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At least 19 recordsLinked to original sources
PubMed1993

Serositis: comparative analysis of histological findings and pathogenetic mechanisms in nonbacterial serosal inflammation.

Peritonitis is the established term for infective inflammation of the peritoneum, while serositis generally refers to nonorganismal inflammation in any serous cavity, including the peritoneum. In continuous ambulatory peritoneal dialysis (CAPD) literature, however, culture-negative peritoneal inflammation is referred to as "sterile" or "chemical" peritonitis. These terms not only imply unwarranted etiologic assumptions, but may also deflect attention from the existence of medical conditions to which the peritoneum is subject. This is evident in CAPD literature where there is little recognition that the peritoneum, as a member of the serosa and a secretor of lamellar bodies, is prey to a wide range of disorders. Thus before, during, and after CAPD, the membrane is liable to fall victim to disease states unconnected with the process of dialysis. Significant peritoneal pathology occurs as part of a pan-serositis, which may be metabolic (uremia, cholesterolosis), autoimmune (systemic lupus erythematosus, rheumatoid disease, acute rheumatism, endocrinopathies), genetic (recurrent hereditary polyserositis), allergic (eosinophilic serositis), and granulomatous in nature. This paper presents a comparative analysis of histopathological presentation and pathogenetic mechanisms involved in all forms of peritoneal serositis. It incorporates recent advances in molecular biology of the membrane into a holistic reappraisal of peritoneal pathology, revealing hitherto unrecognized homologies in peritoneal reaction to diverse disorders.

Animals↗
PubMed1976

Metabolic evidence that serosal sodium does not recycle through the active transepithelial transport pathway of toad bladder.

The possibility that sodium from the serosal bathing medium "back diffuses" into the active sodium transport pool within the mucosal epithelial cell of the isolated toad bladder was examined by determining the effect on the metabolism of the tissue of removing sodium from the serosal medium. It was expected that if recycling of serosal sodium did occur through the active transepithelial transport pathway of the isolated toad bladder, removal of sodium from the serosal medium would reduce the rate of CO2 production by the tissue and enhance of stoichiometric ratio of sodium ions transported across the bladder per molecula of sodium transport dependent CO2 produced simultaneously by the bladder (JNa/JCO2). The data revealed no significant change in this ratio (17.19 with serosal sodium and 16.13 after replacing serosal sodium with choline). Further, when transepithelial sodium transport was inhibited (a) by adding amiloride to the mucosal medium, or (b) by removing sodium from the mucosal medium, subsequent removal of sodium from the serosal medium, or (c) addition of ouabain failed to depress the basal rate of CO2 production by the bladder [(a)rate of basal, nontransport related, CO2 production (JbCO2) equals 1.54 +/- 0.52 with serosal sodium and 1.54 +/- 0.37 without serosal sodium; (b) Jb CO2 equals 2.18 +/- 0.21 with serosal sodium and 2.09 +/- 0.21 without serosal sodium; (c) 1.14 +/- 0.26 without ouabain and 1.13 +/- 0.25 with ouabain; unite of JbCO2 are nmoles mg d.w.-1 min-1]. The results support the hypothesis that little, if any, recycling of serosal sodium occurs in the total bladder.

Amiloride↗
PubMed1976

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. I. Effects of different medium potassium concentrations on electrical parameters.

When serosal medium potassium was decreased from the usual concentration of 3.5 mM, the short-circuit current (SCC) of hemibladders in chambers immediately and transiently increased. The maximum SCC attained was greater the greater the decrease in serosal potassium, and was twice the initial SCC when the final serosal medium was potassium-free. The SCC then fell to its previous level for final serosal potassium concentrations greater than 2 mM and to less than its previous level for those less than 2 mM, being lowest (15% of previous levle) in potassium-free sodium Ringer's. When serosal medium potassium was increased from 3.5 mM by substituting potassium for sodium, SCC transiently decreased and then recovered to its previous level. Steady SCC was the same in serosal media of 2-116 mM potassium; conductance increased and p.d. decreased after incubation in 50-116 mM potassium serosal media. Short-circuit current and p.d. transiently increased (decreased) whenever serosal medium potassium was decreased (increased); conductance increased with any change in serosal potassium. Changing mucosal medium potassium concentration between 0 and 50 mM did not affect SCC. The initial transient increase and subsequent decrease in SCC on removing serosal potassium were partially prevented by 3.5 mM rubidium or caesium, or by 116 mM choline in the serosal medium. The transient changes in SCC were due partly to changes in transepithelial sodium transport.

Animals↗
PubMed1976

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. II. Effects of different medium potassium concentrations on epithelial cell composition.

Epithelial cells from hemibladders incubated in potassium-free sodium Ringer's serosal medium lost potassium, both in exchange for serosal sodium and with chloride and water. Cellular sodium of mucosal origin did not change. The loss of cellular potassium, chloride and water closely followed the fall in short-circuit current (SCC). One third as much potassium, chloride and water were lost in 1 mM potassium serosal medium; SCC fell 1/3 as much. Potassium-free choline Ringer's serosal medium abolished the initial increase in SCC and reduced the fall in cellular potassiu, chloride and water and in SCC. Ouabain (10(-2)M) in potassium-free medium prevented the initial increase in SCC and the loss of cellular chloride and water. Ouabain (5 X 10(-4)M) caused loss of cellular potassium in exchange for mucosal and serosal sodium, effects different from those of absence of serosal potassium although SCC was similarly inhibited. Sodium-free mucosal medium abolished SCC and prevented the initial transient of SCC and diminished loss of cellular potassium, chloride and water on removing serosal potassium. When serosal potassium concentration was increased considerably, cells gained potassium, chloride and water, and in 116 mM potassium media, lost sodium of serosal origin. A hypothesis is advanced to explain the transients in SCC on changing serosal potassium concentration. The fall in cellular potassium, not water, probably inhibits sodium transport in media of less than 2 mM potassium.

Animals↗
PubMed1988

Influence of serosal Cl on transport properties and cation activities in frog skin.

The effects of serosal substitution of isosmotic Na2SO4-Ringer solution for NaCl-Ringer solution were studied in the short-circuited frog skin (Rana pipiens, Northern variety). Despite prompt changes of transepithelial measurements, initial cellular effects were slight. After 30 to 45 min, however, the transcellular current had decreased and the cell electrical potential had depolarized, in association with decrease of the apical membrane fractional resistance and basolateral membrane conductance. Apical membrane slope conductance was unaffected. Similar effects were obtained with isolated epithelia. With the use of gluconate or NO3 in place of Cl, the effects on cellular current and conductance were minimal or insignificant, despite changes of the cell potential, fractional resistance, and basolateral conductance similar to those seen with sulfate. Following prolonged exposure to serosal SO4-Ringer, the extent of depolarization induced by raising the serosal K concentration decreased, indicating diminution of basolateral K conductance and the existence of other basolateral conductances. Equilibration in serosal gluconate-Ringer enhanced polarization on serosal restoration of Cl or removal of Na, again indicating a time-dependent change in the basolateral conductance pattern. Depolarization on removal of serosal Cl was not attributable to inhibition of the pump. Nor was it the result of decrease of the K equilibrium potential EK: exposure to serosal SO4-Ringer decreased cell K activity aKc from 104 +/- 6 to 58 +/- 4 mM (n = 5), but EK was reduced only slightly; exposure to serosal gluconate increased aKc and EK. Serosal sulfate lowered the cell Na activity aNac, but the electrochemical potential difference for Na across the apical surface was unaffected. The concurrent decrease of both aKc and aNac following serosal substitution of SO4 for Cl raises questions concerning mechanisms of osmoregulation.

Amiloride↗
PubMed1975

Galactose transport across the serosal border of rabbit ileum and its role in intracellular accumulation.

Unidirectional fluxes of D-galactose across the brush and serosal border of rabbit ileum were determined using the method described previously (Naftalin, R. J. and Curran, P.F. (1974) J. Membrane Biol. 16, 257-278). With ringer [Na] equals 75 meguiv., the Km for galactose influx across the brush-border is 5mM, with 0.1 mM ouabain present K-m equals 50 mM, the V (2.0 munol - CM-2-H-1) remains unaltered. The Michaelis parameters for galactose influx across the serosal border are K-m equals 59 plus or minus 9 mM and V equals 4.7 plus or minus 0.24 mumol-cm-2-h-1 and for efflux K-m equals 85 plus or minus 10 mM and V equals 6.8 plus or minus 0.7 mumol-CM-2-H-1. 2. 2-Deoxy-D-glucose and methyl beta-D-glucopyranoside inhibit galactose entry exclusively at the serosal and mucosal borders respectively, while 3-O-methyl-D-glucose inhibits galactose influx at both borders. 0.1 mM ouabain increases the K1 of 3-O-methylglucose for the serosal transport system (100 mM) is unaffected by ouabain. Inhibition of mucosal galactose transport by ouabain or by competition with other sugars results in a reciprocal increase in exit permeability and decrease in entry permeability. Inhibition of serosal galactose transport results in inhibition of both the entry and exit permeability, entry is more affected. 3. There is a small degree of permeability asymetry at the serosal border to galactose which is reduced by ouabain or removel of Na+ from the Ringer. Uptake of 14C-labelled galactose from the serosal solution into the tissue is also inhibited by addition of ouabain or Na+ removal. It is therefore considered that there is a weak active transport system for galactose at the serosal border. 4. Net transepithelial galactose flux is sufficiently high and serosal permeability to galactose sufficiently low to be consistent with the view that galactose is concentrated within the tissue fluid, after conviction (Naftalin, R.J. and Holman, G.D. (1974) Biochim. Biophys. Acta., 373, 453-470) across the mucosal border because it is reflected at the serosal boundary.

Animals↗
PubMed1975

D-galactose accumulation in rabbit ileum. Effects of theophylline on serosal permeability.

The effects of theophylline and dibutyryl cyclic AMP, on in vitro unidirectional galactose fluxes across the mucosal and serosal borders of rabbit ileum have been studied. 1. When Ringer [galactose] = 2mM, theophylline and dibutyryl cyclic AMP reduce both mucosal-serosal and serosal-mucosal galactose flux by approx. 50%. The K1 for theophylline inhibition of flux in both directions is 2 mM. 1 mM dibutyryl cyclic AMP elicits a maximal inhibitory response. Concurrent with the inhibition in transmural galactose fluxes, theophylline and dibutyryl cyclic AMP increase the tissue accumulation of [galactose] and the specific-activity ratio R of 3H : 14C-labelled galactose coming from the mucosal and serosal solutions respectively. It is deduced that theophylline and dibutyryl cyclic AMP are without effect on the mucosal unidirectional permeability to galactose but cause a symmetrical reduction in serosal entry and exit permeability. 2. Reduction in the asymmetry of the mucosal border to galactose by reducing Ringer [Na], raising Ringer [galctose] or adding ouabain reduces the theophylline-dependent increase in galactose accumulation. 3. Hypertonicity in the serosal solution increases the permeability of the serosal border to galactose and reduces tissue galactose accumulation. Serosal hypertonicity partially reverses the theophylline-depedent effects on galactose transport. Replacing Ringer chloride by sulphate abolishes the theophylline-dependent effects on galactose transport. 4. It is considered that the theophylline-dependent increase in galactose accumulation results from the reduction in serosal permeability. This is shown to be a quantitatively consistent inference. 5. Further support for the view that the asymmetric transport of galactose in rabbit ileum results from convective-diffusion is presented.

Animals↗
PubMed1990

Prognostic significance of serosal invasion and free intraperitoneal cancer cells in gastric cancer.

Survival rates after curative gastrectomy for advanced gastric cancer among 238 patients in whom the cancer was invading the serosa were compared with 283 patients without serosal invasion. Generalized Wilcoxon estimates for 5-year survival rate were 47.1 per cent for patients exhibiting serosal invasion and 75.9 per cent for patients without serosal invasion. The frequency of lymph node metastasis increased proportionately with the extent of serosal invasion: 18.4 per cent in cases of S0; 53.8 per cent in cases of S1; 80.0 per cent in cases of S2; and 91.4 per cent in cases of S3. The higher the aggregate total of S (serosal invasion) and n (lymph node metastasis) factors, the lower the 5-year survival rate. In addition, patients with serosal invasion had a propensity for peritoneal dissemination of cancer cells; the percentage of cases with intraperitoneal free cancer cells increased with the extent of serosal invasion. It is worth noting that when cancer infiltration proceeded to the deeper layers and was accompanied by nodal metastasis, cancerous invasion of the perinodal fatty tissue was frequently evident. Therefore, unfavourable prognosis after curative resection in gastric cancer patients with serosal invasion may be largely dependent on whether or not the cancer has invaded the peritoneal cavity and the perinodal fatty tissue.

Adult↗
PubMed1976

Effects of serosally added sugars on the transepithelial electrical properties of the perfused goldfish intestine.

1. A study has been made of the effect of serosally added sugars on the transmural potential difference and electrical resistance of the perfused goldfish intestine. 2. Addition of glucose at the serosal side resulted in a decrease of the transmural potential difference independent of the presence or absence of glucose at the mucosal side. The transepithelial resistance did not change. 3. The serosal glucose effect persisted in the presence of phlorizin at the mucosal side. 4. With the activity transported non-metabolized glucose analogue 3-oxy-methylglucose the same effects were observed as with glucose. 5. Replacement of NaCl by cholineCl, RbCl or LiCl at both sides of the intestine had a diminishing effect on the glucose evoked potentials and on the transepithelial conductance. 6. Phlorizin in concentrations lower than 10(-4) M, at the serosal side did not influence neither the mucosal nor the serosal glucose effects. 7. Ouabain at the serosal side inhibited the serosal glucose effect and decreased the transepithelial conductance. 8. The results support the concept that sugar transport at the serosal side of the epithelial cell has features in common with the sodium-dependent sugar transport mechanism at the mucosal side.

Animals↗
PubMed1979

Pathways for bicarbonate transfer across the serosal membrane of turtle urinary bladder: studies with a disulfonic stilbene.

Bicarbonate is transferred across the serosal (S) membrane of the epithelial cells of the turtle bladder in two directions. Cellular HCO3- generated behind the H+ pump moves this membrane into the serosal solution. This efflux of HCO3- is inhibited by SITS (4-isothiocyano-4'-acetamido-2,2'-disulfonic stilbene). When HCO3- is added to the serosal solution it is transported across the epithelium in exchange for absorbed Cl-. This secretory HCO3- flow traverses the serosal cell membrane in the opposite direction. In this study the effects of serosal addition of 5 x 10(-4) M SITS on HCO3- secretion and Cl- absorption were examined. The rate of H+ secretion was brought to zero by an opposing pH gradient, and 20 mM HCO3- was added to S. HCO3- secretion, measured by pH stat titration, was equivalent to the increase in M leads to S Cl- flux after HCO3- addition. Neither the S leads to M flux of HCO3- nor the M leads to S flux of Cl- were affected by SITS. In the absence of electrochemical gradients, net Cl- absorption was observed only in the presence of HCO3- in the media; under such conditions, unidirectional and net fluxes of Cl- were not altered by serosal or mucosal SITS. H+ secretion, however, measured simultaneously as the short-circuit current in ouabain-treated bladders decreased markedly after serosal SITS. The inhibition of the efflux of HCO3- in series with the H+ pump and the failure of SITS to affect HCO3- secretion and Cl- absorption suggest that the epithelium contains at least two types of transport systems for bicarbonate in the serosal membrane.

Animals↗
PubMed1982

Serosal Na/Ca exchange and H+ and Na+ transport by the turtle and toad bladders.

A Na/Ca exchange system has been described in the plasma membrane of several tissues and seems to regulate the concentration of calcium in cytosol. Replacement of extracellular Na by sucrose increases calcium uptake into and decreases calcium efflux from the cell, leading to an increase in cytosolic calcium. The effect of an increase in cytosolic calcium mediated by the Na/Ca exchange system on H+ and Na transport in the turtle and toad bladder was investigated by replacing serosal Na isosmotically by sucrose or choline. Replacement of serosal by sucrose was associated with a significant inhibition of H+ secretion or Na transport which was reversible by addition of NaCl. Replacement of mucosal Na by sucrose failed to alter H+ secretion. Removal of serosal Na was associated with a significant increase in 45Ca uptake which could be blocked by pretreatment with lanthanum chloride. Pretreatment with lanthanum chloride blunted the inhibitory effect of replacement of serosal Na by sucrose on H+ and Na transport, thus suggesting that the increase in calcium uptake and the inhibition of transport are causally related. Under anaerobic conditions the rate of H+ or Na transport are linked to the rate of lactate production. The inhibition of Na or H+ transport by removal of serosal Na was accompanied by a proportional decrease in lactate production, thus suggesting that an increase in cytosolic calcium does not inhibit transport by uncoupling glycolysis from transport. Replacement of serosal Na by sucrose did not alter the force of the H+ or Na pump but led to an increase in resistance of the active pathway of H+ and Na transport. The inhibition of Na transport by replacement of serosal Na with sucrose could be reversed by addition of amphotericin B, an agent which increases luminal permeability to Na, thus suggesting that decreased Na entry across the apical membrane is the mechanism responsible for the inhibition of Na transport. The results of the present studies strongly suggest that an increase in cytosolic calcium through the serosal Na/Ca exchange system inhibits H+ and Na transport in the turtle and toad bladder probably by increasing the resistance of the luminal membrane.

Amphotericin B↗
PubMed1976

Evidence for carrier-mediated uptake and efflux of sugars at the serosal side of the rat intestinal mucosa in vitro.

A modification of the everted sac technique is described which allows several sacs to be prepared rapidly and simultaneously from the same segment of rat intestine. 2. A method has been developed for comparing the transport of two sugars by measuring changes in the ratios of their concentrations as they pass across the intestinal wall. 3. With this method significant differences were observed between the D-[3H]galactose and L-[14C]glucose ratios in the mucosal epithelium, the serosal tissue and the serosal compartment. These results indicate that both the efflux of galactose from the serosal side of the mucosal epithelium and the uptake of the sugar into the mucosa are carrier-mediated processes. 4. The mediated efflux of galactose at the serosal side of the epithelial layer is inhibited by the presence of phlorizin on the mucosal side and to some extent by any reduction in the mucosal Na+ concentration. Both of these treatments inhibited galactose uptake at the brush border. Serosal efflux of the sugar appeared to be saturated at high concentrations of D-galactose. 5. Pre-treatment of the sacs with mercuric chloride considerably reduced D-galactose uptake from the luminal side, but did not affect its efflux relative to L-glucose at the serosal side of the mucosal epithelium. 6. Carrier-mediated sugar uptake into the mucosal epithelium from the serosal side was also examined. The role of the bidirectional, carrier-mediated sugar transport processes at the serosal pole of the mucosal epithelial cell in transintestinal transport is discussed.

Animals↗
PubMed1987

Relationship between area of serosal invasion and prognosis in patients with gastric carcinoma.

We examined the relationship between the spatial extent of invasion of the gastric serosa in patients with gastric carcinoma and their postoperative 5-year survival rate. At the time of surgical resection of gastric cancer, intraperitoneal free cancer cells were detected by lavage of the Douglas cavity in 135 of 309 (44%) patients with gross evidence of serosal invasion. Examination of the relationship between the presence of intraperitoneal free cancer cells and serosal area invaded by the tumor revealed that only 22% of cases with an area of serosal invasion 10 cm2 or less were positive for free cancer cells, but such cells were found in 72% of cases with an area of serosal invasion greater than 20 cm2. The 5-year survival rate was 31% in patients with an area of serosal invasion of less than 10 cm2, whereas the rate was only 8% in patients with an area of serosal invasion greater than 20 cm2. Not only the presence of serosal invasion by a tumor but also the spatial extent of the invasion are significant factors that influence the prognosis of patients with gastric carcinoma.

Gastrectomy↗
PubMed1989

Width of serosal invasion and prognosis in advanced human gastric cancer with special reference to the mode of tumor invasion.

We studied the influence of the width of serosal invasion on the prognosis, in relation to the mode of invasion, in 142 patients who had curative resection for gastric carcinoma that invaded beyond the muscularis propria. The mode of invasion was classified into infiltrative and expanding types. Average diameter of tumor at the serosal or subserosal layer for the infiltrative type was 4.2 +/- 3.2 cm, a value significantly greater than that of 2.5 +/- 2.0 cm for the expanding type (P less than 0.01). The 5-year survival rate of patients with the infiltrative type carcinoma was significantly lower (36.8%) than that with the expanding type carcinoma (50.0%) (P less than 0.05). In the infiltrative type, the survival time of patients with a serosal invasion exceeding 2 cm was significantly shorter than when the serosal invasion was less than 2 cm (P less than 0.05). In the expanding type, however, the prognosis was good until the width of serosal invasion extended to 4 cm or greater. The difference in survival according to the width of serosal invasion did not always depend on the incidence of positive lymph nodes in both types of carcinomas. Therefore, influence of the width of serosal invasion on the prognosis for advanced gastric carcinomas differs between infiltrative and expanding types.

Female↗
PubMed1995

Macroscopic intraoperative diagnosis of serosal invasion and clinical outcome of gastric cancer: risk of underestimation.

Data on 715 Japanese patients with gastric cancer were studied retrospectively with regard to the relationship between macroscopic and microscopic diagnoses of serosal invasion and clinicopathological factors affecting the accuracy of the macroscopic diagnosis. Although there was no macroscopic evidence of serosal invasion intraoperatively (S0 or S1), there was histological evidence of cancer cells on the serosal surface in 69 patients (9.7%). In these serosal invasion-positive cases, the tumors were larger; were located more commonly in the upper third, lesser and greater curvatures of the stomach; were Borrmann type 3 or type 4 tumors, and of an undifferentiated histologic type with an infiltrative growth pattern more commonly, and had more extensive lymphatic and vascular vessel invasion and lymph node metastasis (P < 0.01). Total gastrectomy was done more often for the serosal invasion-positive group, but the extent of lymph node dissection was comparable. Cases of a noncurative resection because of a positive surgical margin were more frequent in the serosal invasion-positive group (8/69 vs. 14/646, P < 0.01), and most had undifferentiated and infiltrative cancers. The 10-year survival rates were 49.2% and 85.5% for patients with and without serosa invasion, respectively. These findings clearly show that the serosal surface, especially in cases of the undifferentiated or infiltrative type of gastric cancer, must be closely inspected intraoperatively.

Aged↗
PubMed1979

Reversible inhibition by lanthanum of the hydrosmotic response to serosal hypertonicity in toad urinary bladder.

In the urinary bladder of amphibia, hypertonicity of the serosal bath (SH) evokes an increase in transepithelial water permeability, the characteristics of which resemble the response to antidiuretic hormone (ADH). The ionic dependency, in particular for Ca2+, appears very similar for SH- and ADH-induced water fluxes. In the present experiments La3+ was used as a probe to study the Ca2+-dependency of the hydrosmotic response to SH in isolated urinary bladder of the toad Bufo marinus. Addition of La3+ (5 mM) on the serosal side of the membrane produced a significant and reversible increase in basal transepithelial water flux. The hydrosmotic response elicited by adding 250 mM mannitol to the serosal Ringer's solution was inhibited by 30% in the absence of serosal Ca2+. Similarly, the hydrosmotic response to SH was inhibited by 37%, 30% and 40% when 5 mM La3+ was added to the serosal medium 30 min before, concommitantly with, or 60 min after induction of SH. The inhibition of transepithelial water flux observed in the absence of serosal Ca2+ or in the presence of serosal La3+ was reversible. The results support a critical role for Ca2+ in the modulation of transepithelial water permeability in the urinary bladder of amphibia. Ca2+ presumably exerts its effects at a post-cyclic AMP step.

Animals↗
PubMed1984

Electrogenic Cl- absorption by Amphiuma small intestine: dependence on serosal Na+ from tracer and Cl- microelectrode studies.

The Na+ requirement for active, electrogenic Cl- absorption by Amphiuma small intestine was studied by tracer techniques and double-barreled Cl- -sensitive microelectrodes. Addition of Cl- to a Cl- -free medium bathing in vitro intestinal segments produced a saturable (Km = 5.4 mM) increase in short-circuit current (ISC) which was inhibitable by 1 mM SITS. The selectivity sequence for the anion-evoked current was Cl- = Br- greater than SCN- greater than NO-3 greater than F- = I-. Current evoked by Cl- reached a maximum with increasing medium Na concentration (KM = 12.4 mM). Addition of Na+, as Na gluconate (10 mM), to mucosal and serosal Na+-free media stimulated the Cl- current and simultaneously increased the absorptive Cl- flux (JCl m----s) and net flux ( JClnet ) without changing the secretory Cl- flux ( JCls ----m). Addition of Na+ only to the serosal fluid stimulated JClm ----s much more than Na+ addition only to the mucosal fluid in paired tissues. Serosal DIDS (1 mM) blocked the stimulation. Serosal 10 mM Tris gluconate or choline gluconate failed to stimulate JClm ----s. Intracellular Cl- activity ( aiCl ) in villus epithelial cells was above electrochemical equilibrium indicating active Cl- uptake. Ouabain (1 mM) eliminated Cl- accumulation and reduced the mucosal membrane potential (psi m) over 2 to 3 hr. In contrast, SITS had no effect on Cl- accumulation and hyperpolarized the mucosal membrane. Replacement of serosal Na+ with choline eliminated Cl- accumulation while replacement of mucosal Na+ had no effect. In conclusion by two independent methods active electrogenic Cl- absorption depends on serosal rather than mucosal Na+. It is concluded that Cl- enters the cell via a primary (rheogenic) transport mechanism. At the serosal membrane the Na+ gradient most likely energizes H+ export and regulates mucosal Cl- accumulation perhaps by influencing cell pH or HCO-3 concentration.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1982

Effects of a small serosal hydrostatic pressure on sodium and water transport and morphology in rabbit gall-bladder.

1. In order to investigate the mechanism of serosal pressure-induced inhibition of isosmotic fluid transport, the effect of 4.5 cm water serosal pressure on spontaneous water transfer (J(v)) in rabbit gall-bladders was measured (in the presence of a supporting soft nylon net on the mucosal side) in a modified Ussing chamber. This allowed unidirectional Na(+) fluxes ([Formula: see text] and [Formula: see text]), transepithelial potential difference and resistance (R(t)) to be measured simultaneously. The effects of the serosal pressure were also investigated by light and electron microscopy.2. During pressure application, R(t) increased due to a covering effect of the mucosal support. The serosal pressure caused a parallel decrease in J(v) and net Na(+) transport ([Formula: see text]) across the free epithelial surface of 80-85%. About 85% of the decrease in [Formula: see text] was due to a decrease in [Formula: see text].3. After inhibition of 93% of fluid absorption by serosal 10(-3)M-ouabain, pressure-induced change in J(v) was only 8% of the spontaneous fluid transport rate.4. Control Na(+) flux ratio ([Formula: see text]) was 3.5. The pressure-induced increase in steady-state [Formula: see text] of 30-35% therefore contributed little to the decrease in [Formula: see text]. Further, this increase in [Formula: see text] was completely prevented by mucosal 10(-3) M-amiloride.5. All pressure-induced effects on transport and electrical parameters were reversible.6. The light microscopical and scanning electron microscopical results showed that half of the epithelial surface was covered by the nylon net following serosal pressure application. Ruptures in the epithelium were not seen. Thin section and freeze fracture electron microscopy demonstrated continuous, well developed tight junctions both in control and experimental condition.7. It is concluded that a serosal pressure of only 4.5 cm water causes inhibition of a cellular active Na(+) and water transport with only minimal, if any, contribution from paracellular filtration. This would seem incompatible with the concept that an active ion transport mechanism localized in the basolateral cell membrane is responsible for transepithelial fluid transport. The possibility of a mechanical fluid transport mechanism via elements of a tubulo-cisternal endoplasmic reticulum is raised.

Amiloride↗