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PubMed1977

Effects of Gaseous CO2 and bicarbonate on the growth of Neisseria gonorrhoeae.

The quantitative and qualitative growth response of Neisseria gonorrhoeae strains was assessed under the following conditions: incubation in a candle jar (approximately 2.5% ambient CO2) on medium without bicarbonate, incubation in air on medium without bicarbonate, incubation in air on medium with bicarbonate, and incubation in air in a sealed jar on medium with bicarbonate. Incubation in the presence of ambient CO2 (candle jar) resulted in the highest plating efficiencies for the three laboratory strains 9, 62, and 2686. The addition of NaHCO3 to the medium enhanced the growth response in air of all three strains, particularly if incubation was carried out in a closed environment (sealed jar). The qualitative growth response of 34 clinical isolates and laboratory strains was assessed under the same conditions of incubation after the plating of an inoculum containing approximately 2 X 10(6) bacteria. The strains were divided into different classes based on their growth responses. About 40% of the strains grew as well on bicarbonate-containing medium incubated in air in sealed jars as they did on medium without bicarbonate incubated in a candle jar. Ten percent of the strains showed only slight growth on bicarbonate containing medium incubated in sealed jars and appeared to have an almost obligate requirement for ambient CO2. Twenty percent of the strains apparently had partially lost their requirement for gaseous C02 and showed slight growth in air on medium without bicarbonate and slight to moderate growth in air on medium containing NaHCO3. The remaining 30% seemed to have completely lost their requirement for gaseous C02 and/or the bicarbonate anion and grew almost as well in air on medium without bicarbonate as they did in either ambient C02 (candle jar) or on medium containing bicarbonate incubated in a sealed jar. These results suggest that N. gonorrhoeae strains may vary widely in their requirements for CO2 and/or the HCO3-anion. Incubation in the presence of ambient CO2 tends to maximize the growth response on solid medium of those strains, which require it for growth. The presence of ambient CO2 is particularly important if growth is to be obtained after the plating of small inocula. Medium conatining 0.1% NaHCO3, if incubated in a closed environment (sealed jar), apperas to be equivalent to medium without bicarbonate incubated in ambient CO2 in supporting the growth of some but not all strains of N. gonorrhoeae.

Air↗
PubMed1997

Reappraisal of bicarbonate secretion by the human oesophagus.

BACKGROUND AND AIMS: Administration of omeprazole to healthy volunteers was recently reported to increase proximal duodenal mucosal bicarbonate secretion. As human oesophagus also secretes bicarbonate, the hypothesis was tested that omeprazole may stimulate oesophageal bicarbonate secretion and thus contribute to the therapeutic efficacy of the drug in gastro-oesophageal reflux disease. SUBJECTS AND METHODS: In nine healthy volunteers, oesophageal "steady state" perfusion of a 10 cm open segment of distal oesophagus was performed twice in random order. The volunteers were pretreated with either 60 mg/day omeprazole for three days and 80 mg intravenous omeprazole before perfusion or 600 mg/day ranitidine for three days and 50 mg/h intravenously during the perfusion. Saliva and samples of aspirate from the perfused oesophagus and stomach were collected and bicarbonate concentrations were measured. RESULTS: The median rates (95% confidence intervals) of intrinsic oesophageal bicarbonate secretion, corrected for contaminating salivary and gastric bicarbonate, were 89 (33-150) and 121 (63-203) mumol/h/10 cm (p > 0.5) in omeprazole and ranitidine treated subjects respectively. Salivary and gastric bicarbonate contaminating the oesophagus accounted for 14% and 3%, respectively, of total oesophageal bicarbonate output. CONCLUSIONS: Bicarbonate secretory capacity of the human oesophagus is less than previously assumed, and the clinical relevance of intrinsic oesophageal bicarbonate for mucosal defence may be overestimated. As omeprazole and ranitidine did not affect bicarbonate secretion differently there was no evidence that omeprazole acts on bicarbonate secretory cells in the oesophageal mucosa.

Adult↗
PubMed1983

Flow dependence of proximal tubular bicarbonate absorption.

Rat proximal convoluted tubules were microperfused in vivo to examine the effect of flow rate on bicarbonate absorption. When tubules were perfused with 25 mM bicarbonate, increases in perfusion rate from 15 to 33 to 49 nl/min caused bicarbonate absorption to increase from 105 +/- 4 to 176 +/- 8 to 209 +/- 7 pmol X mm-1 X min-1, respectively. Only 15% of this stimulation could be attributed to a flow-induced increase in the measured axial luminal bicarbonate concentration profile. In addition, effects of flow on passive bicarbonate diffusion or convection could not account for the observed stimulation. When tubules were perfused with 58 mM bicarbonate (a concentration previously shown to achieve maximal rates of proton secretion), increasing flow rate from 15 to 49 nl/min did not stimulate bicarbonate absorption. Thus, when examined as a function of mean luminal bicarbonate concentration, increases in flow increased the rate of proton secretion without affecting the maximal rate. The data are most consistent with flow-dependent stimulation of bicarbonate absorption, secondary to flow-dependent changes in luminal bicarbonate concentration, occurring by two mechanisms: 1) flow-dependent increases in the measured axial luminal bicarbonate concentration profile and 2) flow-dependent decreases in radial luminal bicarbonate concentration gradients.

Absorption↗
PubMed1985

Sodium-dependent bicarbonate absorption by cortical thick ascending limb of rat kidney.

In vitro microperfusion experiments were performed to investigate the mechanism of bicarbonate absorption in the cortical thick ascending limb of the rat. Tubules were perfused at 1.0-1.5 nl X min-1 X mm-1 and bicarbonate concentration was 25 mM in the perfusate and bath. Bicarbonate absorption rates were determined by microcalorimetry. Control tubules absorbed bicarbonate at a mean rate of 9.5 +/- 0.6 pmol X min-1 X mm-1. The limiting luminal bicarbonate concentration was approximately 5 mM for tubules perfused at slow rates with 25 mM bicarbonate in the bath. Acetazolamide (10(-4)M) in the bath reduced bicarbonate absorption by 76% without significant effect on transepithelial voltage. Removing sodium from the perfusate and bath or removing potassium from the bath reduced bicarbonate absorption and transepithelial voltage to near zero. Adding amiloride (5 X 10(-4) or 10(-3) M) to the perfusate reduced bicarbonate absorption by 60-75% without detectable effect on transepithelial voltage. Adding furosemide (10(-4)M) to the perfusate increased bicarbonate absorption significantly by 40-50% while decreasing transepithelial voltage from 17 to 1.8 mV. Thus, bicarbonate absorption by cortical thick ascending limbs requires carbonic anhydrase activity and sodium transport but is not dependent on transepithelial voltage. When considered together, the results are consistent with mediation of the bicarbonate absorption by apical membrane sodium-hydrogen exchange.

Absorption↗
PubMed1985

Bicarbonate transport by isolated perfused rat collecting ducts.

Previously, bicarbonate transport was measured in isolated perfused rabbit cortical collecting ducts (CCD) and outer medullary collecting ducts (OMCD). Rabbit CCD either absorbed or secreted bicarbonate in vitro, depending on whether the animals were treated with NH4Cl or NaHCO3, but the OMCD absorbed bicarbonate regardless of the treatment. The general significance of these findings (particularly the bicarbonate secretion) was questioned because rabbits are herbivores that normally excrete alkaline urine. Therefore, we have now studied rats, an omnivorous species, that normally excrete acid urine. The overall pattern of bicarbonate transport in rats was similar to that previously found in rabbits. CCD from rats given NaHCO3 initially secreted bicarbonate, but those from rats given NH4Cl absorbed bicarbonate. Rat OMCD all absorbed bicarbonate, regardless of the treatment. The significant differences between the results with rats and rabbits were 1) a marked shift in bicarbonate transport in control and bicarbonate-loaded rat (but not rabbit) CCD with time of perfusion in vitro from secretion toward absorption; this implies an additional regulatory mechanism in rats; and 2) rat OMCDs absorbing bicarbonate more than three times faster than rabbit OMCD. These results provide additional evidence that conditioned changes in cortical collecting duct bicarbonate transport, now observed in two different species, play a significant role in the control of net acid excretion.

Animals↗
PubMed1969

On the influence of extracellular fluid volume expansion on bicarbonate reabsorption in the rat.

Bicarbonate reabsorption is classically regarded as a rate-limited process characterized by saturation kinetics. The tubular maximum (Tm), however, varies with glomerular filtration rate. Thus bicarbonate reabsorption, in common with sodium reabsorption, is characterized by glomerulo-tubular balance. The examination of bicarbonate reabsorption is accomplished using the bicarbonate titration technique; however, this method in its traditional form leads to marked expansion of extracellular fluid (ECF) volume. The possibility exists, therefore, that glomerulo-tubular balance for bicarbonate is altered by the volume expansion and thus that the classic pattern of reabsorption may actually reflect inhibited bicarbonate reabsorptive capacity. The present studies were performed in rats to examine this possibility. Bicarbonate titration studies were performed in two groups of animals: (a) those in which ECF volume expansion was minimized; and (b) those in which ECF volume expansion was exaggerated. In the first group, no Tm for bicarbonate was observed either in the majority of individual rats studied or in a group plot for all rats studied despite the fact that plasma bicarbonate concentrations were increased to values in excess of 60 mEq/liter. In the second group, a clear Tm was demonstrated both in individual animals and in group data and there was a lowered threshold for the excretion of bicarbonate. The data thus lend support to the view that the "normal" Tm for bicarbonate may actually represent an inhibited level of bicarbonate reabsorption induced by ECF volume expansion.

Animals↗
PubMed1996

Importance of gastrin-releasing peptide on acid-induced secretin release and pancreaticobiliary and duodenal bicarbonate secretion.

BACKGROUND: Exogenous gastrin-releasing peptide (GRP) stimulates the release of secretin from the small intestine and pancreaticobiliary bicarbonate secretion in pigs. As acid is the principal stimulant of secretin release, the purpose of this study was to examine the importance of GRP in acid-induced secretin release and to determine whether GRP contributes to the regulatory function of acid-induced pancreaticobiliary bicarbonate secretion in anaesthetized pigs. METHODS AND RESULTS: Intravenous infusion of GRP (500 pmol/kg.h) increased significantly portal vein plasma concentrations of secretin from 1.3 to 5.4 pmol/l and GRP from 0.5 to 340 pmol/l, pancreatic bicarbonate secretion from 0.01 to 5.9 mmol/h, and hepatic bicarbonate secretion from 0.3 to 3.3 mmol/h, whereas duodenal mucosal bicarbonate secretion remained unchanged. Intravenous infusion of the GRP antagonist BIM-26226 completely abolished the GRP-induced secretin release and pancreatic and hepatic bicarbonate secretion. Furthermore, repeated infusions of GRP did not cause desensitization, and BIM-26226 therefore proved to be an effective GRP antagonist. Duodenal perfusion with acid (pH 1.5, 3.8 mmol/h) significantly increased portal vein plasma concentrations of secretin from 0.4 to 2.8 pmol/l, pancreatic bicarbonate secretion from 0.005 mmol/h to 0.19 mmol/h, hepatic bicarbonate secretion from 0.63 to 2.17 mmol/h, and duodenal mucosal bicarbonate secretion from 0.1 to 1.20 mmol/h. Of importance, infusion of BIM-26226 did not significantly alter the effect of intraduodenal acidification on plasma secretin release and pancreaticobiliary and duodenal bicarbonate secretion. CONCLUSIONS: Thus, we conclude that GRP likely plays an insignificant role in a possible peptidergic regulation of acid-induced intestinal secretin release and that GRP has no regulatory function in acid-induced pancreaticobiliary bicarbonate secretion. Furthermore, GRP has no effect on duodenal bicarbonate secretion.

Animals↗
PubMed2005

Sodium bicarbonate and hydrogen peroxide: the effect on the growth of Streptococcus mutans.

PURPOSE: This in vitro experiment studied the effects of sodium bicarbonate and hydrogen peroxide on the cariogenic bacteria Streptococcus mutans through analysis with a spectrophotometer. METHODS: The growth of S. mutans was analyzed using seven different environments. Twelve wells in each of the seven rows of a multi-well plate were used to incubate the test materials. In combinations of 10 microl distilled water, 100 microl broth, 10 microl 10% sucrose, 10 microl S. mutans, 10 microl 10% sodium bicarbonate, and 10 microl 3% hydrogen peroxide, seven different environments were created for testing. Environments had either sodium bicarbonate or hydrogen peroxide with S. mutans, or a combination of sodium bicarbonate and hydrogen peroxide with S. mutans. The plate was incubated at 37 degrees C and measured at 0, 18, 20, 22, 24, 26, 28, 30, and 42 hours by optical density with a spectrophotometer. RESULTS: Results showed bacterial growth was prevented by sodium bicarbonate, hydrogen peroxide, and the combination of sodium bicarbonate and hydrogen peroxide. Although hydrogen peroxide is bacteriocidal and sodium bicarbonate is bacteriostatic, there were no significant differences among the three treatment groups in spectrophotometer readings at any of the nine readings over 42 hours. CONCLUSION: There was no significant difference among the effects of hydrogen peroxide, sodium bicarbonate, or the sodium bicarbonate and hydrogen peroxide combination, as measured by optical density. The hydrogen peroxide, sodium bicarbonate, and the sodium bicarbonate and hydrogen peroxide combination prevented bacterial growth of S. mutans. The results show that products containing these agents have the ability to stop the growth of S. mutans. Products containing sodium bicarbonate and/or hydrogen peroxide may be useful to caries-prone patients. More studies are needed to confirm these results on patients.

Dentifrices↗
PubMed2006

Acid-base profile and predictors of metabolic acidosis in patients undergoing peritoneal dialysis with lactate- and bicarbonate-buffered peritoneal dialysis solutions.

Metabolic acidosis correction is one of the goals of renal replacement therapy. Correction of acidosis in peritoneal dialysis (PD) may be affected by PD modalities such as automated PD (APD) or by new solutions containing a combination of bicarbonate and lactate as a buffer [bicarbonate continuous ambulatory PD (CAPD)]. The aim of the present study was to examine the acid-base status of our PD population and to compare the effects of APD, lactate CAPD, and bicarbonate CAPD on serum bicarbonate levels. We studied 35 stable patients undergoing APD (n = 15), lactate-buffered (35 mEq/L) CAPD (n = 14), and bicarbonate/lactate-buffered CAPD (n = 6) for 48.5 +/- 38.1 months. Most of our patients had serum bicarbonate levels in the normal range. In 3 patients (8%), HCO3 was below 22 mEq/L, and in 8 patients (22%; APD = 2, lactate CAPD = 2, bicarbonate CAPD = 4), HCO3 was above 28 mEq/L. We found no statistically significant correlations between HCO3 serum levels and PD prescription, peritoneal membrane characteristics, or intake of calcium carbonate and sevelamer hydrochloride. Patients on bicarbonate CAPD had higher HCO3 serum levels, but this difference disappeared when corrections for duration of dialysis, residual urine volume, and PD adequacy indices were applied. In the studied PD population, adequate correction of metabolic acidosis was achieved, as reflected in serum bicarbonate levels. We observed no difference in serum bicarbonate levels between APD and lactate CAPD patients. The new bicarbonate-buffered PD solutions are more biocompatible and can result in higher serum bicarbonate levels. However, a significant number of PD patients on bicarbonate-buffered solutions may become alkalotic. The clinical significance of these results needs further examination in prospective studies.

Acid-Base Equilibrium↗
PubMed1986

Human duodenal mucosal bicarbonate secretion. Evidence for basal secretion and stimulation by hydrochloric acid and a synthetic prostaglandin E1 analogue.

The factors responsible for prevention of duodenal mucosal injury are not known. This series of experiments was performed to determine whether the human duodenum secretes bicarbonate that could prevent mucosal damage. To isolate a 4-cm segment of proximal (i.e., the duodenal bulb) or distal duodenum free of contamination from either gastric or pancreaticobiliary secretion, or both, methods were developed using occlusive balloons. The test segment was perfused with NaCl (2 ml/min, 37 degrees C) containing [14C]PEG as a nonabsorbable marker, and bicarbonate output was quantitated. Mean (+/- SE) basal proximal duodenal bicarbonate output was 143 +/- 17 mumol/cm X h. A 5-min infusion of 25, 50, and 100 mM HCl directly into the isolated proximal duodenal test segment increased bicarbonate output to 167 +/- 29, 199 +/- 19, and 278 +/- 49 mumol/cm X h, respectively, during the hour after acidification. Distal duodenal acidification (25, 50, and 100 mM) also increased bicarbonate output from the isolated proximal duodenal test segment. A synthetic prostaglandin E1 analogue, misoprostol (1.67-13.3 micrograms/min), infused directly into proximal or distal test segments significantly stimulated bicarbonate outbreak; peak responses were 644 +/- 35 mumol/cm X h and 171 +/- 20 mumol/cm X h (p less than 0.001), respectively. Thus, in humans, the proximal and distal duodenal mucosa secretes bicarbonate at rest; direct acidification of the proximal duodenum stimulates bicarbonate output; acidification of the distal duodenum beyond the isolated test segment also increased proximal duodenal bicarbonate output; and a synthetic prostaglandin E1 analogue stimulated both proximal and distal bicarbonate output; however, distal duodenal bicarbonate output was significantly less, indicating a proximal-to-distal gradient in bicarbonate secretion.

Adult↗
PubMed2004

Heat-stable enterotoxin of Escherichia coli stimulates a non-CFTR-mediated duodenal bicarbonate secretory pathway.

The cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is an important pathway for duodenal mucosal bicarbonate secretion. Duodenal biopsies from CF patients secrete bicarbonate in response to heat-stable enterotoxin from Escherichia coli (STa) but not cAMP. To explore the mechanism of STa-induced bicarbonate secretion in CF more fully, we examined the role of CFTR in STa-stimulated duodenal bicarbonate secretion in mice. In vivo, the duodenum of CFTR (-/-) or control mice was perfused with forskolin (10(-4) M), STa (10(-7) M), uroguanylin (10(-7) M), 8-bromoguanosine 3',5'-cGMP (8-Br-cGMP) (10(-3) M), genistein (10(-6) M) plus STa, or herbimycin A (10(-6) M) plus STa. In vitro, duodenal mucosae were voltage-clamped in Ussing chambers, and bicarbonate secretion was measured by pH-stat. The effect of genistein, DIDS (10(-4) M), and chloride removal was also studied in vitro. Control, but not CF, mice produced a significant increase in duodenal bicarbonate secretion after perfusion with forskolin, uroguanylin, or 8-Br-cGMP. However, both control and CF animals responded to STa with significant increases in bicarbonate output. Genistein and herbimycin A abolished this response in CF mice but not in controls. In vitro, STa-stimulated bicarbonate secretion in CF tissues was inhibited by genistein, DIDS, and chloride-free conditions, whereas bicarbonate secretion persisted in control mice. In the CF duodenum, STa can stimulate bicarbonate secretion via tyrosine kinase activity resulting in apical Cl(-)/HCO(3)(-) exchange. Further studies elucidating the intracellular mechanisms responsible for such non-CFTR mediated bicarbonate secretion may lead to important therapies for CF.

Animals↗
PubMed1989

Bicarbonate abolishes intracellular alkalinization in mitogen-stimulated 3T3 cells.

An increase in intracellular pH (pHi) following mitogenic stimulation has been reported in a variety of mammalian cells (W. Moolenaar, Annu. Rev. Physiol., 48:363-376, 1986; E. Rozengurt, Science, 234:161-166, 1986). This increase is currently believed to constitute a "permissive" signal in the process of cell activation (A.E. Lagarde and J.M. Pouyssegur, Cancer Biochem. Biophys. 9:1-14, 1986). Since the majority of studies of this phenomenon have been conducted in the nonphysiological milieu of bicarbonate-free solutions, we have undertaken a study of the effects of bicarbonate and CO2 on mitogen-induced intracellular alkalinization in NIH 3T3 cells. Using nuclear magnetic resonance (NMR) spectroscopy and novel 31P NMR pH indicators (2-amino-phosphono-carboxylic acids) we found that mitogen induces an increase in pHi of 0.16 units only in cells bathed in medium containing low concentrations of bicarbonate (less than 1 mM) and not in cells bathed in medium containing physiological levels of bicarbonate (10-30 mM). In addition to abolishing the mitogen-induced alkalinization, bicarbonate stabilizes pHi at 7.25 units as the external pH (pHe) is varied from 7.0 to 7.6. In contrast, in a bicarbonate-free medium pHi increases from 6.9 to 7.3 over the same range of external pHs. At a constant external pH, increasing the bicarbonate/CO2 concentration results in an increase in pHi from 6.9 in bicarbonate-free solution to 7.25 in a bicarbonate-buffered medium. This relationship is hyperbolic with half-maximal effect occurring at a concentration of 0.4 mM bicarbonate at pH 7.05 and 37 degrees C. Our results suggest that the observations of mitogen-induced alkalinization may be due to the use of nonphysiological bicarbonate-free media. Since this increase in pHi is not observed in physiological media where bicarbonate concentrations are usually greater than 20 mM, we conclude that an increase in pHi is not an obligatory or usual part of the cellular response to growth factors in vivo.

Animals↗
PubMed1982

Carbonic anhydrase independent bicarbonate reabsorption.

The present study was designed to define the prerequisites of carbonic anhydrase independent bicarbonate reabsorption. In free flow experiments during systemic application of carbonic anhydrase inhibitor benzolamide (50 mg/kg B. W.) bicarbonate recovery in % of filtered load was found to be 74 +/- 8% in late proximal convoluted tubules, 39 +/- 6% in distal convoluted tubules and 32 +/- 4% in urine, indicating that most of carbonic anhydrase independent bicarbonate reabsorption occurs in tubule segments prior to distal convoluted tubules. In vivo continuous microperfusion experiments in proximal convoluted tubules demonstrated that luminal benzolamide (0.5 mmol/l) virtually abolishes net bicarbonate fluxes, when bicarbonate concentration in the luminal perfusate (25 mmol/l) is close to peritubular plasma concentration (24.4 mmol/l). In contrast, a significant downhill reabsorptive flux occurs, when perfusate bicarbonate concentration is 75 mmol/l and a significant downhill secretory flux is observed, when the perfusate is initially free of bicarbonate. The corresponding apparent permeabilities are 1.0 +/- 0.1 X 10(-6) cm2/s for influx and 1.6 +/- 0.4 X 10(-6) cm2/s for efflux of bicarbonate. Clearance studies reveal that carbonic anhydrase dependent and independent bicarbonate reabsorption are not saturable but depend on the rate of volume reabsorption in the kidney. In conclusion, passive movements of bicarbonate do occur in proximal convoluted tubules and most likely contribute to carbonic anhydrase independent bicarbonate reabsorption.

Absorption↗
PubMed1985

Rheogenic sodium-bicarbonate cotransport in the peritubular cell membrane of rat renal proximal tubule.

The mechanism of bicarbonate transport across the peritubular cell membrane was investigated in rat kidney proximal tubules in situ by measuring cell pH and cell Na+ activity in response to sudden reduction of peritubular Na+ and/or HCO3-. The following observations were made: 1. sudden peritubular reduction of either ion concentration produced the same transient depolarizing potential response; 2. bicarbonate efflux in response to peritubular reduction of bicarbonate was accompanied by sodium efflux; 3. sodium efflux in response to peritubular sodium removal was accompanied by cell acidification indicating bicarbonate efflux; 4. all aforementioned phenomena were inhibited by SITS (10(-3) mol/l) except for a small SITS-independent sodium efflux and depolarization which occurred in response to peritubular sodium removal and was not accompanied by cell pH changes; 5. bicarbonate efflux and accompanying potential changes in response to reduction of peritubular bicarbonate virtually vanished in sodium-free solutions. From these observations we conclude that bicarbonate efflux proceeds as rheogenic sodium-bicarbonate cotransport with a stoichiometry of bicarbonate to sodium greater than 1. The question which of the charged species of the bicarbonate buffer system moves cannot yet be decided. Attempts to determine the stoichiometry from the SITS-inhibitable initial cell depolarization and from the SITS-inhibitable initial fluxes suggest a stoichiometry of 3 HCO3-: 1 Na+. In addition to sodium-dependent bicarbonate flux, evidence was obtained for a sodium-independent transport system of acids or bases which is able to regulate cell pH even in sodium-free solutions.

Animals↗
PubMed1982

A demonstration of bicarbonate production by the normal human stomach in vivo.

Bicarbonate secretion by the stomach may play a role in gastric mucosal protection, and we have therefore examined bicarbonate secretion in the human stomach. Gastric bicarbonate production and contamination with salivary and duodenal bicarbonate was measured in healthy volunteers using an intubation technique. The stomach and duodenum were perfused with nonabsorbable markers and the pH, PCO2, marker, and amylase concentrations measured in 10-min gastric and duodenal aspirates. These measurements enabled calculation of gastric bicarbonate content and the amount of bicarbonate contributed by saliva and duodenogastric reflux. Acid secretion was suppressed by intravenous cimetidine. Validation studies demonstrated a good correlation between instilled and calculated recovered bicarbonate (r = 0.97, P less than 0.001, N = 6), and marker recovery was consistent in each subject. Over a 6-h period, gastric pH ranged from 6 to 7 and PCO2 from 20 to 40 mm Hg. Gastric bicarbonate output stabilized at 326--392 mumol/hr and mean bicarbonate concentration ranged from 2.3 to 20.0 mmol/liter. Approximately two thirds of this bicarbonate was free, 11% was derived from duodenogastric reflux, and 3% from swallowed saliva. This study demonstrates secretion of bicarbonate by the human stomach in vivo at a rate equivalent to 10--20% of basal acid secretion.

Adult↗
PubMed1990

Human duodenal mucosal bicarbonate secretion. Evidence suggesting active transport under basal and stimulated conditions.

When the proximal duodenum of animals or humans is perfused with isoosmolar NaCl, bicarbonate enters the luminal effluent. In addition, duodenal bicarbonate output is stimulated by luminal acidification and prostaglandins of the E class. The hypothesis that in vivo human duodenal bicarbonate transport persists in the absence of a plasma-to-lumen bicarbonate gradient and therefore is probably an active transport process was tested. In healthy subjects, a 4-cm segment of the proximal duodenum was isolated from gastric and pancreaticobillary secretions. Net duodenal bicarbonate secretion remained similar to basal levels during luminal perfusion with either 24 or 32 mM bicarbonate (each isoosmolar with plasma by the addition of NaCl). In addition, peak increases in acid-induced bicarbonate outputs with luminal perfusion of 154 mM NaCl and 32 mM NaHCO3 (+122 mM NaCl) were similar. Moreover, prostaglandin E2-stimulated bicarbonate secretion with perfusion of 154 mM NaCl and 32 mM NaHCO3 (+122 mM NaCl) was similar. It was concluded that in humans, proximal duodenal mucosal bicarbonate transport remains unaltered in the absence of a plasma-to-lumen bicarbonate gradient at rest and after stimulation with HCl or prostaglandin E2. These observations suggest that human proximal duodenal bicarbonate secretion involves active transport.

Adult↗
PubMed2004

Mobilization of arsenic from subsurface sediments by effect of bicarbonate ions in groundwater.

Arsenic leaching by bicarbonate ions has been investigated in this study. Subsurface sediment samples from Bangladesh were treated with different carbonate and bicarbonate ions and the results demonstrate that the arsenic leaching efficiency of the carbonate solutions decreased in the order of Na2CO3>NaHCO3>BaCO3>MnCO3. Sodium carbonate and bicarbonate ions extracted arsenic most efficiently; Na2CO3 leached maximum 118.12 microg/l of arsenic, and NaHCO3, 94.56 microg/l of arsenic from the Ganges delta sediments after six days of incubation. The arsenic concentrations extracted in the batch experiments correlated very well with the bicarbonate concentrations. The kinetics study of arsenic release indicates that arsenic-leaching rate increased with reaction time in bicarbonate solutions. Bicarbonate ions can extract arsenic from sediment samples in both oxic and anoxic conditions. A linear relationship found between arsenic contents in core samples and those in leachates suggests that dissolved arsenic concentration in groundwater is related to the amount of arsenic in aquifer sediments. In batch experiment, bicarbonate solutions effectively extracted arsenic from arsenic adsorbed iron oxyhydroxide, reflecting that bicarbonate solutions may mobilize arsenic from iron and manganese oxyhydroxide in sediments that are ubiquitous in subsurface core samples. Carbonate ion may form complexes on the surface sites of iron hydroxide and substitute arsenic from the surface of minerals and sediments resulting in release of arsenic to groundwater. Like in the batch experiment, arsenic and bicarbonate concentrations in groundwater of Bangladesh correlated very well. Therefore, bicarbonate leaching is presumed to be one important mechanism to mobilize arsenic in bicarbonate dominated reducing aquifer of Bangladesh and other parts of the world as well.

Arsenic↗
PubMedDate not supplied

Effects of sodium bicarbonate on fluid, electrolyte and acid-base balance in racehorses.

Sodium bicarbonate given by nasogastric tube has been used by some trainers as the key ingredient in a 'milkshake'. It has been suggested that such treatment given 3-5 h prior to racing may enhance a horse's racing performance by increasing the blood buffering capacity and enhancing lactate clearance from skeletal muscle, thereby delaying the onset of fatigue. Several experiments were conducted to examine the effects on fluid, electrolyte and acid-base values of 0.5 g kg-1 dose of sodium bicarbonate, were examined. The effects of fasting, the simultaneous administration of glucose (0.5 g kg-1) or the withholding of water were also examined to determine whether they influenced the uptake and elimination of sodium bicarbonate. Six Thoroughbred horses were used, each wearing a urine and faecal collection harness. Prior to sodium bicarbonate administration, venous blood, urine and faecal samples were collected for 24 h to establish control values. After administration of sodium bicarbonate (0.5 g kg-1) in 2 l of water, samples were collected at various times for up to 46 h. There were significant increases in water consumption, from 0.5-2.3 l h-1 at 2 h post-administration. Urine output increased by approximately three fold and did not return to control levels until 18 h post-administration. Urinary sodium concentration increased from 95 +/- 16 mmol l-1 (mean +/- SEM) to peak values of 349 +/- 12 mmol l-1 at 12 h. In the 24 h after sodium bicarbonate administration, approximately 80% of the sodium intake (NaHCO3+feed) was excreted in the urine. There was no significant change in the total urinary potassium and chloride excretion. Faecal water content did not change following sodium bicarbonate administration, but there was an increase in faecal sodium content. The mean increase in venous blood bicarbonate concentration was 7.6 +/- 0.4 mmol l-1 after the 0.5 kg-1 dose. Water deprivation for 6 h after sodium bicarbonate administration, fasting or the co-administration of glucose did not affect the peak blood bicarbonate concentration or the time to peak concentration. However, the withholding of water did result in a faster rate of decrease in blood bicarbonate concentration when water was resupplied.

Acid-Base Equilibrium↗