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PubMed1985

New observations on bicarbonate-pH effects on thickness changes of rabbit corneas under silicone oil in vitro.

Specular microscopy was used to measure thickness changes of stroma-endothelium preparations from rabbit corneas in vitro. The preparations were first bathed on both sides for 90 min with different bicarbonate-Ringer solutions (2 to 50 mM bicarbonate) maintained in equilibrium with 5% CO2-air (pH 6.2 to 7.9). During this equilibration, the stroma attained a stable thickness that was inversely related to the hydrostatic pressure (20 to 100 cm H2O) applied to the endothelial surface. After equilibration and at 20 cm H2O pressure, covering the anterior stromal surface with silicone oil (Dow Corning 200 dielectric fluid, 20 cs viscosity) resulted in stromal thinning. The rate of this deturgescence increased (from 5 to 75 micron/h) as the equilibration solution bicarbonate level increased from 2 to 30 mM. The net size of the thickness change was also related to the equilibration bicarbonate level. However, indirect studies on the cornea using phenol red indicator and pH electrode measurements of solutions revealed that the stromal bathing solutions became more alkaline under the silicone oil layer. CO2 is soluble in silicone oil. Implications of these CO2 and pH effects on mechanisms of corneal deturgescence are discussed.

Animals↗
PubMed1990

Human duodenal mucosal bicarbonate secretion--physiological and clinical aspects.

Over the past few years, we have addressed some of the components that regulate human duodenal bicarbonate secretion (DBS) using a technique for the isolation of a 4-cm duodenal segment from gastric, pancreaticobiliary and distal intestinal secretions. Our observations are summarized as follows. Resting DBS is, to a large extent, maintained by vagal innervation; atropine decreases basal bicarbonate secretion by approximately 80%. Luminal acidification with HCI (H+) is a major physiological stimulus of DBS, resulting in a prompt and significant increase of 3- to 4-fold. H(+)-stimulated DBS is likely to be mediated, at least in part, by prostaglandins of the E class, and by VIP. Each of the latter stimulates DBS independently in a dose-related manner. Since atropine is without effect on the response induced by luminal H+ and sham feeding, in both cases DBS is probably stimulated via a non-cholinergic pathway(s). Moreover, since basal, H(+)- and PGE2-stimulated proximal DBS are unaltered when the plasma-to-lumen bicarbonate concentration gradient is abolished, it may be concluded that DBS in humans involves active transport processes. It is significant that compared to normal subjects, patients with duodenal ulcers show markedly diminished basal and H(+)-stimulated proximal DBS. Furthermore, there is surprisingly little overlap between duodenal ulcer (DU) patients and normal subjects. These findings suggest that an intrinsic cellular or subcellular defect in proximal duodenal mucosal bicarbonate secretion is present in patients with duodenal ulcer disease.

Acid-Base Equilibrium↗
PubMed2001

The stoichiometry of the electrogenic sodium bicarbonate cotransporter pNBC1 in mouse pancreatic duct cells is 2 HCO(3)(-):1 Na(+).

The electrogenic sodium bicarbonate cotransporter pNBC1 is believed to play a major role in the secretion of bicarbonate by pancreatic duct cells, by transporting bicarbonate into the cell across the basolateral membrane. Thermodynamics predict that this function can be achieved only if the reversal potential of the cotransporter is negative to the cell's membrane potential, or equivalently that the HCO3-:Na+ stoichiometry is not larger then 2:However, there are no data available on either the reversal potential or the HCO3-:Na+ stoichiometry of pNBC1 in pancreatic cells. We studied pNBC1 function in mouse pancreatic duct cells. RT-PCR analysis of total RNA revealed that these cells contain the message for pNBC1, but not for kNBC1, NBC2 or NBC3. To measure cotransporter activity, mouse pancreatic duct cells were grown to confluence on a porous substrate, mounted in an Ussing chamber, and the apical plasma membrane permeabilized with amphotericin B. Ion flux through pNBC1 was achieved by applying Na+ concentration gradients across the basolateral plasma membrane. The current through the cotransporter was isolated as the difference current due to the reversible inhibitor dinitrostilbene disulfonate (DNDS). Current-voltage relationships for the cotransporter, measured at three different Na+ concentration gradients, were linear over a range of about 100 mV. The reversal potential data, obtained from these current-voltage relationships, all corresponded to a 2 HCO3-:1 Na+ stoichiometry. The data indicate that pNBC1 is functionally expressed in mouse pancreatic duct cells. The cotransporter operates with a 2 HCO3-:1 Na+ stoichiometry in these cells, and mediates the transport of bicarbonate into the cell across the basolateral membrane.

Animals↗
PubMed1984

Permeability of the human placenta to bicarbonate: in-vitro perfusion studies.

The effect of maternal acidosis on fetal acid-base balance was studied in a dual circuit perfusion of a single cotyledon in normal, term, human placentas. Both the fetal and maternal (intervillous) circulations were perfused with a Krebs-Ringer solution adjusted to pH values between 7.35 and 7.45. After a control period, the perfusate in the maternal circulation was replaced by an acidified medium (mean pH 7.06) for 30 min. This was followed by a second control period of 30 min during which the acidified maternal perfusate was replaced with the original medium. During the 30 min of maternal acidosis, fetal vein pH was not significantly altered despite the large decrease in maternal artery pH, but there was an efflux of total CO2 (tCO2) from the placenta into the maternal circulation which was not matched by an influx of tCO2 from the fetal circulation. The tCO2 transferred was in the form of bicarbonate rather than dissolved CO2, but the maximal rate of tCO2 transfer of in the form of bicarbonate was lower than the rate of placental transfer of tCO2 necessary in vivo. It is probable therefore that bicarbonate does not play a major role in placental CO2 transfer but the placental tissue bicarbonate pool may play an important part in buffering the fetus against changes in maternal pH or blood gas status.

Acidosis↗
PubMed1998

Bicarbonate and bicarbonate/lactate peritoneal dialysis solutions for the treatment of infusion pain.

A randomized, double-blind, cross-over study was undertaken to determine the effects of novel bicarbonate (38 mM) and bicarbonate (25 mM)/lactate (15 mM) containing peritoneal dialysis (PD) solutions on infusion pain in patients who experienced inflow pain with conventional lactate (40 mM) solution. Pain was assessed using a verbal rating scale and the validated McGill Pain Questionnaire (MPQ). Eighteen patients were recruited to the study. Both novel solutions resulted in highly statistically significant reductions in inflow pain compared to the control lactate solution, as assessed with both the verbal rating scale and the MPQ. For all pain variables assessed, the bicarbonate/lactate solution was more effective than the bicarbonate solution in alleviating pain. In conclusion, both solutions reduced the infusion pain experienced with control solution, but the bicarbonate/lactate solution appears to be the most effective. In contrast to the most widespread current treatment, which is the manual injection of sodium bicarbonate, the bicarbonate/lactate solution does not have the associated increased risk of peritonitis.

Bicarbonates↗
PubMed1982

Utilization of bicarbonate for base repletion in hemodialysis.

Because of physiochemical considerations, acetate rather than bicarbonate has traditionally been used as the base repletion agent in dialysate. There are major differences in the mechanisms through which these agents neutralize the body's acid load in the circumstance of dialysis. Acetate dialysis relies on metabolism of acetate to generate bicarbonate. Loss of bicarbonate into the dialysate requires that acetate dialysis supply base far in excess of that required to buffer metabolic hydrogen ion generation alone. Consequently, net accrual of base is difficult to quantitate and may be inadequate to neutralize the excess hydrogen ion, leading to chronic buffer depletion. However, acute acid-base problems are usually avoided because of the indirect nature of base addition. In contrast, net base accrual with bicarbonate dialysis occurs in a direct and quantitative manner. While inadequate base repletion is avoided, the direct addition of base requires much tighter control if undesirable acute changes in blood pH are to be avoided.

3-Hydroxybutyric Acid↗
PubMed1990

Kinetic modeling of intradialytic and interdialytic pH shifts during and after acetate and bicarbonate hemodialysis.

A kinetic model involving intraerythrocytic and whole blood H+ concentrations during and after bicarbonate and acetate hemodialysis is proposed to account for experimental data. A two-compartment model appeared to be the simplest kinetic model to explain the decrease in proton concentration during bicarbonate hemodialysis and its increase between two dialysis sessions, whether acetate or bicarbonate. This model takes into account the hemoglobin buffer power and the cellular metabolic acidosis. During acetate hemodialysis, one must introduce a new compartment to explain the initial increase in H+ concentration in erythrocytes. This compartment, which generates protons, seems to correspond to the carbonic anhydrase cycle. The various parameters obtained show no significant variations between patients receiving bicarbonate hemodialysis. For acetate hemodialysis, the model describes equally well patients with a great initial increase in H+ concentration and those with a slight initial increase. The variations observed in the parameters are due mainly to the carbonic anhydrase compartment. It is suggested the magnitude of this initial increase and the degree of acetate intolerance are correlated.

Acetates↗
PubMed2002

Hypertonic sodium bicarbonate for Taxus media-induced cardiac toxicity in swine.

OBJECTIVE: To determine whether intravenous (IV) hypertonic sodium bicarbonate is effective in the reversal of QRS widening associated with severe Taxus intoxication. METHODS: Seventeen anesthetized and instrumented swine were poisoned with an IV extract of Taxus media until doubling of the QRS interval on electrocardiography was achieved. After poisoning (time zero), the animals received either 4 mL/kg IV 8.4% sodium bicarbonate (experimental group; 6 animals), a similar volume of 0.7% NaCl in 10% mannitol (mannitol group; 6 animals), or nothing (control group; 5 animals). The main outcome parameter was QRS duration. Secondary outcome parameters were mean arterial pressure (MAP), heart rate (HR), and cardiac index (CI = cardiac output/kg). Additionally, arterial pH, partial pressure of carbon dioxide (pCO(2)), and plasma-ionized calcium, sodium, and potassium were monitored. RESULTS: Taxus toxicity, defined as a 100% increase in QRS duration, was produced in all animals. The animals were similar in regard to baseline and time 0 physiologic parameters as well as amount of Taxus media extract administered. From times 5 through 30 minutes, following assigned treatment, significant increases in QRS duration were detected in the experimental and mannitol groups compared with the control group. A significant lowering of MAP was found in the experimental group compared with the control group. No significant difference between groups was noted in HR or CI. The swine treated with hypertonic sodium bicarbonate had a statistically significant increase in pH, plasma sodium concentration, and base excess compared with the other groups. CONCLUSIONS: Hypertonic sodium bicarbonate was ineffective in reversing the widening of QRS interval associated with Taxus poisoning in this swine model.

Animals↗
PubMed1976

Significance of the extracellular bicarbonate buffer system to anaerobic glycolysis in hypoxic muscle.

1. The influence of the carbon dioxide-bicarbonate buffer system on anaerobic energy production during severe hypoxia was studied in isolated right hemidiaphragms of rats.--2. When the tissue was incubated in a Ringer solution containing 25 mM HCO-3 aerated with 7% CO2 in N2 at pH 7.4, the lactate production and lactate content of the tissue increased.--3. At an extracellular (tissue bath) pH OF 6.9 the lactate production was stimulated when carbon dioxide and bicarbonate were changed to 19% and 25 mM, respectively. This stimulatory effect disappeared when these values were lowered to 7% and 7 mM.--4. At pH 7.4 the stimulatory effect of the carbon dioxide-bicarbonate system persisted when the buffer value was lowered from 60 to 3 mM by changing the system from an open (i.e. continuous gas equilibration) to a closed one (i.e. without any gas phase). Decreasing the glucose in the media from 22 to 0 mM reduced the lactate production and abolished the stimulatory effect of the carbon dioxide--bicarbonate system.--5. There was no direct effect of this system on the glycolytic enzymes (i.e. lactate production and activity of phosphofructokinase of homogenates).

Animals↗
PubMedDate not supplied

Accidental acute metabolic acidosis due to inappropriate selection of bicarbonate concentrate.

Haemodialysis using a bicarbonate concentrate (bicarbonate dialysis) is the treatment modality of choice for correction of metabolic acidosis in chronic renal failure. However, improper ratios of acid and bicarbonate concentrates in dialysis fluid can result in an iatrogenically induced metabolic acidosis. The following report presents a case of acute metabolic acidosis, which resulted from the accidental use of an inappropriate bicarbonate concentrate for haemodialysis treatment. Awareness of the problem and a rapid examination of the dialysis fluid in patients who unexpectedly deteriorate rather than improve with haemodialysis may help in averting potentially severe complications due to errors in the concentrate selection. Conductivity cell devises are not suitable for the control of the acid-base composition of the dialysis fluid (dialysate), therefore, monitoring of the dialysate pH in addition to conductivity should become part of the equipment in haemodialysis machines.

Acidosis↗
PubMed1966

The relation between the concentrations of bicarbonate and protein in the pancreatic juice in the dog.

1. In accordance with the admixture theory of the exocrine pancreatic secretion a linear relation between concentrations of bicarbonate and protein in the pancreatic juice is to be expected.2. Pancreatic juice was obtained through a Thomas cannula in three unanaesthetized dogs during digestion of a meal.3. The actual concentration of bicarbonate and protein showed a good approximation to a straight-line relation.4. The calculated concentration of bicarbonate in the distal secretion was nearly identical with the highest concentration of bicarbonate obtained in the pancreatic juice after stimulation with secretin.

Animals↗
PubMed1976

The bicarbonate ion pump in the endothelium which regulates the hydration of rabbit cornea.

1. Studies were made on the short-circuit current (s.c.c.) and fluid transport across rabbit corneal endothelium. 2. Normal s.c.c. of 27 muA.cm-2 is reduced to 19 muA.cm-2 in CO2-free Ringer, to 9 muA. cm-2 in HCO-3 -free Ringer and to zero in CO2 and HCO-3 -free Ringer. 3. Carbonic anhydrase inhibitors reduce s.c.c. from 27 to 19 muA.cm-2. Removal of exogenous CO2 causes no further reduction in s.c.c. 4. In CO2-free Ringer, net exogenous bicarbonate translocation is equal to s.c.c. 5. In all cases studied, net fluid transport across the endothelium in open circuit is directly proportional to s.c.c. 6. It is concluded that the endothelial 'pump' which regulates corneal hydration operates by 'pumping' bicarbonate ions into the aqueous humour. 7. Under physiological conditions, two thirds of the substrate is supplied by exogenous bicarbonate ions and one third is supplied by conversion of exogenous CO2 by intracellular carbonic anhydrase. 8. Metabolic CO2 does not participate significantly in the process, probably because it is at too low a concentration to compete effectively with exogenous CO2. 9. Electron histochemical studies suggest that carbonic anhydrase is located immediately underneath the posterior membrane of the endothelium, across which the active bicarbonate ion flux passes.

Animals↗
PubMed1998

Sodium bicarbonate ingestion does not attenuate the VO2 slow component during constant-load exercise.

We examined the effects of sodium bicarbonate ingestion on the VO2 slow component during constant-load exercise. Twelve physically active males performed two 30-min cycling trials at an intensity above the lactate threshold. Subjects ingested either sodium bicarbonate (BIC) or placebo (PLC) in a randomized, counterbalanced order. Arterialized capillary blood samples were analyzed for pH, bicarbonate concentration ([HCO3-]), and lactate concentration ([La]). Expired gas samples were analyzed for oxygen consumption (VO2). The VO2 slow component was defined as the change in VO2 from Minutes 3 and 4 to Minutes 28 and 29. Values for pH and [HCO3-] were significantly higher for BIC compared to PLC. There was no significant difference in [La] between conditions. For both conditions there was a significant time effect for VO2 during exercise; however, no significant difference was observed between BIC and PLC. While extracellular acid-base measures were altered during the BIC trial, sodium bicarbonate ingestion did not attenuate the VO2 slow component during constant-load exercise.

Adult↗
PubMed2002

The cation transporters rOCT1 and rOCT2 interact with bicarbonate but play only a minor role for amantadine uptake into rat renal proximal tubules.

In renal proximal tubules, the organic cation transporters rOCT1 and rOCT2 are supposed to mediate the first step in organic cation secretion. We investigated whether previously described differences in amantadine and tetraethylammonium (TEA) uptake into isolated renal proximal tubules could be explained by differences in their transport by rOCT1 and rOCT2. By expressing rOCT1 and rOCT2 in Xenopus oocytes and HEK 293 cells, we demonstrated that both transporters translocated amantadine. In Xenopus oocytes, the inhibitory potency of several rOCT1/2 inhibitors was similar for amantadine compared to TEA uptake and supports amantadine transport by rOCT1 and rOCT2. In proximal tubules, procainamide, quinine, cyanine(863), choline, and guanidine in concentrations that inhibit rOCT1/2-mediated TEA or amantadine uptake in Xenopus oocytes exhibited no effect on amantadine uptake. At variance, these inhibitors blocked TEA uptake into proximal tubules. Amantadine and TEA transport were sensitive to modulation by 25 mM bicarbonate. The effect of bicarbonate on organic cation transport was dependent on substrate (amantadine or TEA), cell system (oocytes, HEK 293 cells, or proximal tubules), and transporter (rOCT1 or rOCT2). In proximal tubules, only amantadine uptake was stimulated by bicarbonate. The data suggested that rat renal proximal tubules contain an organic cation transporter in addition to rOCT1 and rOCT2 that mediates amantadine uptake and requires bicarbonate for optimal function. TEA uptake by the basolateral membrane may be mediated mainly by rOCT1 and rOCT2, but these transporters may be in a different functional or regulatory state when expressed in cells or oocytes compared with expression in vivo.

Amantadine↗
PubMed2006

Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate.

OBJECTIVE: This study aimed to determine the extent of agreement between central venous and arterial values for pH, bicarbonate, base excess, and lactate in a group of intensive care unit (ICU) patients. METHODS: A prospective study of a convenience sample of patients deemed by their treating doctor to require blood gas analysis as part of their clinical care in ICU. It compared pH, bicarbonate, base excess and lactate on arterial and central venous samples taken within five minutes of each other. Data were analysed using bias (Bland-Altman) methods. RESULTS: A total of 168 matched sample pairs from 110 patients were entered into the study. All variables showed close agreement. The mean difference between arterial and venous values of pH was 0.03 pH units, for bicarbonate 0.52 mmol/l, for lactate 0.08 mmol/l, and for base excess 0.19 mmol/l. All showed acceptably narrow 95% limits of agreement. CONCLUSION: Central venous pH, bicarbonate, base excess, and lactate values showed a high level of agreement with the respective arterial values, with narrow 95% limits of agreement. These results suggest that venous values may be an acceptable substitute for arterial measurement in this clinical setting.

Acid-Base Imbalance↗
PubMed1984

Effect of vasoactive intestinal polypeptide and somatostatin on secretion of epidermal growth factor and bicarbonate from Brunner's glands.

The effect of VIP and somatostatin on secretion of epidermal growth factor and bicarbonate from Brunner's glands was investigated in the rat. Vasoactive intestinal polypeptide infused in doses of 10 and 100 ng/kg/h significantly increased epidermal growth factor and bicarbonate output, but the concentrations did not change. Somatostatin infused at doses of 1, 10, 100 and 1000 ng/kg/h against a background of VIP 100 ng/kg/h inhibited in dose-dependent fashion the stimulated epidermal growth factor and bicarbonate outputs from rat Brunner's gland pouches. Also basal secretion was inhibited by somatostatin. Infusion of antisomatostatin serum stimulated Brunner's gland secretion. By immunohistochemical studies of rat duodena, it was found that epidermal growth factor, is almost exclusively present in the secretory cells of Brunner's glands. It is concluded that VIP stimulates secretion of epidermal growth factor and bicarbonate from Brunner's glands, an effect which is inhibited by somatostatin. A possible role for somatostatin in the control of Brunner's gland secretion is suggested.

Animals↗
PubMed1987

Effect of luminal pH on the output of bicarbonate and PGE2 by the normal human stomach.

The gastric output of bicarbonate and prostaglandin E2 has been calculated using a perfusion technique before and after instillation of 100 mM hydrochloric acid into the stomach of seven healthy volunteers. A significant increase in bicarbonate output occurred from 258 +/- 38 mumol/30 min during the basal period to 531 +/- 86 mumol/30 min after return of the intragastric pH to neutral (p less than 0.05). Prostaglandin E2 output also increased significantly from 410 +/- 136 pmol/30 min to 1002 +/- 194 pmol/30 min (p less than 0.05). The changes were caused mainly by an increase in gastric secretory volume with only non-significant increases in concentrations of bicarbonate and prostaglandin E2. The results suggest that mechanisms exist to adjust the rate of gastric bicarbonate secretion to the prevailing intraluminal pH and that this may occur through the release of prostaglandin E2.

Adult↗
PubMed1989

Duodenal mucosal bicarbonate secretion in man. Stimulation by acid and inhibition by the alpha 2-adrenoceptor agonist clonidine.

A multi-channel small diameter tube was used to study the secretion of bicarbonate by 3 cm long segments of the proximal duodenum isolated between balloons. The tube had an outer diameter of 5.3 mm and two central and four smaller, peripheral channels. Measurements of infused phenol red, 14C-PEG and vitamin B12 and of trypsin activity were performed to rule out contamination of the perfusate by gastric and pancreatic secretions. Basal secretion of bicarbonate by the duodenal mucosa in healthy subjects varied between 135 and 220 mumol/cm of intestine per hour. Perfusion of the lumen with acid (100 mM HCl for five minutes) increased the secretion to greater than 400 mumol/cm/h and the alpha 2-adrenoreceptor agonist clonidine (150 micrograms iv) decreased the HCO3- secretion by 70 mumol/cm/h. Clonidine simultaneously reduced the mean arterial blood pressure and plasma noradrenaline concentration, but did not affect the plasma glucose or adrenaline concentration. Duodenal bicarbonate secretion is important in the protection of this mucosa against acid discharged from the stomach. Increased sympathetic activity may, by inhibiting the bicarbonate secretion, decrease the protection in proximal duodenum in man and facilitate ulceration.

Adult↗