VP. However, PMA increased by threefold the number of apical endosomes with high Pf formed in response to serosal VP. Pf of endosomes containing the VP-sensitive water channel decreased fourfold by increasing membrane fluidity with hexanol or chloroform (0-75 mM); Pf of phosphatidylcholine liposomes (0.002 cm/s) increased 2.5-fold under the same conditions. Endosome Pf was mildly pH dependent, strongly inhibited by HgCl2, but not significantly altered by GTP gamma S, Ca, ATP + protein kinase A, and phosphatase action. We conclude that: (a) water channels cycled in endocytic vesicles are functional and not subject to physiological regulation, (b) VP and forskolin do not have cAMP-independent cellular actions, (c) activation of protein kinase C stimulates trafficking of water channels, but does not increase the number of apical membrane water channels induced by maximal VP, and (d) water channel function is sensitive to membrane fluidity. By using VP and PMA together, large quantities of endosomes containing the VP-sensitive water channel are labeled with fluid-phase endocytic markers.

Animals↗
PubMed1996

Cytologic diagnosis of primary serous lymphoma.

Lymphomas arising primarily in serosal surfaces have recently been described. Although these "body-cavity" lymphomas usually present as an effusion, the role of cytologic diagnosis has not been fully explored. The authors present seven cases of primary serous lymphoma. All were large cell lymphomas (5 B cell types, 2 T cell types). Three distinct clinical presentations were seen. Four patients had the rapid onset of pleural effusions without an associated mass in the setting of immunodeficiency (3 with AIDS, 1 with Castleman's disease). Cytologic examination of the effusion was positive in all cases for B-cell lymphoma. All four patients died of their disease in less than 6 months. Two other patients with AIDS and T-cell lymphomas both of which were associated with a serosal mass as well as an effusion. Although cytologic examination revealed numerous atypical lymphoid cells, clonality could not be demonstrated. One patient survived for more than 1 year, the other lymphoma was an incidental finding at autopsy. Finally, one B-cell lymphoma arose in a patient with chronic pleuritis. Pleural decortication was required to identify the neoplastic cells. The authors conclude that primary serosal lymphomas have characteristic clinical presentations, and that although cytologic and flow cytometric examination of effusions is necessary for the diagnosis of immunodeficiency associated B-cell lymphomas, tissue biopsy will likely be required in patients with immunodeficiency-associated T-cell lymphomas or lymphomas associated with chronic pleuritis.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Detection of N-(deoxyguanosin-8-yl)-2-fluorenamine in DNA of peritoneal serosa and liver after intraperitoneal exposure of rats to N-hydroxy-N-2-fluorenylbenzamide or N-hydroxy-N-2-fluorenylacetamide.

DNA adduct formation was examined in rat peritoneal serosa, a tumor target for i.p. administered aqueous suspensions of N-hydroxy-N-2-fluorenylbenzamide (N-OH-2-FBA) and N-hydroxy-N-2-fluorenylacetamide (N-OH-2-FAA), and compared to that in the liver, which is a tumor target for N-OH-2-FAA in the male rat. 32P-Postlabeling analyses showed the presence of a single adduct, N-(deoxyguanosin-8-yl)-2-fluorenamine (dG-C8-FA), from activation of both hydroxamic acids by the serosa and liver in vitro and in vivo. The relatively low levels of dG-C8-FA (60-80 fmol/micrograms DNA) from N-OH-2-FBA in vitro were increased 2.7- and 35-fold upon the addition of acetyl coenzyme A (AcCoA) to the serosal cytosol and hepatic cytosol or microsomes respectively. By contrast, addition of AcCoA led to a decrease (approximately 34%) in the high level of dG-C8-FA (4330 fmol/micrograms DNA) from activation of N-OH-2-FAA by hepatic cytosol and did not alter the levels from activation by hepatic microsomes and serosal cytosols (530 and 78.3 fmol/micrograms DNA respectively). These data and the previously reported hydroxamic acid activation enzyme activities in the serosa and liver indicated that the precursor of dG-C8-FA, N-acetoxy-N-2-fluorenamine, was formed from N-OH-2-FAA chiefly via an intramolecular N,O-acetyltransfer and from N-OH-2-FBA via a two-step sequence of N-debenzoylation and AcCoA-dependent O-acetylation. The levels of dG-C8-FA were approximately 2- to 3-fold higher in the serosal DNA (up to 515 and 1012 fmol/micrograms DNA) after one (30 mumol/rat) and ten or eleven (cumulative dose of approximately 275 mumol/rat) injections of N-OH-2-FBA or N-OH-2-FAA than in the hepatic DNA. This correlated with the carcinogenicities of the hydroxamic acids, but was inversely proportional to the rates and extents of their activation in vitro. Multiple injections affected hepatic enzyme activities related to the activation of the hydroxamic acids in that the cytosolic N-debenzoylation of N-OH-2-FBA increased (approximately 1.7-fold) whereas N-OH-2-FAA acetyltransferase and sulfotransferase activities decreased. The effect of treatment with N-OH-2-FBA was greater than that with N-OH-2-FAA and was greater on the sulfotransferase activity (approximately 88% decrease). The latter suggested that N-OH-2-FBA, although a poor acceptor for an enzymatic sulfate transfer, may be carcinogenic for the rat liver.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetyl Coenzyme A↗
PubMed1981

Influence of cadmium on the intestinal uptake and absorption of calcium in the rat.

To determine the effects of cadmium on the intestinal absorption of calcium, everted gut sacs from rats orally dosed with 0, 0.05, 0.5 or 5.0 mg Cd daily for 3 weeks were placed in media containing 4 x 10(-5) M Ca. Tissue content of calcium after 1 hour incubation was approximately 1.5 times greater for the 5-mg Cd dose. Serosal fluid content of calcium was decreased by the 0.5- and 5-mg Cd/day doses. In other experiments, gut sacs were incubated in bathing media containing 4 x 10(-5) Ca and Cd in concentrations of 10(-4) to 10(-2) M. Tissue and serosal fluid uptake of calcium decreased as Cd concentration increased. To determine the effects of cadmium on the accumulation of calcium against a concentration gradient, equimolar concentrations of Cd were placed in the mucosal and serosal fluids. Cadmium was added to the mucosal fluid. The accumulation of calcium was abolished by 1.5 x 10(-4) M Cd while at 10(-6) M Cd the accumulation was decreased to one-third the control value. The results indicate that acute or chronic exposure of the intestine to cadmium decreases the intestinal absorption of calcium.

Animals↗
PubMed1983

Effects of zinc on mucosal copper binding and on the kinetics of copper absorption.

The kinetics of serosal copper transfer and the distribution of copper between metallothionein (MT) and a high-molecular-weight protein fraction (HMWPF) within the mucosal cells were examined, using isolated duodenal segments from rats fed different amounts of zinc. No difference in the Vmax or Km for serosal transfer could be detected between the different zinc groups, suggesting that zinc did not affect this aspect of copper absorption. When intestinal segments from rats fed the low zinc diet were incubated in high copper media, the majority of the copper was associated with the HMWPF, while those from rats fed the high zinc diet had the largest proportion bound to MT. All the intestines incubated in the low copper media, regardless of rat zinc status, had the majority of copper associated with MT. These results suggested that with the low zinc diet, the limited amount of MT present was saturated, and the excess copper was bound to the HMWPF. With larger intakes of zinc, MT synthesis was induced, and the larger amount of this protein was not as readily saturated, resulting in less copper binding to the HMWPF and more to MT. It is suggested that zinc interferes with copper absorption by inducing MT, which sequesters copper in the mucosal cells, making it unavailable for serosal transfer. The copper bound to the HMWPF is available for transfer.

Animals↗
PubMed1992

Paracellular calcium transport across the small intestine.

Concentration and voltage dependence of unidirectional 45Ca transport measurements indicated that approximately 60-70% of the mucosa-to-serosa calcium flux measured across the short-circuited rat duodenum, jejunum and ileum is paracellular, with only 30-40% of the mucosa-to-serosa calcium transport cellular. The calcium flux from serosa to mucosa was purely paracellular in all segments. Duodenal calcium serosal-to-mucosal flux was of the same order of magnitude as the mucosal-to-serosal paracellular movement. However, the serosal-to-mucosal flux of jejunum and ileum was twice as high. Therefore, net calcium absorption occurs only in the duodenum, whereas calcium is secreted in the jejunum and ileum by a passive paracellular route, presumably involving an anomalous solvent drag effect. Administration of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) led to an increase in the transcellular mucosa-to-serosa flux in the duodenum only. It also led to a stimulation of paracellular calcium flux in both directions in all three intestinal segments, with no change in net paracellular calcium absorption. Thus, the only vitamin D-related increase in calcium absorption was due to the increase in duodenal transcellular absorption. The mechanism by which 1,25-(OH)2D3 increased paracellular flux is not known but may have resulted from an osmotic effect on the intercellular spaces.

Animals↗
PubMed2002

Quercetin-3-glucoside is transported by the glucose carrier SGLT1 across the brush border membrane of rat small intestine.

In the present study we investigated a possible involvement of the intestinal sodium-dependent glucose transporter (SGLT)1 in the absorption of quercetin-3-glucoside (Q3G). Pieces of rat jejunum or proximal colon were mounted in Ussing-type chambers and incubated under short-circuited conditions. Test flavonols were added to the mucosal or serosal bathing solution (initial concentration, 100 micromol/L) and disappearance from the donor compartment was monitored for 2 h. With jejunal tissue, only 13.6 +/- 3.5% of the initial dose of Q3G was found in the mucosal compartment 2 h after mucosal addition. Simultaneous addition of D-glucose (10 mmol/L) significantly reduced the disappearance of Q3G (remaining concentration, 33.4 +/- 6.9%) as did a Na(+)-free buffer solution containing phloridzin (final mucosal concentration of Q3G, 54.2 +/- 7.7%). In these experiments, disappearance of Q3G was paralleled by the appearance of quercetin in the mucosal solutions. In contrast, D-fructose (10 mmol/L) did not influence the disappearance of Q3G (Na(+)-free conditions). With proximal colon, 78.2 +/- 11.5% of the initial concentration of Q3G was still present in the mucosal solution after 2 h. When added to the serosal side, the concentration of Q3G decreased only slightly (jejunum, 96.1 +/- 2.1%; proximal colon, 90.7 +/- 1.2%). The concentration of rutin did not change after mucosal or serosal addition. Neither transport of intact glycosides nor of free quercetin from the donor into the acceptor compartment was observed under our experimental conditions. Taken together, the results clearly indicate a role of SGLT1 in mucosal uptake of the Q3G.

Animals↗
PubMed2006

Conversion of the methionine hydroxy analogue DL-2-hydroxy-(4-methylthio) butanoic acid to sulfur-containing amino acids in the chicken small intestine.

dl-Methionine or its corresponding hydroxy analogue, DL-2-hydroxy-(4-methylthio) butanoic acid (DLHMB), are commonly added to commercial animal diets to satisfy the TSAA requirement. The utilization of DLHMB as a supplementary source of Met begins with its conversion to L-Met via a 2-step mediated process. L-Methionine can then be transsulfurated to L-Cys, which, in turn, can be catabolized to taurine (TAU). In the present study, the capacity of the chicken small intestine to convert DLHMB to L-Met and to use this amino acid as a source for L-Cys and TAU production was evaluated. The appearance of Met in the serosal compartment of everted sacs incubated with DLHMB is higher in the presence of an H(+) gradient (mucosal pH 5.5 vs. 7.4). Serosal Cys and TAU concentration was compared in everted sacs incubated at a mucosal pH of 5.5 with DLHMB or L-Met, and the results show significantly higher values after incubation with the hydroxy analogue. Regional comparisons indicate no significant differences in the appearance of serosal Met and Cys, although lower values were obtained for TAU in the duodenum than in the jejunum and ileum. The profile of non-S amino acids was also determined and revealed no significant differences between DLHMB- and L-Met-incubated sacs. In conclusion, Cys and TAU content in chicken enterocytes is higher when DLHMB is used as a Met source.

Amino Acids, Sulfur↗
PubMed2006

Clostridium perfringens alpha toxin affects electrophysiological properties of isolated jejunal mucosa of laying hens.

Bacteria that colonize the intestinal tract can invade epithelial cells or produce toxins that cause diarrhoeal diseases. Proliferation of Clostridium perfringens and production of alpha-toxin, a phospholipase C, is the major factor for necrotic enteritis in poultry. However, little is known about the functional importance of luminal alpha-toxin during intestinal infection. The purpose of this study was to investigate the effects of purified alpha toxin of Clostridium perfringens on the electrophysiology of the laying hen's stripped jejunum in Ussing chambers. The effects were investigated in Experiment 1 after toxin addition to the mucosal and serosal side of the tissue, and a second experiment was performed to study the effect of the toxin on sodium-dependent glucose transport. Mucosal exposure of jejunal tissue sheets to 100 units of alpha toxin/L did not elicit electrophysiologic changes. The addition of purified alpha toxin to the serosal side induced a biphasic increase in short-circuit current (ISC) after 15 and 100 min. The magnitude of the increase of ISC of both peaks was similar, but the second phase response lasted longer. The tissue conductivity tended (P = 0.07) to be lower after 2 h of toxin addition compared with basal value when no toxin was added. In the second experiment, adding D-glucose on the mucosal side of the jejunum increased (P < 0.05) the ISC from a baseline value of 42 +/- 28 microA/cm2 to a maximal value of 103 +/- 27 microA/cm2. Preincubation with alpha-toxin almost fully inhibited this stimulation of ISC by D-glucose. The conductance of the tissues was not affected by the toxin addition. These findings indicate that alpha toxin not only causes electrogenic secretion of anions, probably due to the stimulation of chloride secretion, but also diminishes electrogenic Na+/glucose cotransport from the mucosal to serosal side in the small intestine of poultry.

Animals↗
PubMed1999

Intestinal cytokine response after gut ischemia: role of gut barrier failure.

OBJECTIVE: To investigate the effect of intestinal ischemia with and without a reperfusion injury on intestinal cytokine production and gut permeability. SUMMARY BACKGROUND DATA: In humans and in animal models, the gut has been implicated as a cytokine-producing organ after ischemia/reperfusion (I/R)-type injuries. Because of the limitations of in vivo models, it has been difficult to demonstrate directly that the gut releases cytokines after an I/R injury or whether there is a relation between the magnitude of the ischemic process and the cytokine response. METHODS: Ileal mucosal membranes from rats subjected to sham or 45 or 75 min of superior mesenteric occlusion (SMAO) or 45 minutes of SMAO and 30 minutes of reperfusion (SMAO 45/30) were mounted in the Ussing chamber system. Levels of tumor necrosis factor-alpha and interleukin-6 were serially measured in the mucosal and serosal reservoirs of the Ussing system, as was mucosal permeability as reflected by the passage of bacteria or phenol red across the ileal membrane. In a second group of experiments, Escherichia coli C25 was added to the mucosal reservoir to determine if the cytokine response would be increased. RESULTS: Mucosal and serosal levels of tumor necrosis factor-alpha were equally increased after SMAO, with the highest levels in the 75-minute SMAO group. The highest levels of interleukin-6 were found in rats subjected to 75 minutes of SMAO or SMAO 45/30; the serosal levels of interleukin-6 were four to sixfold higher than the mucosal levels. The addition of E. coli C25 resulted in a significant increase in the amount of interleukin-6 or tumor necrosis factor-alpha recovered from the mucosal reservoir. Increased ileal membrane permeability was observed only in rats subjected to 75 minutes of SMAO or SMAO 45/30. CONCLUSION: These results directly document that the levels of tumor necrosis factor-alpha and interleukin-6 released from the gut increase after an ischemic or I/R injury, such as SMAO, and that there is a relation between the magnitude of the gut ischemic or I/R insult and the cytokine response.

Animals↗
PubMed1999

Effects of low-dose dopexamine on splanchnic oxygenation during major abdominal surgery.

OBJECTIVE: To study the influence of low-dose dopexamine on splanchnic oxygenation during major abdominal surgery. DESIGN: Prospective, randomized, placebo-controlled study. SETTING: University hospital. PATIENTS: Eighteen adult patients undergoing elective major abdominal surgery. INTERVENTIONS: The patients received either dopexamine at 1 microg/kg/min (group A, n = 9) or 0.90% saline as control (group B, n = 9). MEASUREMENTS AND RESULTS: To assess the splanchnic oxygenation, intestinal tissue PO2 (PtissO2) and gastric intramucosal Pco2 (PmucCO2) were measured, and the PCO2 gap (PmucCO2 - PaCO2) was calculated at baseline (T1) and after an infusion period of 60 mins (T2). There was no difference between the groups in the global oxygen transport parameters. Low-dose dopexamine increases PtissO2 on the serosal side of the small bowel (deltaPtissO2, 17+/-24 mm Hg in group A vs. -5+/-10 in group B). The changes in PtissO2 at the serosal side of the colon after dopexamine demonstrated a nonsignificant increase (deltaPtissO2, 7+/-11 mm Hg in group A vs. -11+/-23 mm Hg in group B). In both groups, the Pco2 gap (group A, 6+/-7 mm Hg [T1] and 5+/-6 mm Hg [T2], vs. group B, 9+/-10 mm Hg [T1] and 12+/-10 mm Hg [T2]) remained unchanged compared with the baseline. CONCLUSION: It is concluded that low-dose dopexamine improves PtissO2 at the serosal side of the gut, preferably at the small bowel. However, low-dose dopexamine did not improve gastric PmucCO2.

Abdomen↗
PubMed1998

Calcium-activated potassium conductances on cultured nontransformed dog pancreatic duct epithelial cells.

Pancreatic duct epithelial cells (PDECs) mediate the pancreatic secretion of fluid and electrolytes. Membrane K+ channels on these cells regulate intracellular K+ concentration; in combination with the Na+/H+ antiport and Na+,K+ adenosine triphosphatase (ATPase), they may also mediate serosal H+ secretion, balancing luminal HCO3- secretion. We describe the K+ conductances on well-differentiated and functional nontransformed cultured dog PDECs. Through 86Rb+ efflux studies, we demonstrated Ca(2+)-activated K+ channels that were stimulated by A23187, thapsigargin, and 1-ethyl-2-benzimidazolinone, but not forskolin. These conductances also were localized on the basolateral membrane because 86Rb+ efflux was directed toward the serosal compartment. Of the K+ channel blockers, BaCl2, charybdotoxin, clotrimazole, and quinidine, but not 4-aminopyridine, apamin, tetraethylammonium, or iberiotoxin, inhibited 86Rb+ efflux. This efflux was not inhibited by amiloride, ouabain, and bumetanide, inhibitors of the Na+/H+ antiport, the Na+,K(+)-ATPase pump, and the Na+,K+,2Cl- cotransporter, respectively. When apically permeabilized PDEC monolayers were mounted in Ussing chambers with a luminal-to-serosal K+ gradient, A23187 and 1-ethyl-2-benzimidazolinone stimulated a charybdotoxin-sensitive short-circuit current (Isc) increase. Characterization of K+ channels on these cultured PDECs, along with previous identification of Cl- channels (1), further supports the importance of these cells as models for pancreatic duct secretion.

Animals↗
PubMed2005

Effect of red wine on the intestinal absorption of thiamine and folate in the rat: comparison with the effect of ethanol alone.

BACKGROUND: This work aimed to investigate, in the rat, the acute in vitro effect of red wine and the effect of chronic red wine ingestion on the intestinal absorption of thiamine and folate and to compare them with the effects of ethanol alone. METHODS: The effects of red wine and of an ethanol solution (same ethanol concentration as that in the red wine, i.e., 12% [v/v]) on rat jejunal apparent permeability (Papp) to H-thiamine and H-folate in the mucosal-to-serosal direction were investigated. Red wine and ethanol were tested both chronically (21-day consumption) and acutely in vitro. RESULTS: Acutely, both red wine and ethanol 12% (v/v) (both diluted 1:5) reduced (to 65 and 60% of control, respectively) the mucosal-to-serosal Papp to H-thiamine across rat jejunum. Chronic (21-day) ethanol (12% [v/v]) consumption also decreased the Papp to H-thiamine (to 33% of control), but red wine consumption for the same period did not change it. Mucosal-to-serosal Papp to H-folate across rat jejunum was not changed by chronic ingestion of red wine or ethanol. Similarly, it was not affected by acute exposition of the tissue to red wine or ethanol. Acute ethanol (0.05% [v/v]) did not affect the Papp to H-thiamine or H-folate in jejunal tissues obtained from control and red wine-treated rats, but it significantly increased the Papp to both H-thiamine and H-folate (to 183 and 197% of control, respectively) in tissues from chronically ethanol-treated rats. CONCLUSIONS: Acute and chronic red wine or ethanol had no effect on the intestinal absorption of folate. However, ethanol, both acutely and chronically, decreased the jejunal absorption of thiamine, and red wine reduced the jejunal absorption of thiamine, but only when tested acutely. These findings show that it is not correct to extrapolate from results obtained with ethanol alone on intestinal permeability to the effect of alcoholic beverage consumption.

Animals↗
PubMed2005

Postoperative ascites associated with intraperitoneal antiseptic lavage.

BACKGROUND: Peritonitis is the established term for infective inflammation of the peritoneum, whereas serositis generally refers to aseptic inflammation of a serous cavity, including the peritoneum. Serositis may be metabolic, viral, autoimmune, drug induced, genetic, allergic or granulomatous, or due to chemical antiseptics. CASES: In our gynecological department, 4 patients had peritonitis and ascites after laparotomy. CONCLUSION: Based on the investigation, we think that the solution used for peritoneal lavage (0.1% octenidine dihydrochloride and 2% phenoxyethanol) played a role in the tissue toxicity that caused chemical serositis with effusion.

Ascites↗
PubMed2005

Activation of splanchnic and pelvic colonic afferents by bradykinin in mice.

BACKGROUND: Lumbar splanchnic (LSN) and sacral pelvic (PN) nerves convey different mechanosensory information from the colon to the spinal cord. Here, we determined whether these pathways differ also in their chemosensitivity to bradykinin. METHODS: Using a novel in vitro mouse colon preparation, serosal afferents were recorded from the LSN and PN and distinguished based on their mechanosensitivity to von Frey filaments (70-4000 mg) and insensitivity to colonic stretch (1-5 g) or fine mucosal stroking (10 mg). Bradykinin was applied into a ring around mechanoreceptive fields. RESULTS: The LSN and PN afferents had different dynamic responses to mechanical stimuli: PN afferents required lower intensity stimuli, evoked larger responses, and displayed more maintained responses than LSN afferents. Bradykinin (1 micromol L-1) excited 66% (27 of 41) of LSN afferents. Responses to probing were potentiated after bradykinin. The concentration-dependent (EC50: 0.16 micromol L-1) response was reversed by the B2-receptor antagonist HOE-140 (10 nmol L-)). Twelve bradykinin responsive afferents were mechanically insensitive. More LSN serosal afferents responded to bradykinin than PN afferents (11%, P<0.001) , with larger responses (P<0.05). No mechanically insensitive PN afferents were recruited by bradykinin. CONCLUSIONS: Bradykinin potently stimulates most splanchnic serosal afferents via B2-receptors, but few pelvic afferents. Mechanically insensitive afferents recruited by bradykinin are exclusive to the LSN.

Animals↗