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PubMed2005

Effect of oral sodium bicarbonate supplementation on interdialytic weight gain, plasma sodium concentrations and predialysis blood pressure in hemodialysis patients.

BACKGROUND: Correction of metabolic acidosis in dialysis patients should be considered of paramount importance. However, consuming sodium bicarbonate tablets during the interdialytic interval to reach predialysis bicarbonate levels of 23--24 mmol/l is not widespread due to the fear of greater interdialytic weight gain and fluid overload. For this reason we investigated in a cross-sectional and in an interventional study the effect of oral sodium bicarbonate supplementation on body weight gain, plasma sodium concentrations and predialysis blood pressure in a group of stable uremic patients on regular hemodialysis (HD) treatment. STUDY DESIGN: 110 patients (67 men, 43 women), mean age 67+/-15 (range 22--89) years, on regular chronic HD treatment for 6--372 (median 48) months were studied. 70 patients were on regular oral bicarbonate supplementation for at least 4 weeks (group A), 40 patients were not on oral bicarbonate supplementation (group B). The following parameters were recorded: dry body weight (DBW), interdialytic weight gain (IWG), body mass index (BMI), plasma sodium (Na), serum pH, serum bicarbonate (sBic), K(t)/V, normalized protein catabolic rate (PCRn), predialysis systolic (SBP) and diastolic (DBP) blood pressure, and bicarbonate therapy (g/day). 18 patients not on oral bicarbonate supplementation with sBic levels</=20 mmol/l were started on oral bicarbonate therapy and were prospectively followed in the context of an interventional study of correction of chronic metabolic acidosis. The same parameters were recorded before (pre) and after (post) 4 months of oral bicarbonate supplementation. RESULTS: Serum pH and sBic concentrations were significantly higher in patients in group A compared to patients in group B (pH 7.37 +/- 0.02 group A vs. 7.33+/- 0.02 group B: p<0.001: sBic 23.8+/-1.4 group A vs. 20.9+/-1.4 group B: p<0.0001). Age, DBW, BMI, IWG, SBP, DBP, Na, K(t)/V and PCRn did not differ between groups. The mean daily dose of oral sodium bicarbonate administered to patients in group A was 1.9+/-0.9 (range 1--5, median 2) g/day. Also in the 18 patients who started bicarbonate treatment, a significant increase in serum pH and sBic concentrations and a significant reduction in PCRn were observed. No significant change in DBW, IWG, SBP, DBP and Na concentrations after 4 months of treatment was found. CONCLUSIONS: Our data show that in stable uremic patients on regular HD treatment, oral daily administration of sodium bicarbonate is effective in correcting mild-moderate chronic metabolic acidosis, and does not cause increased interdialytic body weight gain, different plasma sodium concentrations and different systolic-diastolic blood pressure levels compared to patients not on oral sodium bicarbonate supplementation.

Acidosis↗
PubMed1978

Bicarbonate secretion by rabbit cortical collecting tubules in vitro.

We previously reported that rabbit renal cortical collecting tubules can secrete bicarbonate in vitro (i.e., there can be net transport from bath to lumen, causing the concentration in the lumen to increase). Net bicarbonate secretion was observed most often when rabbits had been pretreated with NaHCO(3) and were excreting alkaline urine before being killed for experiments. The purpose of the present studies was to elucidate the mechanism involved by testing the effects of ion substitutions and drugs on collecting tubules that were secreting bicarbonate. Acetazolamide inhibited net bicarbonate secretion, suggesting that the process is dependent upon carbonic anhydrase. Net bicarbonate secretion also decreased when sodium in the perfusate and bath was replaced by choline, but not when chloride was replaced by nitrate or methylsulfate. Ouabain had no significant effect. Amiloride caused net bicarbonate secretion to increase. The rate of net secretion did not correlate with transepithelial voltage. The results are compared to those in turtle urinary bladders that also secrete bicarbonate. There are no direct contradictions between the results in the two tissues, i.e., in turtle bladders acetazolamide also inhibited bicarbonate secretion and ouabain had no effect. Nevertheless, it seems unlikely that net secretion of bicarbonate by collecting tubules involves specific exchange for chloride, as has been proposed for turtle bladders, because replacement of chloride by other anions did not inhibit bicarbonate secretion by collecting tubules. It was previously shown that the collecting tubules in vitro also may absorb bicarbonate, especially when the rabbits have been treated with NH(4)Cl and are excreting acid urine before being killed. The effects of drugs on net bicarbonate secretion found in the present studies are compared to their previously reported effects on net bicarbonate absorption and the possibility is discussed that bicarbonate absorption and secretion are independent processes, as was previously proposed for turtle bladders.

Acetazolamide↗
PubMedDate not supplied

Sodium bicarbonate versus THAM in ICU patients with mild metabolic acidosis.

BACKGROUND: Sodium bicarbonate is despite its side effects, considered the standard alkali therapy in metabolic acidosis. THAM is an alternative alkalizing agent; however, there are limited data on the use of THAM in metabolic acidosis. The aim of this study was to compare the efficacy and adverse effects of a single dose of sodium bicarbonate and THAM in intensive care unit (ICU) patients with mild metabolic acidosis. METHODS: 18 adult ICU patients with mild metabolic acidosis (serum bicarbonate < 20 mmol/L) were randomized to a single dose of either sodium bicarbonate or THAM, administered over a 1-hour period, and titrated to buffer the excess of acid load. RESULTS: Sodium bicarbonate and THAM had equivalent alkalinizing effect during the infusion period. This was still present 4 hours after start of infusion of sodium bicarbonate, and until 3 hours after start of infusion of THAM. Serum potassium levels decreased after sodium bicarbonate infusion, and remained unchanged after THAM. After sodium bicarbonate, sodium increased, and after THAM, serum sodium decreased. CONCLUSIONS: Sodium bicarbonate and THAM had a similar alkalinizing effect in patients with mild metabolic acidosis; however, the effect of sodium bicarbonate was longer lasting. Sodium bicarbonate did decrease serum potassium, and THAM did not; THAM is therefore not recommended in patient with hyperkalemia. As sodium bicarbonate leads to an increase of serum sodium and THAM to a decrease, THAM may be the alkalinizing agent of choice in patients with hypernatremia. Similarly, because sodium bicarbonate increases PaCO2 and THAM may even decrease PaCO2, sodium bicarbonate is contraindicated and THAM preferred in patients with mixed acidosis with high PaCO2 levels.

Acidosis↗
PubMed1989

Acid base correction in bicarbonate CAPD patients.

Bicarbonate has been proposed as buffer in CAPD solutions in recent years instead of lactate and acetate. The present study is designed to evaluate peritoneal bicarbonate kinetics using bicarbonate solutions. Seventy kinetic studies have been performed in 7 patients treated with 2 CAPD solutions containing 35 mmol/l (A) and 27 mmol/l (B) of bicarbonate. The changes in dialysate bicarbonate concentration at different dwell times were correlated with bicarbonate blood levels. Furthermore after 2 hours of dwell time and at subsequent observations, no differences in dialysate bicarbonate concentration were found between A and B solutions at the same bicarbonatemia. Thus a feedback between bicarbonate absorption and bicarbonate blood concentration was observed. If the amount of bicarbonate transferred to the patient is over the metabolic acid production, bicarbonatemia will rise: consequently bicarbonate dialysate absorption will decrease. After a few days, an equilibrium point will be reached. In this condition the bicarbonate absorption is equal to metabolic acid production and, in stable clinical conditions, a stable acid base status will be maintained by the patient. Our studies empirically demonstrated that the equilibrium is reached when a difference of 5 mmols between blood and inlet dialysate bicarbonate concentration is observed. Consequently to achieve 25 mmol/l of bicarbonatemia, the bicarbonate concentration of CAPD solution should be about 30 mmol/l.

Acetates↗
PubMed1988

The ATP-sensitive potassium channel in pancreatic B-cells is inhibited in physiological bicarbonate buffer.

The effects of bicarbonate buffer (HCO3-/CO2) on the activity of the two K+ channels proposed by some to control the pancreatic B-cell membrane response to glucose were studied. Single K+-channel records from membrane patches of cultured B-cells dissociated from adult rat islets exposed to a glucose- and bicarbonate-free medium (Na-Hepes in place of bicarbonate) exhibit the activity of both the ATP-sensitive as well as the [Ca2+]i-activated K+ channels. However, in the presence of bicarbonate-buffered Krebs solution, the activity of the ATP-sensitive K+ channel is inhibited leaving the activity of the K+ channel activated by intracellular [Ca2+]i unaffected. In the absence of bicarbonate (Hepes/NaOH in place of bicarbonate), lowering the external pH from 7.4 to 7.0 also has differential effects on the two K+ channels. While the K+ channel sensitive to ATP is inhibited, the K+ channel activated by a rise in [Ca2+]i is not affected. To determine whether the response of the B-cell in culture to bicarbonate is also present when the B-cell is functioning within the islet syncytium, the effects of bicarbonate removal on membrane potential of B-cells from intact mouse islets were compared. These studies showed that glucose-evoked electrical activity is also blocked in bicarbonate-free Krebs solution. Furthermore, in the absence of bicarbonate and presence of glucose (11 mM), electrical activity was recovered by lowering the pHo from 7.4 to 7.0. The ATP-sensitive K+-channel activity is greatly reduced by physiologically buffered solutions in pancreatic B-cells in culture. The most likely explanation for the bicarbonate effects is that they are mediated by cytosolic pH changes. Removal of bicarbonate (keeping the external pH at 7.4 with Hepes/NaOH as buffer) would increase the pHi. Since the activity of the [Ca2+]i-dependent K+ channels is not affected by the removal of the bicarbonate buffer, our patch-clamp data in cultured B-cells indicate an involvement of [Ca2+]i-activated K+ channels in the control of the membrane potential. For the B-cell in the islet, we propose that the burst pattern of electrical activity (Ca2+ entry) is controlled, at least in part, by the [Ca2+]i-activated K+ channel.

Adenosine Triphosphate↗
PubMed1996

Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol.

Acute treatment of hyperkalemia in patients with end-stage renal disease requires temporizing measures to shift potassium rapidly from the extracellular to the intracellular fluid compartments until hemodialysis can be initiated. Whereas insulin and albuterol are effective in lowering plasma potassium acutely, bicarbonate by itself is not. Bicarbonate administration may, however, potentiate the effects of insulin and albuterol on plasma potassium. Using a prospective cross-over design, we investigated the acute effects of (1) isotonic bicarbonate, (2) isotonic saline, (3) insulin + bicarbonate, (4) insulin + saline, (5) albuterol + bicarbonate, and (6) albuterol + saline on plasma potassium as well as blood bicarbonate and pH in nondiabetic hemodialysis patients. After obtaining a baseline blood sample, the subjects received one of the six treatment protocols, with plasma potassium measured every 15 minutes over 1 hour. Neither isotonic bicarbonate nor isotonic saline decreased plasma potassium significantly (-0.03 +/- 0.06 mmol/L v -0.01 +/- 0.10 mmol/L at 60 minutes; P = 0.60). Intravenous insulin decreased plasma potassium by a similar degree when given in conjunction with bicarbonate or saline (-0.81 +/- 0.05 mmol/L v -0.85 +/- 0.06 mmol/L at 60 minutes; P = 0.65). Likewise, nebulized albuterol decreased plasma potassium by a similar degree when given with bicarbonate or saline (-0.71 +/- 0.16 mmol/L v -0.53 +/- 0.15 mmol/L at 60 minutes; P = 0.18). The three protocols that included bicarbonate administration resulted in significant increases in blood bicarbonate (P < 0.005) and pH (P < 0.01), whereas the three protocols that included saline did not affect blood bicarbonate or pH. These observations suggest that bicarbonate administration does not potentiate the potassium-lowering effects of insulin or albuterol in hemodialysis patients.

Adrenergic beta-Agonists↗
PubMed1976

Influence of bicarbonate on parathyroid hormone-induced changes in fluid absorption by the proximal tubule.

Segments of the proximal tubule of the rabbit kidney were perfused in vitro in order to examine the influence of bicarbonate on the reduction in fluid absorption that occurs following the acute administration of parathyroid hormone (PTH). Studies were performed using either normal ultrafiltrate as perfusion fluid and normal rabbit serum as bath or low bicarbonate ultrafiltrate as perfusion fluid and low bicarbonate rabbit serum as bath. Low bicarbonate fluids were prepared by replacement of bicarbonate with chloride. In the presence of normal concentrations of bicarbonate, the addition of PTH to the bath (1 U/ml) resulted in a decrease in the fluid absorption rate (Jv) from 1.13 +/- 0.08 to 0.60 +/- 0.04 nl/mm X min (p is less than 0.001) in 23 convoluted segments and from 0.64 +/- 0.05 to 0.46 +/- 0.05 nl/mm - mm (P less than 0.01) in ten straight portions. Simultaneous with the PTH-induced reduction in Jv, the chloride concentration in the collected fluid changed from 119.0 +/- 2.0 to 113.4 +/- 1.1 mEq/liter (P less than 0.01) in the pars convoluta and from 117.7 +/- 0.6 to 114.0 +/- 1.9 mEq/liter (P less than 0.01) in the pars recta. However, there was no change in the net flux of chloride which averaged 42.58 +/- 5.00 pEq/mm - min during the control periods. Additional studies were performed in eight convoluted segments during perfusion on a randomized basis with low bicarbonate fluids as well as during perfusion with fluids having normal levels of bicarbonate. As before, in the presence of normal levels of bicarbonate, PTH reduced Jv from 1.16 +/- 0.15 to 0.68 +/- 0.07 nl/mm - min (P less than 0.001) and the chloride concentration in the collected fluid ([Cl]o) from 118.6 +/- 2.9 to 111.6 +/- 1.3 mEq/liter (P less than 0.005). Substitution of low bicarbonate fluids for normal bicarbonate fluids resulted in a decrease in Jv from 1.16 +/- 0.15 to 0.74 +/- 0.10 nl/mm - min (P less than 0.001). In the presence of low bicarbonate fluids, the addition of PTH resulted in no further decrease in Jv (0.74 +/- 0.10 vs. 0.72 +/- 0.10 nl/mm - min). These data indicate that in the proximal tubule the PTH-induced reduction in fluid absorption may be mediated by changes in bicarbonate absorption.

Absorption↗
PubMed2004

The bicarbonate transport metabolon.

To allow cells to control their pH and bicarbonate levels, cells express bicarbonate transport proteins that rapidly and selectively move bicarbonate across the plasma membrane. Physical interactions have been identified between the carbonic anhydrase isoform, CAII, and the erythrocyte membrane Cl- /HCO3(-) anion exchanger, AE1, mediated by an acidic motif in the AE1 C-terminus. We have found that the presence of CAII attached to AE1 accelerates AE1 HCO3(-) transport activity, as AE1 moves bicarbonate either into or out of the cell. In efflux mode the presence of CAII attached to AE1 will increase the local concentration of bicarbonate at the AE1 transport site. As bicarbonate is transported into the cell by AE1, the presence of CAII on the cytosolic surface accelerates transport by consumption of bicarbonate, thereby maximizing the transmembrane bicarbonate concentration gradient experienced by the AE1 molecule. Functional and physical interactions also occur between CAII and Na+/HCO3(-) co-transporter isoforms NBC1 and NBC3. All examined bicarbonate transport proteins, except the DRA (SLC26A3) Cl-/HCO3(-) exchange protein, have a consensus CAII binding site in their cytoplasmic C-terminus. Interestingly, CAII does not bind DRA. CAIV is anchored to the extracellular surface of cells via a glycosylphosphatidyl inositol linkage. We have identified extracellular regions of AE1 and NBC1 that directly interact with CAIV, to form a physical complex between the proteins. In summary, bicarbonate transporters directly interact with the CAII and CAIV carbonic anhydrases to increase the transmembrane bicarbonate flux. The complex of a bicarbonate transporter with carbonic anhydrase forms a "Bicarbonate Transport Metabolon."

Animals↗
PubMed1990

Effect of acid-base balance on biliary bicarbonate secretion in the isolated perfused guinea pig liver.

Secretin-induced choleresis is of ductal origin and involves bicarbonate transport. Its mechanism is unknown. To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on secretin-stimulated bicarbonate transport, states of acute metabolic and respiratory acidosis or alkalosis were created in isolated perfused guinea pig livers with or without secretin infusion. During spontaneous secretion conditions, biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.62) or perfusate PCO2 (23.9-59.7) but was significantly correlated with perfusate bicarbonate concentration (17.5-37.9 mM). Under secretion infusion (25 mU/min), bile flow and biliary bicarbonate concentration increased significantly (109 and 51%, respectively). Biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.60) but was significantly correlated both with perfusate bicarbonate concentration (14.6-36.8 mM) and PCO2 (25.8-54.3 mmHg). Spontaneous and secretin-induced bile flow were correlated with biliary bicarbonate concentration. The correlation between biliary bicarbonate secretion and PCO2 during secretin-induced choleresis supports the hypothesis that secretin-induced biliary bicarbonate secretion could, at least in part, involve a transport of H+ (or OH-) rather than HCO3- itself and that intracellular pH could play a role in the regulation of this secretion. Amiloride (5 X 10(-4) M) did not influence secretin-induced biliary bicarbonate secretion. This result suggests that the Na(+)-H+ exchange is not involved in bicarbonate secretion by ductular cells.

Acid-Base Equilibrium↗
PubMed1989

Control of bicarbonate transport in collecting tubules from normal and remnant kidneys.

Bicarbonate transport in the rabbit cortical collecting tubule (CCT) and outer medullary collecting tubule (MCT) in vitro was studied under two types of conditions that were anticipated to alter distal tubule bicarbonate transport: 1) reduction of renal mass, and 2) acid and base loading in vivo. Bicarbonate secretion (both total and acetazolamide sensitive) and bicarbonate reabsorption (studied separately) in CCT and bicarbonate reabsorption in the MCT were not different between tubules from normal and remnant kidneys. The control or conditioning of the separate processes of bicarbonate secretion and bicarbonate reabsorption was also studied in CCT from normal and remnant kidneys. Bicarbonate secretion was not increased by base-loading animals with either normal or remnant kidneys. In contrast, bicarbonate secretion was consistently decreased by acid loading (studied in CCT from remnant kidneys). Bicarbonate reabsorption in the CCT was not altered by acid or base loads given to animals with normal kidneys. And bicarbonate reabsorption in MCT was not increased by acid loading of animals with remnant kidneys. These studies demonstrate that bicarbonate transport (and its conditioning by acid or base loads in vivo) in both CCT and MCT in vitro is not altered by reduction of renal mass in rabbits. The predominant conditioning effect of acid or base loads in vivo is for acid loads to inhibit CCT bicarbonate secretion.

Acid-Base Equilibrium↗
PubMed1970

Regulation of renal bicarbonate reabsorption by extracellular volume.

The ability of the kidney to reabsorb bicarbonate is held to be a function of plasma CO(2) tension, carbonic anhydrase activity, and potassium stores. The effects of alterations of extracellular volume on bicarbonate reabsorption were studied in dogs whose arterial Pco(2) was kept constant at 40 mm Hg (range 35-45 mm Hg). The effect of extracellular volume expansion was studied in dogs receiving hypertonic bicarbonate and isotonic saline, isotonic saline alone (two of the animals in this group received HCl to lower the plasma bicarbonate concentration), and isotonic bicarbonate. The results were similar in each group. Extracellular volume expansion depressed bicarbonate reabsorption. This depression was related not to changes in glomerular filtration rate (GFR) or bicarbonate concentration, but to the increase of fractional sodium excretion. In addition, volume expansion with bicarbonate increased chloride excretion. Bicarbonate loading was performed in two groups of dogs in which effective expansion of extracellular volume was minimized by hemorrhage or acute constriction of the thoracic vena cava. Both groups demonstrated enhanced bicarbonate reabsorption relative to that seen in the volume-expanded groups. Release of the caval ligature promptly decreased bicarbonate reabsorption. Plasma potassium decreased in all animals studied, but the changes in bicarbonate reabsorption noted could not be related to the decrease. This study demonstrates that the state of effective extracellular volume is a major determinant of bicarbonate reabsorption by the kidney.

Animals↗
PubMed1979

Loop of Henle bicarbonate accumulation in vivo in the rat.

We have carried out perfusion studies on hydropenic and bicarbonate-loaded rats to provide direct in vivo observations on bicarbonate accumulation in the short loops of Henle. Analysis of early distal tubular fluid was made during bicarbonate-free saline perfusion from the end proximal to the early distal site, documenting accumulation of "new" bicarbonate. During perfusion in hydropenic rats, steady-state bicarbonate concentrations were suggested by early distal values of approximately equal to mM, which were independent of perfusion rate and virtually indistinguishable from bicarbonate concentration measured during free flow when filtered bicarbonate was allowed to enter the loop. Thus, loop bicarconate accumulation was apparently sufficient to allow new bicarbonate to enter at a rate comparable to that delivered to the early distal site during free flow, recognizing of course that free-flow delivery rates are the result of complex components of filtration and bidirectional fluxes. In bicarbonate-loaded rats, however, bicarbonate accumulation rates although higher than in hydropenia, were much lower than free-flow delivery rates. Furthermore, early distal bicarbonate concentrations during bicarbonate loading fell as perfusion rate increased, presumably because of a limitation to increasing ionic bicarbonate entry.

Animals↗
PubMed1983

Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.

Studies were undertaken to define the pattern of proximal tubular bicarbonate reabsorption and its relation to tubular and capillary PCO2 in rats with chronic metabolic alkalosis (CMA). CMA was induced by administering furosemide to rats ingesting a low electrolyte diet supplemented with NaHCO3 and KHCO3. Proximal tubular bicarbonate reabsorption and PCO2 were measured in CMA rats either 4-7 or 11-14 d after furosemide injection, in order to study a wide range of filtered bicarbonate loads. A group of nine age-matched control animals, fed the same diet but not given furosemide, was studied for comparison. In a third group of controls, the filtered load of bicarbonate was varied over the same range as in the CMA rats by plasma infusion and aortic constriction. The CMA rats had significant alkalemia and hypokalemia (4-7 d: pH 7.58, HCO3 38.3 meq/liter, K+ 2.1 meq/liter; 11-14 d: pH 7.54, HCO3 38.1 meq/liter, K+ 2.5 meq/liter). Nonetheless, proximal bicarbonate reabsorption was not significantly different from that seen in control rats at any given load of filtered bicarbonate (from 250 to 1,300 pmol/min). In both control and CMA rats, 83-85% of the filtered bicarbonate was reabsorbed by the end of the accessible proximal tubule. These observations indicate that proximal bicarbonate reabsorption is determined primarily by the filtered load in chronic metabolic alkalosis. When single nephron glomerular filtration rate (SNGFR) is reduced by volume depletion in the early postfurosemide period, the filtered load and the rate of proximal bicarbonate reabsorption remain at or below control levels, maintaining metabolic alkalosis. In the late postfurosemide period, however, SNGFR returned to control levels in some instances. In these animals, both the filtered load and rate of proximal reabsorption were increased above the highest levels seen in control animals. The PCO2 gradient between the peritubular capillaries and arterial blood (Pc-Art) was significantly higher in CMA than in control, even though the rate of proximal bicarbonate reabsorption did not differ. Thus, proximal bicarbonate reabsorption did not appear to be the primary determinant of Pc-Art PCO2. PCO2 in the early proximal (EP) tubule was significantly higher than in either the late proximal (LP) tubule or peritubular capillaries in both control and CMA rats. The EP-LP PCO2 gradient correlated directly with proximal bicarbonate reabsorption (P less than 0.05). The small elevation in PCO2 in EP may be related to CO2 generated at this site in the process of bicarbonate reabsorption.

Absorption↗
PubMed1997

Inhibition of biliary bicarbonate secretion in ethinyl estradiol-induced cholestasis is not associated with impaired activity of the Cl-/HCO-3 exchanger in the rat.

BACKGROUND/AIMS: Bicarbonate is a major component of bile salt independent bile flow, which is impaired in ethinyl estradiol (EE)-cholestasis. To examine this subject in EE-cholestasis, we studied: 1) basal and glucagon-stimulated biliary bicarbonate secretion both in vivo and in the isolated perfused rat liver (IPRL); 2) H+/HCO-3 transport processes in isolated rat hepatocyte couplets. METHODS: Rats received EE (5 mg.kg b.w.-1) for 5 days. Intracellular pH (pHi) was measured (BCECF-AM) using a single-cell microfluorimetric setup. RESULTS: Bile flow was markedly (p < 0.01) decreased in EE-treated rats. Bicarbonate concentration in bile was decreased (p < 0.01) and bicarbonate secretion was 2.5-fold lower in EE-treated animals than in controls, both in bile-fistula rats [19.5 +/- 5.1 (n = 23) vs 54.2 +/- 5.7 (n = 20) nmol.min-1g liver-1; p < 0.01] and in the IPRL [11 +/- 2 (n = 8) vs 24 +/- 3 (n = 8) nmol.min-1.g liver-1; p < 0.01]. In control IPRL, a bile/perfusate gradient for bicarbonate is maintained, while it is lost in EE-treated IPRL because of the lower bicarbonate concentration in bile. Glucagon stimulated bile flow and bicarbonate secretion to a similar extent in EE-treated and control IPRL (+25% vs +23%). Resting pHi of EE-treated hepatocyte couplets was higher in comparison with controls in KRB [7.25 +/- 0.07 (n = 35) vs 7.20 +/- 0.05 (n = 33); p < 0.02] but similar in Hepes [7.08 +/- 0.07 (n = 24) vs 7.05 +/- 0.06 (n = 26)]. Basal activity of the Cl-/HCO-3 exchanger was similar in EE-treated and control hepatocyte couplets [H+ flux = 2.87 +/- 1.12 (n = 18) vs 3.01 +/- 1.23 mM/min (n = 15)] and was stimulated to a similar extent by glucagon. Na+/HCO3-symport activity was increased in EE-treated hepatocyte couplets (p < 0.05) while the Na+/H+ exchanger was unchanged. CONCLUSIONS: Bicarbonate biliary secretion is markedly impaired during EE-cholestasis in association with a marked decrease of bile salt independent bile flow. However, the Cl-/HCO-3 exchanger and its hormonal regulation are normal, indicating that the lower bicarbonate excretion in EE-cholestasis is not due to a compromised activity of this anion exchanger. Since the bile/perfusate gradient for bicarbonate is dissipated in EE-treated IPRL, the impaired bicarbonate excretion could be caused by a reflux of biliary bicarbonate via leaky tight junctions.

Animals↗
PubMed1983

Characteristics of bicarbonate, sodium, and chloride fluxes in the rabbit corneal endothelium.

Unidirectional fluxes of bicarbonate, sodium and chloride were measured across the isolated rabbit corneal endothelium. Bicarbonate and sodium fluxes were measured between 13 and 37 degrees C and were found to be temperature-sensitive. Ouabain (10(-6)M), which inhibits endothelial fluid transport, reduced the net bicarbonate flux by 32% but had no significant effect on sodium fluxes. Amiloride (10(-4)M) did not alter sodium transport, but slightly increased the unidirectional bicarbonate fluxes. Sodium fluxes were unchanged in chloride-free and potassium-free Ringer solutions, and net sodium transport was unaffected in the presence of carbonic anhydrase, acetazolamide, or low (5 mM) bicarbonate Ringer, but was reduced by 45% in bicarbonate-free Ringer. A net chloride flux was found in the same direction (stroma to aqueous) as bicarbonate and sodium. This chloride flux (2.18 muEq/cm2/hr) was of the same magnitude as bicarbonate but was sodium-independent. These findings suggest that: (1) like bicarbonate and fluid transport, sodium transport is bicarbonate-dependent, temperature-sensitive, and chloride-independent; (2) sodium transport is not stoichiometrically coupled to bicarbonate; and (3) neither sodium nor bicarbonate transport are coupled to that of chloride.

Acetazolamide↗
PubMed2005

Sodium bicarbonated mineral water decreases postprandial lipaemia in postmenopausal women compared to a low mineral water.

The role of bicarbonated mineral waters on lipid metabolism and lipoprotein concentrations in man has scarcely been investigated. The present study aimed to investigate whether drinking sodium bicarbonated mineral water affects postprandial cholesterol and triacylglycerol metabolism in postmenopausal women. In a three-way, randomised, crossover study, eighteen healthy postmenopausal women consumed two sodium bicarbonated mineral waters (bicarbonated mineral water 1 and bicarbonated mineral water 2) and a low mineral water (500 ml of each) with a standard fat-rich meal (4552 kJ; 75.3 g fat). The bicarbonated waters were rich in sodium and bicarbonate and bicarbonated mineral water 1 contained 5.7 times more fluoride than bicarbonated mineral water 2. Fasting blood samples and postprandial blood samples were taken at 30, 60, 120, 240, 360 and 420 min after the end of the meal consumption. Cholesterol and triacylglycerols were determined in serum and chylomicrons. A significant water consumption effect was observed in the total area under the curve (TAUC) of serum and chylomicron triacylglycerols (ANOVA, P=0.008 and P=0.027, respectively). TAUC of serum triacylglycerols for bicarbonated mineral water 2 was significantly lower compared to low mineral water (Bonferroni, P=0.039). Peak concentration of serum triacylglycerols showed a significant water effect (P=0.025). Changes in chylomicron cholesterol were not significantly affected by the type of water. Bicarbonated mineral waters 1 and 2 did not show any significant differences. Drinking sodium bicarbonate-rich mineral waters reduces postprandial lipaemia in healthy postmenopausal women compared to drinking a low mineral water.

Analysis of Variance↗
PubMed2000

Addition of sodium bicarbonate to lidocaine decreases the duration of peripheral nerve block in the rat.

BACKGROUND: Adding sodium bicarbonate to lidocaine to enhance its efficacy during peripheral nerve block is controversial. The authors studied the effect of adding sodium bicarbonate to lidocaine with and without epinephrine versus equivalent alkalinization by sodium hydroxide (NaOH) on onset, degree, and duration of peripheral nerve block. METHODS: Part I examined alkalinization by sodium bicarbonate versus NaOH to pH 7.8 on 0.5% lidocaine, with and without epinephrine (1:100,000), prepared from crystalline salt. Part II examined 0.5% and 1.0% commercial lidocaine solutions, with and without epinephrine, either unalkalinized or alkalinized with sodium bicarbonate or NaOH. With NaOH, pH was adjusted to 7.8, but with sodium bicarbonate, no pH adjustments were made to simulate clinical conditions. RESULTS: In part I, addition of either NaOH or sodium bicarbonate to 0.5% lidocaine without epinephrine produced a faster onset than did unalkalinized lidocaine, without effecting degree or duration of block. In solutions with epinephrine there were no differences in onset, degree, or duration between lidocaine alkalinized with sodium bicarbonate versus NaOH. In part II, addition of sodium bicarbonate or NaOH to 1.0% commercial lidocaine without epinephrine did not accelerate onset compared with the unalkalinized solution. However, adding sodium bicarbonate decreased the degree and duration of block by 25% and more than 50%, respectively, compared with lidocaine unalkalinized and alkalinized with NaOH. With epinephrine, sodium bicarbonate hastened onset without effecting degree and duration compared with the unalkalinized solution. CONCLUSIONS: With 1% commercial lidocaine without epinephrine, sodium bicarbonate decreases the degree and duration of block. However, in solutions with epinephrine, sodium bicarbonate hastens onset, without effecting degree or duration.

Anesthetics, Local↗
PubMed1996

Secretin-induced plasma bicarbonate decrease as a simple indicator of exocrine pancreatic function.

During a secretin-cerulein test for exocrine pancreatic function, venous acid-base analysis was performed before and 30 and 45 min after the intravenous injection of secretin (1 clinical unit/kg body weight). A decrease in plasma bicarbonate was observed in persons with normal exocrine pancreatic function as defined by normal bicarbonate and enzyme secretion in the secretin-cerulein test (n = 39). Bicarbonate values were 94.8 +/- 3.6% (mean +/- SD) of the initial concentration after 30 min and 92.9 +/- 3.9% after 45 min. In contrast, there was no statistically significant decrease in plasma bicarbonate in patients with global pancreatic exocrine deficiency (n = 15). In normal exocrine pancreatic function, the maximal plasma bicarbonate decrease was 2.17 +/- 1.12 mM (mean +/- SD; n = 39). In patients with global exocrine deficiency, however, a maximal plasma bicarbonate decrease of 0.54 +/- 0.68 mM (n = 15) was obtained. The difference was highly significant (p < 0.001). In patients with partial exocrine deficiency (isolated decrease in bicarbonate secretion or reduced excretion of a single enzyme), values were also significantly lower (1.44 +/- 1.40 mM; n = 14; p < 0.05). The maximal plasma bicarbonate decrease correlated with the bicarbonate secretion into the duodenal juice (r = 0.62, p < 0.001). If a maximal plasma bicarbonate decrease > or = 0.9 mM was considered normal, determination of plasma bicarbonate following secretin administration allowed us to detect the presence of global exocrine deficiency with a sensitivity of 87% and a specificity of 87%. The secretin-induced plasma bicarbonate decrease may therefore be used as a new simple tubeless test to evaluate exocrine pancreatic function.

Acid-Base Equilibrium↗