Increase In HCO3 Research Articles

Simple acid-base disorders

This article reviews normal acid-base regulation, related laboratory tests, and the potential disorders if the body's ability to compensate is disrupted. Acid derived from the oxidation of proteins and through tissue metabolism must be excreted or neutralized daily by the kidneys and lungs to maintain a proper acid-base balance. Acid-base homeostasis is normally maintained by chemical buffering, changes in renal hydrogen-ion excretion, and alterations in the rate and volume of alveolar ventilation. Metabolic disorders are characterized by disturbances in bicarbonate (HCO3-) concentration, and respiratory disorders develop with primary alterations in the partial pressure of carbon dioxide (Pco2). Metabolic acidosis is characterized by low pH, low serum HCO3- concentrations, and a compensatory decrease in Pco2 with hyperventilation. Bicarbonate administration can correct this disorder, and equations for calculating the necessary amount of HCO3- are presented. Metabolic alkalosis is characterized by a primary increase in HCO3-, compensatory hypoventilation, and an increase in Pco2 (hypercapnia). The drug therapy for this disorder is directed at either saline-responsive alkalosis or saline-resistant alkalosis. Formulas for estimating the volume requirements of patients and appropriate doses of acidifying agents are presented. Respiratory acidosis and alkalosis are also discussed. The initial therapy for the hypercapnia associated with respiratory acidosis requires reversing the underlying pulmonary disease with steroids, bronchodilators, or antibiotics. The increased Pco2 in this conditions must be lowered slowly to avoid precipitating cardiac arrhythmias and seizures. The correction of respiratory alkalosis requires elevating the Pco2 and again treating the underlying disease. Pharmacists should be knowledgeable about acid-base regulation and the disorders that frequently occur with disease because drugs are capable of inducing or exacerbating these disorders and are often key elements in therapy.

Scale Formation During Alkaline Flooding

Summary Alkaline chemicals in enhanced recovery operations are used (1) as preflush agents, (2) with polymers and surfactants, and (3) as a principal recovery agent. In these chemical flooding techniques, the precipitation reactions of multivalent hardness ions with alkalis are of particular concern. These reactions may be prevented at the injection wells through adequate preflushing and/or the use of good-quality softened water; filtration can remove any precipitates that form at the surface. In the formation, precipitates that form at the surface. In the formation, many reactions occur that alter the injected slug significantly. Those include dissolution, mixing, neutralization, and ion exchange. Such reactions may lead to beneficial fluid diversion as precipitates form and block high-flow channels. At the producing wells, however, precipitation and deposition phenomena are undesirable because scales may form that restrict production and foul well equipment. With the current higher production and foul well equipment. With the current higher concentrations of alkali being used in the field, the development of well scaling has become noticeable and difficult to control by previously accepted practices. This paper describes the progress and experience gained at the Long Beach Unit, Wilmington, CA, alkaline pilot dealing with scales formed in producing wells. These scales have been made up variously of calcium carbonate, magnesium silicate, and amorphous silica. In particular, the reservoir characteristics and chemical conditions leading to the scale formation are discussed in detail, showing what, how, and why the scale forms. For the Wilmington alkaline pilot, the cause appears to be the mixing of very hard waters from one subzone with moderately alkaline water from other subzones. This mixing and the dissolution of formation solids by the alkali have led to scale formation in the producers closest to the injectors. producers closest to the injectors. A few general scale inhibitor formulations, useful for both formation squeeze treatments and continuous sidestream annular injection, have been effective in controlling the carbonate scale under laboratory and field conditions. However, the physical environment and mechanical limitations in the field have resulted in a new deposit, consisting mainly of amorphous silica, against which the current inhibitor systems am ineffective. We suggest field procedures for dealing with such a situation. It is anticipated that the use of appropriate chemicals and methods can lead to cost-effective scale control. Introduction Them is a large body of literature on alkaline flooding and its variations. However, few authors consider associated scale phenomena at the production wells or in laboratory studies, although it is well known that alkaline chemicals react with reservoir rock and fluids to produce precipitates. Mungan mentions briefly that produce precipitates. Mungan mentions briefly that plugging and scaling were noted in some field-test plugging and scaling were noted in some field-test production wells but gives no details. Raimondi et al. production wells but gives no details. Raimondi et al. describing a sodium hydroxide pilot in the North Ward-Estes field, observed increased gypsum scale formation in producers. This reservoir has a high gypsum content. However, no treatment was discussed. The authors also noted an increase in silica content at the producers but did not detect an accompanying increase in pH value or decrease in hardness levels in the produced fluids. The alkaline slug was believed to have been completely consumed by inaction with gypsum. In a field test at the Trekhozernoye deposit in Russia, fluid-flow diversion was reported because of swelling and migrating clays and precipitation of calcium and magnesium carbonates. The produced fluids showed a decrease in Ca++ ion with subsequent increases in HCO3 - ion. In laboratory tests evaluating alkaline flooding for an Alberta reservoir, Novosad and McCaffrey reported a white precipitate in the coreflood effluents that added to the alkali consumption. They also noted that silicates are more effective at precipitation divalent metal ions. Sydansk observed the formation of new, highly hydrated alumina-silicate precipitates in alkaline com tests; these have lower silica/alumina ratios than the original formation clays. Carbonate minerals in the core dissolved first, leading to accelerated alkaline consumption. Significant amounts of silica were dissolved from the rock matrix at elevated temperatures. A number of other studies show that alkalis react strongly with the various reservoir-rock constituents. These inactions can produce very complex ionic effluents downstream in both laboratory com tests and field production wells. Ehrlich and Wygal studied the caustic consumption of a number of clays and minerals in an attempt to quantify the contribution of each to the overall consumption. More recently, this quantification has been extended by Mohnot et al. Holm and Robertson studied the effect of various preflush agents, including alkaline silicates on divalent ion exchange in surfactant flooding. JPT P. 1466

Gastric and duodenal HCO3- transport in vivo: influence of prostaglandins.

Gastric and duodenal HCO3- transport was compared in the same mammalian species (cat) in vivo. The most appropriate technique for detecting HCO3- in the lumen of the stomach was measurement of pH and CO2 tension, whereas in the duodenum it was pH-stat titration. For experiments on gastric HCO3- transport, conscious cats prepared with vagally denervated fundic pouches were used; for those on duodenal transport anesthetized animals with in situ perfused segments were studied. When expressed in terms of gross surface area, basal HCO3- output was six times greater in the duodenum than in the stomach (approximately 1.5 cf. approximately 0.25 mumol X cm-2 X 15 min-1). topical application of 16,16-dimethyl prostaglandin E2 (dmPGE2) to duodenal mucosa caused a concentration-dependent increase in HCO3- output and transmucosal electrical potential difference (PD) over the range 0.01-1.0 microgram X ml-1. PGE2 was approximately 200 times less potent than dmPGE2 as a stimulant of duodenal HCO3- transport. Increases in the rate of luminal HCO3- output following application of dmPGE2 were considerably less in the stomach compared with the duodenum (approximately 50% cf. approximately 1,000% at 1 microgram X ml-1). Intravenous dmPGE2 (1 microgram X kg-1 X h-1) had no effect on either gastric or duodenal HCO3- outputs. Indomethacin (5 mg X kg-1 iv) inhibited duodenal HCO3- output by approximately 50% and reduced PD but did not influence gastric HCO3- output. We propose that in the cat duodenum in vivo local prostaglandins regulate HCO3- transport, but in the cat stomach in vivo they have a less important role.

Bicarbonate effects, electromotive forces and potassium effluxes in rabbit and guinea-pig gall-bladder.

The stimulating effect of external HCO3- on Na+ salt transport has been examined in rabbit and guinea-pig gall-bladder by electrophysiological methods, as a sequel to a previous study carried out by radiochemical techniques. At steady state, cell K+ activity was found to be significantly reduced in the presence of HCO3-, whereas cell Na+ activity significantly increased; in parallel the apical membrane p.d. was depolarized; K+ equilibrium potential was higher than membrane p.d. in every case. The apical p.d. dependence on K+ was unaffected by HCO3-, but in the guinea-pig it was affected by Cl-. Rapid increases in HCO3- concentration on the luminal side caused a depolarization of the apical p.d. of the guinea-pig within about 30 sec, an effect that did not occur if the tissue was pre-treated with 10(-4) M-acetazolamide; the epithelial resistance and apical/basolateral resistance ratio were unchanged in all cases. The primary action of HCO3- is confirmed to be on the apical membrane; an HCO3- conductance does not seem to be present at this level, either in the rabbit or guinea-pig, nor does HCO3- affect Na+ influx through the apical conductive pathway, so that all the stimulating effects of the anion are confirmed to be on the neutral transports of Na+ salts; in spite of this, the apical electromotive force is modified due to the changed cell K+ activity. The rapid depolarization caused by the anion in the guinea-pig is in agreement with an HCO3- electrogenic secretion and/or a basolateral conductance for the anion. Polyelectrolyte dissociation from protons increases in the absence of external HCO3-: the negative charges are mainly counterbalanced by bound Na+ in the rabbit and by free K+ in the guinea-pig. K+ leakage from the cell into the lumen is calculated to be minimal in the rabbit and all K+ lost could be reabsorbed through the paracellular pathways; K+ efflux to the subepithelial layer via conductive routes is insufficient to account for the over-all K+ efflux.

Acid-Base Balance in Callinectes Sapidus During Acclimation from High to Low Salinity

ABSTRACT When transferred from 865 to 250 m-osmol salinity, the blue crab C. sapidus maintains its blood Na+ and Cl− concentrations significantly above those in the medium. When branchial carbonic anhydrase is inhibited by acetazolamide, ion regulation fails and the animals do not survive the transfer. An alkalosis occurs in the blood at low salinity, indicated by an increase in HCO3− and pH at constant . The alkalosis is closely correlated with an increase in the Na+–Cl− difference, a convenient indicator of the overall strong ion difference. The contribution’ of changes in to acid-base changes was negligible, but the change in the total weak acid (proteins) may be important. It is suggested that the change in blood acidbase status with salinity is related to an increase in the strong ion difference, which changes during the transition from osmoconformity to osmoregulation in the blue crab, and which is related to both carbonic anhydrase and ion-activated ATPases.

Cimetidine-induced bicarbonate production in canine gastric pouches

Secretion of HCO 3 − into a mucus-gel “unstirred layer” has been proposed as part of the gastric mucosal defense system. Cimetidine has a cytoprotective effect on salicylate-challenged gastric mucosa independent of its acid-inhibiting property. This study was done to (1) evaluate whether cimetidine increases gastric mucosal HCO 3 and to (2) ascertain if ionic shifts accompany the HCO 3 − to explain the mechanism of its production. Six dogs with Heidenhain gastric pouches were fasted 24 hr prior to testing. Pouch access was provided by a cannula fitted with an airtight apparatus for test solution instillation and removal and transmucosal potential difference (PD) measurement. A test solution composed of 175 m M mannitol, 25 m M NaCl, and 50 m M EPPS buffer was used, its pH adjusted to above 8.0; 14C-labeled polyethylene glycol was added for volumetric determinations. Nine 15-min periods comprised each test: four control periods of iv saline infusion; a fifth period when an iv cimetidine bolus was given; and four test periods when doses of 2.5, 5, or 10 mg/kg/hr cimetidine were infused iv. Test solution (50 ml) was placed in the pouch and an initial sample taken; 15 min later a final sample was taken, the pouch rinsed, and the next period begun. Concentrations of HCO 3 −, Na +, K +, and Cl − were determined for each sample as well as changes in osmolality, pH, volume, and PD. Mean net HCO 3 − increased from 79 μmol/15 min during saline infusions to 109, 124, and 123 μmol/15 min with 2.5, 5, and 10 mg/kg/hr cimetidine iv; all are significantly increased compared to saline controls ( P < 0.01). None of the other measured parameters changed significantly after cimetidine infusion. Cimetidine causes modest but significant increases in gastric mucosal HCO 3 −. The clinical role, if any, of these increases in HCO 3 − in gastric mucosal defense remains to be determined.

Correlated radon and CO2 variations near the San Andreas Fault

Correlations have been observed between groundwater radon and thoron concentrations and carbon dioxide discharges at the Lake Hughes station of the Caltech radon monitoring network. The Lake Hughes site is one of three radon monitoring stations located near the "big bend" segment of the San Andreas fault which began to record anomalous radon levels in August 1981. Two stations, Lake Hughes and Lytle Creek, recorded anomalous increases in radon while the third, Sky Forest, recorded an anomalous decrease. Several weeks after the onset of the anomaly, strongly correlated radon fluctuations began at Lake Hughes and Lytle Creek. These radon spikes also were found to be phase anti‐correlated with barometric pressure fluctuations. Analyses of gas grab samples showed relatively high levels of CO2 and ethylene in borehole air at Lake Hughes and Lytle Creek, while analyses of water samples showed relatively large increases in HCO3− at both sites. Isotopic analysis of one gas sample from Lake Hughes yielded a 13C δ value of −22 ‰, which suggests that the CO2 originates from the oxidation of organic material. The correlation in radon fluctuations at Lake Hughes and Lytle Creek and their common dependence on barometric pressure changes began shortly after the onset of the radon anomaly in August, and probably resulted from the simultaneous saturation of the water in these boreholes with carbon dioxide.

Effect of parathyroid hormone on bicarbonate secretion in the guinea-pig stomach and the amphibian isolated gastric mucosa.

1. The effect of parathyroid hormone on gastric bicarbonate secretion was determined in the anaesthetized guinea pig. Subcutaneous injections of bovine parathyroid hormone (75 U.S.P units day-1 kg-1) for 7 days caused a significant increase in HCO3- output. There was also a rise in K+ output and a slight elevation of H+ secretion. A similar increase in HCO3- output occurred after acute intravenous injection of the hormones (75 U.S.P. units/kg). 2. Both chronic and acute administration of parathyroid hormone caused a significant increase in serum calcium concentration and it is likely that the changes in gastric ion outputs reflect raised calcium levels. Given alone intravenous calcium (1.5 mg/kg body wt.) stimulated gastric secretion of both HCO3- and H+. 3. To determine whether parathyroid hormone had a direct action on gastric ion transport experiments were performed in the amphibian isolate mucosa. Antrum transports HCO3- spontaneously while HCO3- transport in fundus was studied after inhibition of the greater H+ secretion by the histamine H2-receptor antagonist metiamide. Parathyroid hormone at a concentration of 0.2 United States Pharmacopea (U.S.P.) unit/ml in the nutrient-side bathing solution inhibited both antral and fundic HCO3- transport. A higher concentration (2.0 units/ml) had no effect on fundic H+ secretion. 4. The inhibitory effect in vitro was greater in the antrum and parathyroid hormone may almost abolish the active component of HCO3- transport in this tissue. It is likely that any similar inhibition of gastric HCO3- secretion by parathyroid hormone in vivo is masked by the stimulatory effects of released calcium.

Pharmacological studies on iridoid compounds. III. The choleretic mechanism of iridoid compounds.

We made a study on choleretic property and mechanism of action of iridoid compounds as well as dehydrocholate (DHC), cholate (CA), and salicylate (SA), examining their effects on factors such as bile flow, bile acids, electrolytes (Na+, K+, Cl-, and HCO3-), and their metabolites. Each sample showed a characteristic property, respectively. Genipin and patrinoside decreased biliary concentrations of bile acids, Na+, Cl-, and HCO3-, corresponding to their rapid choleretic actions which were due to bile acids independent fraction. The choleretic action of DHC is approximately twice as potent as that of CA. Their actions were due to bile acids-dependent fraction. CA gave a marked increase in Na+ concentration but DHC did not. And both compounds gave a marked diminution in Cl- concentration and weakly decreased HCO3- concentration. SA showed a weak and durable choleretic action and also gave a marked increase in HCO3- concentration. The main metabolite detected from the bile given genipin was genipin-1-O-glucuronic acid (GGA). The periodical pattern of GGA level in bile was in agreement with that of genipin- induced choleretic action, and quantitatively cation, anion gap produced was nearly compensated by biliary concentration of GGA. From out various results, the choleretic mechanism of iridoid compounds is considered to be as follows: The hemiacetal moiety of them undergoes conjugation in the liver to give glucuronide. Glucuronide thus formed is secreted into the biliary tree being coupled mainly with Na+ and water is passively excreted.

Influence of luminal acidification on bicarbonate transport by gastric and duodenal isolated mucosae

Transport of HCO 3 − was measured by pH-stat titration in pairs of amphibian fundic or proximal duodenal mucosae using a modified Ussing chamber. Separate unbuffered solutions bathed the luminal sides of two tissue while their serosal surfaces were in contact with a common buffered solution. Lowering luminal pH bathing one fundic mucosa from 7.40 to 1.85 significantly increased HCO 3 − transport by another fundus. However, acidification of fundic mucosa did not affect duodenal HCO 3 − transport. In duodenal mucosal pairs, lowering pH from 7.40 to 5.46 caused an increase in HCO 3 − transport by the other tissue. Luminal H + ion concentration may therefore regulate HCO 3 − transport via a humoral mechanism.

Gastric HCO3--secretion in the guinea pig.

Measurement of gastric intraluminal PCO2 and pH in the anesthetized guinea pig enabled simultaneous determination of total H+ and HCO3- gastric secretions. There was quantitative agreement between the release of CO2 and decrease in HCO3- after intragastric instillation of HCl. The basal rate of HCO3- secretion (approximately 40 mueq-h-1) was, in most cases, smaller than spontaneous H+ secretion, but gastric net secretory output was alkaline (HCO3- greater than H+) after inhibition of acid secretion with histamine H2-receptor antagonists (cimetidine 20 mg-kg-1 or metiamide 35 mg-kg-1). Carbachol (1-2 microgram-kg-1) stimulated secretion of both HCO3- and H+; only the latter response was sensitive to the histamine antagonists. Atropin (100 microgram-kg-1) blocked stimulation of HCO3- secretion but did not affect the basal output of HCO3-. An increase in HCO3- secretion was associated with an equivalent increase in net Na+ influx and an increase in the net influx of Cl- with H+ plus K+. Intragastric neutralization of H+ by HCO3- is likely to occur at the mucosal surface and may protect the mucosa from the damaging effects of intraluminal acid.

Effect of bicarbonate-rich irrigation waters on the growth, nutrient uptake and synthesis of proteins and carbohydrates in wheat

A greenhouse experiment was conducted to study the effect of increasing levels of HCO3 − ion concentration and residual sodium carbonate (RSC) on the growth, nutrient uptake and synthesis of proteins and carbohydrates in wheat. Wheat could tolerate 8 me/l HCO3 − ion concentration at 40 me/l salt concentration; however, the residual sodium carbonate at this level was more harmful when it was composed of carbonate plus bicarbonate rather than bicarbonate alone. The relative order in yield reduction was: root plant. The uptake of sodium was enhanced and that each of potassium, calcium and magnesium was decreased with the increasing bicarbonate ion concentration. The contents of proteins and carbohydrates, in different forms, were decreased with the increase of HCO3 − levels, particularly above 8 me/l. Contents, both of sugars and proteins, were more in grain than in plant. The specific effect of CO3 = and/or HCO3 − ions seems to inhibit the metabolic processes in the plant and appears responsible for reduction of crop growth, absorption of nutrients and synthesis of proteins and carbohydrates.

Ionic control of renal gluconeogenesis III. The effects of changes in pH, pCO 2, and bicarbonate concentration

The effect of changing pH, pCO 2 and HCO 3 − concentration upon the formation of glucose from a variety of substrates, and the rates of decarboxylation of these substrates was studied in isolated rat renal tubules. A decrease in pH whether brought about by an increase in pCO 2 or a decrease in HCO 3 − concentration led to an increase in glucose production from citrate, glutamine, glutamate and α-ketoglutarate but not from malate or pyruvate. Conversely an increase in pH, whether due to an increase in HCO 3 − concentration or a decrease in pCO 2, led to an inhibition of glucose formation from all substrates. An increase in pH brought about by an increase in HCO 3 − concentration produced a greater inhibition than an increase in pH brought about by a decrease in pCO 2. In both instances alkalosis was associated with a decrease in cellular ATP content. In the case of both citrate and α-ketoglutarate, the rate of substrate disappearance followed the same pattern as glucose production, but in the case of malate and pyruvate their rates of disappearance decreased with a fall in pH even though glucose formation did not change, and their rates of disappearance did not change when pH was increased even though glucose production fell markedly. A change in total HCO 3 − concentration from 30 to 15 mM, maintaining a constant pH of 7.2±0.02, resulted in an increase in glucose formation from citrate, glutamine, and α-ketoglutarate but not from malate or pyruvate. This increase was less than that seen after the pH fell. When HCO 3 − concentration was raised from 30 to 60 mM, at constant pH, there was a fall in rate of glucose formation from all substrates. This fall was comparably to that seen in respiratory alkalosis but less than that seen in metabolic alkalosis. These data, plus data from measurements of metabolic concentrations under different conditions of pH, pCO 2 and HCO 3 − concentration and measurements of substrate decarboxylation in both tubules and isolated renal mitochondria, led to the conclusions that when pH is lowered either by a fall in HCO 3 − or an increase in pCO 2, the major regulator of gluconeogenesis is H + concentration which acts to inhibit citrate synthetase and activate both isocitrate and succinate dehydrogenase, all mitochondria enzymes. Conversely, a decrease in H + concentration could account for only part of the changes observed in alkalosis. The fall in H + concentration led to a decrease in ATP concentration which led in turn to an inhibition of phosphoglycerate kinase. In addition, an increase in HCO 3 − concentration has a specific inhibitory effect upon phosphoenolpyruvate carboxykinase, a cytosolic enzyme.

The effect on blood and urine of the ingestion of sodium bicarbonate.

O·145M NaHCO3 given by stomach tube to conscious dogs caused a fall in plasma solids (protein), decrease in plasma Cl and increase in HCO3; pH of the arterial blood increased but any increase of arterial PCO2, was not significant; plasma K fell. The urine after 0·145M NaHCO3 contained increased amounts of Na with only a small increase in Cl. The increased excretion of Na+ was mainly accompanied by a large excretion of HCO3‐, and the urine became alkaline and contained little NH4+. Changes in the excretion of inorganic PO4, SO4 and K were small.Comparison was made with the effects of the same doses of Na given as 0·122M NaCl+0·023M NaHCO3. This caused an equal fall in plasma solids but no change in plasma Cl, HCO3 and K. The urinary excretion of Na+ increased to rates approximately the same as those produced by NaHCO3 but the main urinary anion was Cl‐, the excretion of which was greatly increased. There was a small excretion of HCO3‐ with larger doses.It is concluded that an important agent determining increased excretion of Na is dilution of the plasma protein, which is common to both types of experiment. The changes in plasma Cl and HCO3 appear to be the factor which determines whether the increased excretion of Na+ is accompanied mainly by HCO3‐ or Cl‐.

Factors modifying renal tubular bicarbonate reabsorption in the dog

1. Acute experiments were carried out on anaesthetized dogs during metabolic alkalosis produced by I.V. administration of NaHCO(3). Partial constriction of one ureter led to a significant rise in the HCO(3) (-) threshold, beyond the simultaneous value for the other kidney. The magnitude of the increase was not correlated with the reduction of glomerular filtration.2. Stop-flow analysis, following complete unilateral obstruction of urine flow, demonstrated proximal as well as distal tubular reabsorption of bicarbonate. At any given plasma P(co2) the detailed configuration of the concentration changes which developed depended on (a) the presence and concentration of mannitol, (b) the duration of urinary stasis, and (c) the plasma concentration of HCO(3) (-).3. If a solution containing 15% (w/v) mannitol was infused I.V., the HCO(3) (-) concentration in free flow urine was lower than in plasma, and it fell further during arrest of flow in the entire column of trapped fluid. If less mannitol was infused, or none at all, interruption of urine flow led to a striking increase of HCO(3) (-) concentration in the distal portion of the occluded column, and to a fall in the fluid arrested in the proximal segments.4. It was demonstrated that the HCO(3) (-) concentration attained after 2(1/2), 6, or 15 min of urinary stasis at any point in the trapped fluid column was due to the combined effects of water reabsorption and HCO(3) (-) reabsorption which proceeded independently, and with a different time course.5. If mannitol was administered the lowest urinary HCO(3) (-) concentration in the series moved progressively to a more distal location with increasing duration of urinary stasis. When HCO(3) (-) concentration peaks were present in distal fluid they were conspicuous only after short interruptions of urine flow; during extended stop-flow periods they became attenuated, or disappeared. If no mannitol was administered this did not occur.6. Provided the plasma level of HCO(3) (-) was sufficiently elevated, mannitol (15%, w/v) was administered, and the time available for reabsorption was lengthened by ureter obstruction, much larger concentration differences between plasma and trapped fluid developed than the largest that are ever found between the plasma and freely draining urine. The magnitude of the largest plasma-urine (P-U) concentration difference for HCO(3) (-) increased with intratubular ;contact time', and no limiting value was found.7. Potassium concentration in distal occluded fluid fell with prolonged duration of stasis. This was related to the slow and progressive diminution of distal HCO(3) (-) concentration. But if instead of bicarbonate a nonreabsorbable anion, such as phosphate, was the dominant distal anion, K(+) concentration in distal fractions remained high and rose further with time.