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PubMed1979

The surface epithelium of teleostean fish gills. Cellular and junctional adaptations of the chloride cell in relation to salt adaptation.

Various species of teleostean fishes were adapted to fresh or salt water and their gill surface epithelium was examined using several techniques of electron microscopy. In both fresh and salt water the branchial epithelium is mostly covered by flat respiratory cells. They are characterized by unusual outer membrane fracture faces containing intramembranous particles and pits in various stages of ordered aggregation. Freeze fracture studies showed that the tight junctions between respiratory cells are made of several interconnecting strands, probably representing high resistance junctions. The organization of intramembranous elements and the morphological characteristics of the junctions do not vary in relation to the external salinity. Towards the base of the secondary gill lamellae, the layer of respiratory cells is interrupted by mitochondria-rich cells ("chloride cells"), also linked to respiratory cells by multistranded junctions. There is a fundamental reorganization of the chloride cells associated with salt water adaptation. In salt water young adjacent chloride cells send interdigitations into preexisting chloride cells. The apex of the seawater chloride cell is therefore part of a mosaic of sister cells linked to surrounding respiratory cells by multistranded junctions. The chloride cells are linked to each other by shallow junctions made of only one strand and permeable to lanthanum. It is therefore suggested that salt water adaptation triggers a cellular reorganization of the epithelium in such a way that leaky junctions (a low resistance pathway) appear at the apex of the chloride cells. Chloride cells are characterized by an extensive tubular reticulum which is an extension of the basolateral plasma membrane. It is made of repeating units and is the site of numerous ion pumps. The presence of shallow junctions in sea water-adapted fish makes it possible for the reticulum to contact the external milieu. In contrast in the freshwater-adapted fish the chloride cell's tubular reticulum is separated by deep apical junctions from the external environment. Based on these observations we discuss how solutes could transfer across the epithelium.

Adaptation, Physiological↗
PubMed1983

Relationship of net chloride flow across the human erythrocyte membrane to the anion exchange mechanism.

The parallel effects of the anion transport inhibitor DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonate) on net chloride flow and on chloride exchange suggest that a major portion of net chloride flow takes place through the anion exchange system. The "slippage" model postulates that the rate of net anion flow is determined by the movement of the unloaded anion transport site across the membrane. Both the halide selectivity of net anion flow and the dependence of net chloride flux on chloride concentration over the range of 75 to 300 mM are inconsistent with the slippage model. Models in which the divalent form of the anion exchange carrier or water pores mediate net anion flow are also inconsistent with the data. The observations that net chloride flux increases with chloride concentration and that the DIDS-sensitive component tends to saturate suggest a model in which net anion flow involves "transit" of anions through the diffusion barriers in series with the transport site, without any change in transport site conformation such as normally occurs during the anion exchange process. This model is successful in predicting that the anion exchange inhibitor NAP-taurine, which binds to the modifier site and inhibits the conformational change, has less effect on net chloride flow than on chloride exchange.

Adult↗
PubMed2005

Preventing adverse events in the pediatric intensive care unit: prospectively targeting factors that lead to intravenous potassium chloride order errors.

OBJECTIVE: To prospectively identify and reduce proximal causes of error contributing to inappropriate intravenous potassium chloride orders and reduce adverse events subsequent to these ordering errors. DESIGN: Pre-post cohort study of the reduction in both proximal causes of error and number of postinfusion elevated serum potassium levels after intervention. SETTING: Sixteen-bed, tertiary care, urban, academic pediatric intensive care unit. PATIENTS: Children 0-18 yrs old receiving intravenous potassium chloride in the pediatric intensive care unit. INTERVENTIONS: A multidisciplinary team determined proximal causes of error that were likely contributors to the occurrence of the outcome measure, elevated potassium levels after intravenous potassium chloride. A mandatory drug request form was designed for physicians ordering intravenous potassium chloride. The drug request form was designed to reduce proximal causes of error and, as a result, elevated potassium levels after intravenous potassium chloride. Demographic and laboratory data on children receiving intravenous potassium chloride in the pediatric intensive care unit and details of the drug order were analyzed. MEASUREMENTS AND MAIN RESULTS: Data from 1,492 intravenous potassium chloride administration-events before implementation of the drug request form were collected. After the drug request form was mandated, 166 consecutively completed forms were collected and analyzed. The incidence of postinfusion elevations in serum potassium decreased from a rate of 7.7% (103 of 1,341) before the drug request form to 0% (0 of 150) after the drug request form (p < .001). Proximal causes of error were also reduced. The number of patients with a creatinine >/=2 mg/dL receiving intravenous potassium chloride decreased from 28.4% to 14.2% (p < .001). The number of intravenous potassium chloride infusions administered to patients where serum potassium value was >4.5 mmol/L decreased significantly (2.9% vs. 0.0%, p < .02). The incidence rates of both verbal orders and failure to write the order in a correct format were reduced to zero. CONCLUSIONS: Simple, blame-free, system-wide interventions designed to reduce proximal causes of error can be an effective, proactive means of reducing the likelihood of medical morbidity.

Adolescent↗
PubMed1985

The role of mitochondria-rich cells in the chloride current conductance across toad skin.

In early studies of salt transport across frog and toad skin, it was assumed that chloride movement is extracellular. However, later studies suggested that chloride movement is largely transcellular. Chloride transport across toad skin is greatly diminished in skins of salt-acclimated toads (Bufo viridis) and was correlated with the number of mitochondria-rich (m.r.) cells in the epithelium. The activated chloride conductance could be recovered upon in vitro incubation with theophylline. It was found that the short-circuit current (Isc) and the chloride conductance (Gcl) in toad skin could be separated experimentally by selective use of synthetic oxytocin (Syntocinon) or theophylline, and by substituting impermeable anions for chloride. With the use of the vibrating probe we demonstrated directly that chloride-dependent peak currents are localized only over m.r. cells, under hyperpolarized (V = -100 mV) conditions. It is concluded that the m.r. cells form the principal site for passive chloride movement across amphibian skin. This cellular pathway is regulated through a cyclic AMP-mediated process. It is suggested that the spatial separation of the sodium and chloride channels is essential to maintain the granulosum cells which are engaged in sodium transport hyperpolarized, and thus providing the driving force for the sodium entry into the cells.

Animals↗
PubMed1987

Influence of chloride concentration and pH on the 36Cl efflux from depolarized skeletal muscle of Rana temporaria.

1. 36Cl- efflux rates were measured in depolarized fibre bundles (predominantly fast fibres) from m. semitendinosus of Rana temporaria in order to investigate the influence of chloride concentration (20-400 mM) and external pH (pHo, 5.5-11.6) on chloride self-exchange. Usually, the bundles were depolarized to a membrane potential of virtually zero ([Cl-]i = [Cl-]o = [Cl-]) in 140 mM-K+ and 20 mM-Cl- combined with either 60 mM-SO4(2-) (+52 mM-sucrose) or 120 mM-methyl sulphate, gluconate or glucuronate. Various values of [Cl-] were obtained by adding KCl to the medium, keeping constant the concentration of relatively impermeant solutes and thus the fibre volume. 2. The chloride permeability, PCl, at pH 7.5 decreased with increasing [Cl-] above 50 mM. At [Cl-] less than 50 mM, PCl was about 4 X 10(-6) cm s-1. 3. PCl at pHo 7.5 and 5.6 was a hyperbolic function of [Cl-1] (greater than or equal to 50 mM), consistent with saturation kinetics of chloride self-exchange. 4. Methyl sulphate inhibited chloride self-exchange and may enter depolarized fibre membranes slowly. Comparison of PCl estimates in SO4(2-), gluconate, and glucuronate suggested that SO4(2-) and gluconate may interfere with chloride self-exchange at low [Cl-], and that glucuronate interferes the least. 5. A change from chloride equilibrium to an inward KCl gradient increased the 36Cl- efflux rate in acid media (pH less than 6.5) and decreased the efflux rate at pHo greater than or equal to 7. The effects were not due to changes of membrane potential and demonstrate a change of transport mode consistent with single-filing at high pH and dominant exchange diffusion at low pH. This result makes interpretation of the saturation kinetics difficult. 6. At constant [Cl-], PCl showed a bell-shaped dependence on pHo with a maximum around pH 8.5. The decrease of chloride permeability as the pH is decreased below 8.5 showed an apparent pK of about 7. PCl fell at very alkaline pH with an apparent pK of about 10. 7. The results are in agreement with previous observations of an external pH-sensitive control of PCl (pK approximately 7) and suggest that, in conditions close to chloride equilibrium, this control includes a transition between a dominant conductive channel conformation at high pH and a dominant non-conductive conformation at low pH.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

The coupled movements of sodium and chloride across the basolateral membrane of frog skin epithelium.

1. When frog skin epithelium was exposed to a chloride-free solution bathing the basolateral side of the frog skin preparation the short-circuit current fell and there was a simultaneous loss of chloride and water from its cells. This effect was partially blocked by furosemide when this drug was added to the basolateral bathing solution. 2. Under control conditions and when added to the solution bathing the basolateral side of the preparation furosemide had no effect on the ion and water contents of the frog skin epithelium. 3. Furosemide but not SITS (4-acetamide-4'-isothiocyanate-stilbene-2,2'-disulphonic acid) or amiloride blocked the recovery of short-circuit current and the reuptake of chloride and water by preparations pre-incubated with chloride-free solution on the basolateral side. The recovery of the short-circuit current was also blocked by the replacement of basolateral potassium by sodium. 4. The effect on the short-circuit current of graded replacements by impermeant ions of sodium or chloride did not show saturation for concentrations of these ions up to their control values. 5. Replacement of basolateral potassium by sodium inhibited the short-circuit current and the recovery observed when potassium was reintroduced in the basolateral bathing solution was blocked by furosemide. 6. The replacement of basolateral sodium or chloride by impermeant ions induced an immediate fall in the intracellular concentrations of both sodium and chloride suggesting that the transport system coupling the movements of the two ions across the basolateral membrane is operative under control conditions. 7. It is proposed that the coupled movements of sodium and chloride across the basolateral membrane of the frog skin epithelium are mediated by a sodium-potassium-2 chloride co-transport system which under control conditions is very near equilibrium.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1990

GTP-binding proteins mediate noradrenaline effects on calcium and chloride currents in rat portal vein myocytes.

1. Membrane currents were recorded by a patch-clamp pipette technique in cultured cells from rat portal vein using the whole-cell mode. 2. Noradrenaline (NA, 10(-5) M) and phorbol-12,13-dibutyrate (PDBu, 10(-7) M) produced an increase in voltage-dependent inward current carried by barium (5 mM), but their effects were not additive. Calcium-activated chloride current was evoked by NA but not by PDBu. 3. The NA-induced increase in peak voltage-dependent inward current was inhibited by intracellular application of GDP-beta-S (10(-3) M) while the effect of PDBu was unchanged. GDP-beta-S blocked the NA-induced chloride current but had no effect on the caffeine-induced chloride current. 4. Inclusion of GTP-gamma-S (10(-5)-10(-4) M) in the pipette solution increased the voltage-dependent inward current and inhibited the NA- or PDBu-induced increase in peak current. GTP-gamma-S potentiated the effect of NA on calcium-activated chloride current. At higher concentrations (10(-3) M), GTP-gamma-S activated the chloride current and prevented the effects of NA or caffeine on this current. 5. The combination of 10(-5) M-aluminium chloride and 10(-2) M-sodium fluoride had an effect similar to that of high concentrations of GTP-gamma-S on both inward current and calcium-activated chloride current. In contrast, arachidonic acid (10(-3) M) had no effect on calcium and chloride conductances activated by NA. 6. Cells responded normally to NA after pre-treatment for 4-30 h with 10 micrograms ml-1 pertussis toxin (PTx). 7. It is concluded that the stimulation of calcium and chloride conductances by NA is mediated through activation of a PTx-insensitive GTP-binding protein. This effect may involve activation of phospholipase C enzyme and production of both D-myo-inositol 1,4,5-trisphosphate which depletes calcium stores and diacylglycerol which activates protein kinase C.

Animals↗
PubMed2004

Reduced pH and chloride levels in exhaled breath condensate of patients with chronic cough.

BACKGROUND: Increased hydrogen and reduced chloride ionic environments of the airways are conducive to the stimulation of cough. However, the constituents of the local milieu of the airways of patients with chronic cough are unknown. METHODS: The pH and chloride levels in exhaled breath condensate and capsaicin cough threshold (C5) were measured in 50 patients with chronic cough and in 16 healthy controls. pH and chloride measurements were repeated after capsaicin challenge in those with cough. The cause of cough was asthma (n = 13), postnasal drip/rhinitis (n = 7), gastro-oesophageal reflux (n = 5), bronchiectasis (n = 5), but remained unidentified in 20. RESULTS: Compared with controls, patients with chronic cough had lower pH (mean 7.9 v 8.3, 95% CI of difference -0.5 to -0.2, p<0.0001), chloride levels (median 4 v 6 mmol/l, 95% CI -3.1 to -0.2, p = 0.007), and C5 (median 3.9 v 125 micro M, 95% CI -270.0 to -17.6, p = 0.002). The pH levels were different in the six subgroups including controls, and were reduced in all diagnostic subgroups of patients with cough compared with controls but did not differ between them. Chloride levels were significantly different in the six subgroups but were lower than controls in only the gastro-oesophageal reflux subgroup. There was a weak but significant correlation between chloride levels and C5 when all participants were analysed together, but not between pH and C5 or chloride levels. pH and chloride levels did not change after capsaicin challenge. CONCLUSIONS: The epithelial lining fluid of patients with chronic cough has a reduced pH and reduced chloride levels which could contribute to the enhanced cough reflex.

Adult↗
PubMed1988

Chloride transport across placental microvillous membranes measured by fluorescence.

Chloride transport across human placental microvillous vesicle membrane was investigated using the fluorescent probe SPQ (6-methoxy-N[3-sulfopropyl]quinolinium). Chloride influx (JCl) was calculated from the initial rate of quenching of intravesicular SPQ fluorescence by chloride. JCl measured by SPQ fluorescence was not significantly different from JCl measured by uptake of 36Cl; SPQ did not affect measurements of JCl.JCl was increased 51% by a 58-mV membrane potential (internal positive). Voltage-stimulated JCl showed a saturable dependence on chloride concentration with a dissociation constant (Kd) of 18 +/- 5 mM and was inhibited by diphenylamine-2-carboxylate with an apparent inhibitory constant of 0.13 +/- 0.03 mM. The activation energy calculated for voltage-stimulated JCl was 4.6 +/- 0.6 kcal/mol. JCl was also stimulated by a reduction in the external pH from 7.0 to 5.5 (internal pH = 7.0). pH-stimulated chloride influx was increased by trans-HCO3 (25 mM) and was inhibited by dihydro-4,4'-diisothiocyano-2,2'-disulfonic stilbene. Uptake of 36Cl into microvillous vesicles was stimulated by trans-Cl. pH-stimulated JCl showed a saturable dependence on chloride with a Kd of 38 +/- 6 mM but was not affected by membrane potential. No evidence was found for Na- or K-coupled chloride cotransport. These findings demonstrate the presence of a saturable chloride conductance and an electroneutral chloride-bicarbonate exchanger in the placental microvillous membrane.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Insulin increases loop segment chloride reabsorption in the euglycemic rat.

To elucidate the nephron segment(s) responsible for insulin's antinatriuretic effect in the mammalian kidney, late proximal, early distal, and late distal tubule micropuncture was performed during base-line and intravenous insulin infusion in glucose-clamped, volume-expanded rats. During insulin infusion, urinary sodium chloride excretion fell. Blood glucose, arterial pressure, whole kidney and single-nephron inulin clearance, fluid, and chloride delivery out of the proximal convoluted tubule remained unchanged. Early distal chloride delivery decreased (P less than 0.001) during insulin administration. Insulin infusion increased calculated loop chloride reabsorption compared with both base-line values and values for time-control rats. Distal convoluted tubule chloride reabsorption was unchanged during insulin administration. We conclude that 1) euglycemic insulin administration reduces urinary chloride excretion in volume-expanded rats by tubular mechanisms; 2) in superficial nephrons, insulin has no effect on proximal tubule fluid or chloride reabsorption but markedly stimulates chloride reabsorption in the loop; and 3) chloride reabsorption in the distal convoluted tubule was unaltered by insulin administration.

Animals↗
PubMed1995

Chloride transport in the rat S1 proximal tubule.

In vivo microperfusion was used to elucidate the modes and regulation of the powerful chloride transport system resident in the rat early (S1) proximal convoluted tubule (PCT). From a complete, glomerular ultrafiltrate-like perfusate, omission of organic solutes reduced chloride absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001). From a high-chloride perfusate (a relatively pure NaCl solution devoid of bicarbonate and organic solutes), luminal addition of the active transport inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632 +/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium isethionate isosmotically replaced bicarbonate and organic solutes, preventing development of a chloride gradient. Intravenous angiotensin II caused a stimulation of chloride absorption from a high-chloride perfusate by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the components of the normal S1 PCT chloride reabsorption (approximately 300 peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following: active transport (40-50%), which can be regulated by angiotensin II; sodium-coupled organic solute transport (30%); and passive, chloride concentration gradient-driven transport (20-25%).

Absorption↗
PubMed1997

Methylene chloride induced mouse liver and lung tumours: an overview of the role of mechanistic studies in human safety assessment.

B6C3F1 mice exposed to high dose levels of methylene chloride by inhalation for 2 years had an elevated incidence of liver and lung tumours. These tumours were not increased in rats or hamsters exposed under the same or similar conditions. This paper gives an overview of research conducted over the last 10 years into the mechanism of action of methylene chloride as a mouse carcinogen and into the relevance of the mouse data to humans exposed to this chemical. Data are presented on the comparative metabolism and pharmacokinetics of methylene chloride in mice, rats, hamsters and humans, on the toxicity of methylene chloride to the target organs in the mouse, and on the genotoxicity of methylene chloride in vitro and in vivo. The enzyme which activates methylene chloride to its carcinogenic form has been isolated, sequenced, and cloned, and its distribution studied within cells, organs and between species. Evidence has been obtained to show the methylene chloride caused cancer in mice as a result of interactions between metabolites of the glutathione S-transferase pathway and DNA. Damage to mouse lung Clara cells and increased cell division are believed to have influenced the development of the lung tumours. The species specificity was a direct consequence of the very high activity and specific cellular and nuclear localisation of a theta class glutathione S-transferase enzyme which was unique to the mouse. Consequently, DNA damage was not detectable in rats in vivo, or in hamster and human hepatocytes exposed to cytotoxic dose levels of methylene chloride in vitro. These results provide evidence that the mouse is unique in its response to methylene chloride and that it is an inappropriate model for human health assessment.

Administration, Inhalation↗
PubMed1991

Cyclic AMP-sensitive chloride efflux in rabbit pancreatic acini.

We studied chloride efflux from isolated rabbit pancreatic acini in suspension, by loading with 36Cl to steady state and rapidly washing acini by filtration to determine 36Cl cpm/micrograms DNA remaining. Linear loss of acinar chloride occurred over 5 min (k = 0.038 +/- 0.008 min-1, n = 5). Forskolin (5 x 10(-5) M) increased the rate of chloride efflux (k = 0.100 +/- 0.016 min-1, n = 5, p less than 0.001) 2.6-fold. At 5 min, forskolin increased acinar cAMP levels (1065 +/- 254 versus 7 +/- 2 pmol/mL, n = 5, p less than 0.005) and percentage of chloride efflux (37.4 +/- 2.3 versus 26.0 +/- 2.2%, n = 13, p less than 0.005). The chloride channel inhibitor anthracene-9-carboxylic acid (10(-3) M) had no effect on chloride loss from acini exposed to vehicle (30.9 +/- 1.9 versus 29.9 +/- 2.3%, n = 4), but completely inhibited forskolin-stimulated efflux at 5 min (40.0 +/- 2.4 versus 29.3 +/- 2.4%, n = 5, p less than 0.005). Manipulation of extracellular calcium concentration demonstrated that chloride efflux was not coupled to zymogen granule amylase release. Secretin (10(-7) M) increased acinar cAMP levels (68 +/- 22 versus 7 +/- 2 pmol/mL, n = 5, p less than 0.05) and significantly increased the loss of chloride from acini (34.9 +/- 1.4 versus 26.1 +/- 1.7%, n = 7, p less than 0.005) without affecting amylase release. Secretagogue-stimulated amylase release by cholecystokinin octapeptide (10(-8) M) and carbamylcholine (10(-5) M), did not increase chloride efflux at 5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Chloride channels of intracellular organelles and their potential role in cystic fibrosis.

Chloride channels were previously purified from bovine kidney cortex membranes using a drug affinity column. Reconstitution of the purified proteins into artificial liposomes and planar bilayers yielded chloride channels. A 64 x 10(3) M(r) protein, p64, identified as a component of this chloride channel, was used to generate antibodies which depleted solubilized kidney membranes of all chloride channel activity. This antibody has now been used to identify a clone, H2B, from a kidney cDNA library. Antibodies, affinity-purified against the fusion protein of H2B, from a kidney cDNA library. Antibodies, affinity-purified against the fusion protein of H2B, also depleted solubilized kidney cortex from all chloride channel activity. The predicted amino acid sequence of p64 shows that it contains two and possibly four putative transmembrane domains and potential phosphorylation sites by protein kinases A and C. There was no significant homology to other protein (or DNA) sequences in the data base including other anion channels or the cystic fibrosis transmembrane conductance regulator. The protein is expressed in all cells tested and probably represents the chloride channel of intracellular organelles. Cystic fibrosis (CF) is associated with a defect in a cyclic-AMP-activated chloride channel in secretory epithelia which leads to decreased fluid secretion. In addition, many mucus glycoproteins show decreased sialylation but increased sulfation. We have recently shown that the pH of intracellular organelles is more alkaline in CF cells, an abnormality that is due to defective chloride conductance in the vesicle membranes. We postulate that the defect in the intracellular chloride channel, and hence the alkalization, could explain the glycosylation abnormalities since the pH optimum of Golgi sialyltransferase is acid while that of focusyl- and sulfotransferases is alkaline. Defects in sialyation of glycolipids might also generate receptors for Pseudomonas, which is known to colonize the respiratory tract of CF patients.

Adenosine Triphosphatases↗
PubMed2000

Osteogenesis from cultured chick periostea has a specific requirement for chloride.

Bone development, like embryonic development in general, depends on a particular internal electrical milieu. Ions are the carriers of currents that maintain this internal environment. In embryonic bone, chloride is a major carrier of such current. To explore the role chloride plays in embryonic bone development we performed several ion-removal experiments, using the chick periosteal osteogenesis (CPO) system as our model. We found that if chloride is reduced in the medium and replaced with a nontoxic anion, alkaline phosphatase (ALP) activity does not rise, nor does osteogenic development occur. However, acid phosphatase (AP) activity is not affected by level of chloride. Experiments using metabolic inhibitors showed that explants cultured in low chloride medium remain viable. Dose-response studies revealed that the response of ALP activity to chloride concentration is sigmoidal, with a [Cl-]0.5 of 45.9 mM. Reciprocal transfers of explants between complete and low chloride medium show that the rise in ALP activity depends on the length of time explants are cultured with chloride. In contrast, such transfer experiments show that osteogenesis requires chloride only during days 2-3 of culture.

Acid Phosphatase↗
PubMed2006

Effects of pH, temperature, and water quality on chloride removal with ultra-high lime with aluminum process.

The ultra high-lime with aluminum process (UHLA) has the ability to remove sulfate and chloride in addition to other scale-forming materials from recycled cooling water. Laboratory experiments have demonstrated that the UHLA process can achieve high chloride removal from recycled cooling water, and an equilibrium model was developed to describe chemical behavior during chloride removal. This paper describes the influence of pH, temperature, and initial chloride concentration on chloride removal by UHLA and identifies the precipitated solids formed during treatment. The optimum pH for maximum chloride removal efficiency was found to be 12 +/- 0.2. Chloride removal efficiency was higher at a high initial chloride concentration than at a low initial chloride concentration with the chemical doses used. Solids formed during UHLA treatment were identified by x-ray diffraction as calcium chloroaluminate, tricalcium hydroxyaluminate, and tetracalcium hydroxyaluminate. This supports the assumption of the equilibrium model that these compounds are present and form a solid solution.

Aluminum↗
PubMed1985

Electron microprobe analysis of chloride secretion in the frog cornea.

Electron microprobe analysis was employed to measure the intracellular electrolyte concentrations of the bullfrog corneal epithelium. Under control conditions, transepithelial potential short-circuited and both sides of the isolated cornea incubated in Conway's solution, the mean intracellular concentrations were 8.0 for sodium, 18.4 for chloride and 117.3 for potassium (mmole/kg wet weight). These values are in good agreement with previously reported ion activities implying that the intracellular activity co-efficient for small ions is close to that of the extracellular space. No significant differences between the nuclear and cytoplasmic concentrations of small diffusible ions were detectable. Similarly, the chloride concentrations in the different epithelial layers were virtually identical and showed parallel changes at varying states of chloride secretion, suggesting that corneal epithelium represents a functional syncytium. The behavior of the intracellular ion concentrations after removal of sodium, chloride or potassium from the outer or inner bath is consistent with a passive electrodiffusive efflux of chloride across the outer membrane and a sodium coupled chloride uptake across the inner membrane. Furthermore, effects of bicarbonate and CO2 on the rate of chloride secretion and on the intracellular sodium and chloride concentrations were observed, indicating a possible role of pH in regulating chloride secretion.

Animals↗
PubMed1975

Chloride compartments in embryonic brain tissue after intracerebral ouabain administration.

The "chloride space" in brain tissue of 15- and 19-day-old chick embryos was studied during the 3 h following intracerebral administration of 3.4-10(-4) M ouabain. Total tissue water, dry substance, plasma and liquor and tissue chloride concentrations were determined. The chloride space in brain tissue was calculated on the basis of the brain-cerebrospinal fluid ratio and the brain-plasma ratio. The chloride concentration in blood plasma was generally unchanged after ouabain treatment. The chloride concentration in cerebrospinal fluid was lower in younger embryos during the whole 3-h period, whereas in 19-day-old embryos only during the 1st h. Tissue chloride concentration was generally elevated, but to a greater extent in younger embryos. Total brain tissue water increased for 3 h after ouabain treatment in 15-day-old embryos and for the first 2 h in 19-day-old embryos. The expansion of chloride space reached a new steady state during the 1st h after ouabain treatment and amounted to 12-15% of control values in 15-day-old embryos. The increase of chloride space in older embryos reached its maximum (14.8% of control values) within the 1st h and gradually decreased thereafter. The age-dependent changes of chloride compartmentation in embryonic brain tissue are discussed in relation to the previously investigated spongy state of the brain tissue in chick embryo.

Animals↗