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PubMed1985

Deoxycorticosterone-stimulated bicarbonate secretion in rabbit cortical collecting ducts: effects of luminal chloride removal and in vivo acid loading.

To assess the role of cortical collecting duct bicarbonate secretion in the regulation of net acid excretion, we have sought to identify what factors influence the secretion rate. Net and unidirectional bicarbonate fluxes were measured in isolated perfused cortical collecting ducts from deoxycorticosterone-treated rabbits. The collecting ducts secreted bicarbonate at 11-24 pmol X mm-1 X min-1, confirming the high rate seen in earlier studies. Oral acid loading (50 mM NH4Cl drinking water) completely inhibited the net bicarbonate secretion. The bath-to-lumen flux was markedly reduced with acid loading, but the lumen-to-bath flux changed very little. In tubules from rabbits treated with deoxycorticosterone (but not NH4Cl), luminal chloride replacement with either sulfate or gluconate completely and reversibly inhibited the net bicarbonate secretion. The bath-to-lumen flux was greatly inhibited, but there was little change in the lumen-to-bath flux. We conclude: 1) High rates of bicarbonate secretion can be induced in rabbit cortical collecting ducts by chronic treatment of the animals with deoxycorticosterone. 2) When deoxycorticosterone-treated rabbits were made acidotic by oral administration of NH4Cl, the bicarbonate secretion was prevented, indicating that the systemic acid-base state of the animal may be an important factor regulating bicarbonate secretion. 3) Replacement of chloride in the lumen with sulfate inhibits bicarbonate secretion in the cortical collecting duct, an effect which may explain in part the decrease in urinary pH in response to sulfate infusions in mineralocorticoid-stimulated animals.

Acid-Base Equilibrium↗
PubMed1986

Bicarbonate transport by amphibian nephron.

To determine the site of bicarbonate reabsorption, tubular fragments from five different segments of the salamander nephron (Ambystoma) were perfused in vitro. Bicarbonate contents (total CO2) of tubular fluid were determined by microcalorimetry. Bicarbonate was not transported by the diluting segment or the mid-distal tubule. Although proximal tubule fragments did appear to reabsorb bicarbonate (10.8 +/- 3.7 pmol X mm-1 X min-1, P less than 0.01, n = 14), the chemical gradients observed were small with respect to the sensitivity of our methods. In the late distal tubule (LDT), bicarbonate reabsorption averaged 28.9 +/- 8.2 pmol X mm-1 X min-1 (P less than 0.01, n = 16). Transport in this segment was inhibited by ethoxzolamide or by perfusing with a sodium-free solution. Ethoxzolamide had no effect on the trans-epithelial voltage. Thus bicarbonate is reabsorbed by the LDT of amphibia via a mechanism that is dependent on carbonic anhydrase and the presence of luminal sodium. The 13 initial collecting tubules (ICT) studied did not appear to reabsorb bicarbonate. On the other hand, some ICT developed substantial bicarbonate gradients. Therefore this nephron segment has the capacity to reabsorb bicarbonate.

Ambystoma↗
PubMed2002

Relation between bicarbonate concentration and voltage dependence of sodium currents in freshly isolated CA1 neurons of the rat.

It recently has been shown that whole cell calcium and sodium currents are modulated by CO(2)/HCO(3)(-)-buffered saline. While the bicarbonate ion, but not CO(2), has been proven to modulate calcium currents, this information is lacking for sodium currents. Furthermore, it is not known whether the strength of modulation dependents on the bicarbonate concentration or whether it is an all-or-nothing phenomenon. To answer these questions, we used the whole cell voltage-clamp technique on freshly isolated hippocampal CA1 neurons from the rat. A voltage step from -130 to -20 mV elicited a sodium current with an amplitude of -5.1 +/- 0.5 nA (mean +/- SE, n = 17) when cells were superfused with HEPES-buffered saline. The amplitude of this current increased during a subsequent superfusion with solutions containing increasing amounts of bicarbonate and CO(2) (%CO(2)/mM HCO(3)(-): 2.5/5.6; 5.0/18; 10/37), with a maximal increment in 10% CO(2)/37 mM HCO(3)(-) of -6.9 +/- 0.8 nA. The increase in amplitude was associated with a linear negative shift (slope: -0.7 mV/mM HCO(3)(-)) of the potential of half-maximal activation (DeltaV(h,a): -19.4 +/- 1.8 mV in 10% CO(2)) but not with an alteration in the maximal conductance (g(max): HEPES: 203.1 +/- 21.0 nS and 10% CO(2)/37 mM HCO(3)(-): 207.3 +/- 21.3 nS). In addition, the potential of half-maximal inactivation (V(h,i)) shifted to more negative potentials (slope: -0.6 mV/mM HCO(3)(-)) with increasing amounts of bicarbonate and CO(2) (HEPES: -53.6 +/- 11.8 mV; 10% CO(2)/37 mM HCO(3)(-): -69.8 +/- 2.1 mV), making the amplitude of the current highly sensitive for small potential changes at resting membrane potential. The same negative shift in voltage dependence arose when cells were exposed to solutions with different amounts of bicarbonate (5.6; 18; 26 mM) but constant CO(2) (5%) with slope rates of -0.5 mV/mM HCO(3)(-) for V(h,a) and -0.5 mV/mM HCO(3)(-) for V(h,i). Again, there was no correlation between bicarbonate concentration and the size of g(max). When currents were evoked in solutions containing a constant concentration (18 mM) of bicarbonate but different amounts of CO(2) (2.5; 5.0 10%), no significant changes have been observed. The present data demonstrate that bicarbonate ions, and not CO(2), modulate voltage-gated sodium currents in a concentration-dependent manner. Because the amplitude of the sodium current becomes highly sensitive to membrane potential changes concomitant with increased bicarbonate amounts, this may be critical for the excitability of the neuronal network in situations (like metabolic acidosis, respiratoric alkalosis and hypercapnia) in which the concentration of this ion can alter.

Algorithms↗
PubMed1996

Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalemia in end-stage renal disease patients.

This study was performed to evaluate the efficacy of various treatment modalities for hyperkalemia in 8 end-stage renal disease (ESRD) patients. Simultaneous administration of sodium bicarbonate and insulin with glucose was compared with infusion of either bicarbonate alone or insulin and glucose. Plasma potassium was measured at the baseline and after 60 min of infusion with each regimen. Infusion of 8.4% solution of sodium bicarbonate at 2 mEq/min for 60 min induced a significant rise in blood bicarbonate from 21.7 +/- 2.1 to 26.3 +/- 1.7 mEq/l (p < 0.01), but failed to lower plasma potassium (6.4 +/- 0.1 vs. 6.3 +/- 0.2 mEq/l, before and after). Intravenous infusion of insulin and glucose (5 mU/kg/min for 60 min) significantly lowered plasma potassium from 6.3 +/- 0.1 to 5.7 +/- 0.1 mEq/l (p < 0.01). The combined infusion of bicarbonate and insulin with glucose showed the greatest decline in plasma potassium, from 6.2 +/- 0.2 to 5.2 +/- 0.1 mEq/l (p < 0.01). With the combined regimen, the increases in plasma bicarbonate (22.3 +/- 1.7 to 25.8 +/- 1.9 mEq/l, p < 0.05) and blood pH (7.36 +/- 0.02 to 7.42 +/- 0.02, p < 0.01) were significant, but somewhat less than those with bicarbonate administration alone. Plasma insulin levels before treatment were similar in all treatment regimens, and increased markedly following the infusion of insulin with glucose, either with or without sodium bicarbonate (9 +/- 1.5 vs. 10 +/- 10 microU/ml before insulin, and 196 +/- 18.0 vs. 201 +/- 26.4 microU/ml after insulin). Plasma epinephrine, norepinephrine, osmolality and plasma aldosterone before and after treatment did not show any significant differences among the 3 different regimens. In conclusion, the ineffectiveness of sodium bicarbonate alone and its synergistic effect with insulin and glucose in acute therapy of hyperkalemia in ESRD patients suggest that mild metabolic acidosis, which is common in patients on maintenance hemodialysis, may contribute to tissue insensitivity to the action of insulin on transcellular potassium shift.

Adult↗
PubMed1982

Does basal cholinergic activity potentiate exogenous secretin for stimulation of pancreatic bicarbonate output in dogs?

In conscious dogs with gastric and pancreatic Thomas fistulas, we studied the effect of atropine sulfate (20 micrograms kg-1 h-1 intravenously) on bicarbonate output basally and in response to intravenous infusion of synthetic secretin (62.5, 125, 250, 500, 1,000 and 2,000 ng kg-1 h-1). We analyzed the data in an attempt to determine whether basal cholinergic activity potentiates the pancreatic bicarbonate response to secretin. Assuming that atropine suppresses all basal cholinergic activity, C (= bicarbonate response to basal cholinergic activity alone) was calculated by subtracting basal pancreatic bicarbonate output with atropine from that without atropine, S (= response to secretin alone) was calculated by subtracting basal pancreatic bicarbonate output with atropine from that in response to secretin with atropine. SwC was defined as the response to secretin acting simultaneously with (w) basal cholinergic activity and was calculated by subtracting basal pancreatic bicarbonate output with atropine from the response to secretin without atropine. If SwC was significantly greater than S + C (= sum of effects of stimulus alone and basal cholinergic activity alone) potentiation between basal cholinergic activity and secretin was assumed to exist. C was 30 +/- 9 mumol 15 min-1 for bicarbonate output. SwC of bicarbonate output was significantly (p less than 0.05) greater than S + C in response to the four lowest doses (62.5-500 ng kg-1 h-1) of secretin. We conclude that potentiation exists between basal cholinergic activity and low doses of exogenous secretin. Thus, basal cholinergic activity is an important modulator of pancreatic bicarbonate response to secretin.

Animals↗
PubMed1970

Mechanism of bicarbonate absorption and its relationship to sodium transport in the human jejunum.

Using a constant perfusion technique, sodium and bicarbonate absorption was studied in human subjects. The following observations were made on sodium absorption from saline solution: (a) the rate of sodium absorption is markedly influenced by bulk water flow, (b) when net water flow is zero, sodium absorption is zero if there are no concentration gradients between plasma and lumen that favor net NaCl diffusion; and (c) the PD between abraded skin and jejunal lumen is near zero when saline is perfused and does not change with partial substitution of sulfate or bicarbonate for chloride. Based on these observations, we conclude that sodium absorption from saline is entirely passive in the human jejunum. On the other hand, in the presence of bicarbonate sodium is absorbed actively against electrochemical gradients. The mechanism of the link between bicarbonate and sodium absorption was studied in normal subjects and in 11 patients with pernicious anemia; the latter were chosen because they do not secrete gastric acid which can react with bicarbonate in the jejunal lumen. We observed that bicarbonate absorption (a) occurs against steep electrochemical gradients, (b) does not generate a potential difference between abraded skin and jejunal lumen, (c) is inhibited by acetazolamide, and (d) generates a high CO2 tension in jejunal fluid. These observations suggest that bicarbonate absorption is mediated by active hydrogen secretion, rather than by bicarbonate ion transport per se, and that the link between sodium and bicarbonate transport is best explained by a sodium-hydrogen exchange process.

Acetazolamide↗
PubMed1972

Glucose-induced alkalosis in fasting subjects. Relationship to renal bicarbonate reabsorption during fasting and refeeding.

This study documents the development of alkalosis in patients returning to caloric intake after a period of starvation and investigates the mechanisms responsible for this metabolic alteration. We studied the acid-base status, bicarbonate reabsorption, acid excretion, and sodium metabolism during fasting and glucose refeeding in 19 patients receiving sodium supplements. Metabolic alkalosis developed promptly in all of the subjects who terminated an 18 day fast with 300 g of glucose daily for 4 days. Tubular maximum reabsorptive capacity for bicarbonate and renal bicarbonate threshold determinations were performed at varying intervals in six and seven subjects, respectively, who had fasted for 3-18 days. The results demonstrated that bicarbonate reabsorptive capacity was normal or low during early fasting, markedly elevated during the 2nd wk; and moderately elevated during the 3rd wk of fasting. Glucose administration at all stages of fasting caused a further increase in bicarbonate threshold. Sodium balance during fasting with sodium supplements was found to follow a triphasic pattern, with the occurrence of a natriuresis during the 1st wk followed by a period of sodium retention after which neutral daily sodium balance was reestablished. Correlation of bicarbonate reabsorption with sodium homeostasis indicated a slight decrease in renal bicarbonate threshold during the natriuretic phase, a marked increase in bicarbonate reabsorption during the period of sodium retention, and a continued moderate elevation of threshold after sodium balance was reestablished. This relationship was interpreted to indicate that changes in bicarbonate reabsorption during fasting and refeeding may be secondary to alterations in the renal reabsorption of sodium.

Absorption↗
PubMed1987

Renal bicarbonate reabsorption in the rat. II. Distal tubule load dependence and effect of hypokalemia.

We studied two groups of rats acutely loaded with bicarbonate, control rats on a standard diet and rats kept on a K-free diet for 3 wk. Compared with controls, K-depleted rats had reduced fractional excretion of bicarbonate despite their elevated filtered bicarbonate load. Distal bicarbonate reabsorption increased in K-depleted rats. In the presence of almost identical early distal bicarbonate loads (481 +/- 40 pmol/min in controls and 444 +/- 50 pmol/min in K depletion), distal bicarbonate reabsorption was significantly enhanced in K depletion (247 +/- 17 pmol/min) as compared with controls (179 +/- 18 pmol/min). These values are significantly different from each other, and both are severalfold higher than bicarbonate reabsorption in nonloaded conditions. In conclusion, distal bicarbonate reabsorption is load dependent, and distal bicarbonate reabsorption is stimulated in K depletion.

Animals↗
PubMed2005

Life-threatening asthma in children: treatment with sodium bicarbonate reduces PCO2.

OBJECTIVES: To assess the effect of administration of sodium bicarbonate on carbon dioxide levels in children with life-threatening asthma (LTA) and to evaluate the clinical effect of this treatment. STUDY DESIGN: Retrospective study. SETTING: A pediatric ICU (PICU) of a tertiary care university hospital. PATIENTS: Seventeen children with LTA who received sodium bicarbonate. MEASUREMENTS AND RESULTS: In January 1999, a new protocol for the treatment of LTA was initiated in our institution, incorporating the use of IV sodium bicarbonate in acidotic patients (pH < 7.15) with refractory status asthmaticus. Since January 1999, sodium bicarbonate was administered to 17 patients; 5 patients received two or three doses of sodium bicarbonate. In three patients, sodium bicarbonate was administered after intubation. Intubation and mechanical ventilation were performed in five patients before admission to the PICU, and in one patient during admission. There was a significant decrease of Pco(2) after sodium bicarbonate infusion (p = 0.007). An improvement of respiratory distress in all but one patient was seen as well. CONCLUSIONS: Administration of sodium bicarbonate in 17 children with LTA was associated with a significant decrease in Pco(2) and an improvement of respiratory distress. The possible benefits of sodium bicarbonate in LTA deserve further study in a controlled, prospective design.

Acidosis↗
PubMed2005

Management of the cardiovascular complications of tricyclic antidepressant poisoning : role of sodium bicarbonate.

Experimental studies suggest that both alkalinisation and sodium loading are effective in reducing cardiotoxicity independently. Species and experimental differences may explain why sodium bicarbonate appears to work by sodium loading in some studies and by a pH change in others. In the only case series, the administration of intravenous sodium bicarbonate to achieve a systemic pH of 7.5-7.55 reduced QRS prolongation, reversed hypotension (although colloid was also given) and improved mental status in patients with moderate to severe tricyclic antidepressant poisoning. This clinical study supports the use of sodium bicarbonate in the management of the cardiovascular complications of tricyclic antidepressant poisoning. However, the clinical indications and dosing recommendations remain to be clarified. Hypotension should be managed initially by administration of colloid or crystalloid solutions, guided by central venous pressure monitoring. Based on experimental and clinical studies, sodium bicarbonate should then be administered. If hypotension persists despite adequate filling pressure and sodium bicarbonate administration, inotropic support should be initiated. In a non-randomised controlled trial in rats, epinephrine resulted in a higher survival rate and was superior to norepinephrine both when the drugs were used alone or when epinephrine was used in combination with sodium bicarbonate. Sodium bicarbonate alone resulted in a modest increase in survival rate but this increased markedly when sodium bicarbonate was used with epinephrine or norepinephrine. Clinical studies suggest benefit from norepinephrine and dopamine; in an uncontrolled study the former appeared more effective. Glucagon has also been of benefit. Experimental studies suggest extracorporeal circulation membrane oxygenation is also of potential value. The immediate treatment of arrhythmias involves correcting hypoxia, electrolyte abnormalities, hypotension and acidosis. Administration of sodium bicarbonate may resolve arrhythmias even in the absence of acidosis and, only if this therapy fails, should conventional antiarrhythmic drugs be used. The class 1b agent phenytoin may reverse conduction defects and may be used for resistant ventricular tachycardia. There is also limited evidence for benefit from magnesium infusion. However, class 1a and 1c antiarrhythmic drugs should be avoided since they worsen sodium channel blockade, further slow conduction velocity and depress contractility. Class II agents (beta-blockers) may also precipitate hypotension and cardiac arrest.

Alkalosis, Respiratory↗
PubMed1981

Effect of acid-base status in vivo on bicarbonate transport by rabbit renal tubules in vitro.

In previous studies, when rabbit cortical collecting ducts were studied under standard conditions in vitro, bicarbonate transport was conditioned by the acid-base status in vivo of the animals from which the tubules were obtained. The collecting ducts absorbed bicarbonate if the animals were acidotic (from ammonium chloride administration), but they secreted bicarbonate if the animals were alkalotic (from sodium bicarbonate administration). The purpose of the present studies was to test whether similar conditioning occurs in other nephron segments. In proximal straight tubules neither the sodium-dependent nor the sodium-independent component of bicarbonate absorption was significantly affected by the acid-base status of the animals from which the tubules were obtained. .In cortical thick ascending limbs, chloride was absorbed, but there was no net transport of bicarbonate by tubules whether they came from acidotic or alkalotic animals. Since cortical thick ascending limbs were not found to transport bicarbonate, they cannot be implicated in the control of bicarbonate excretion. We conclude that the previously observed conditioning of bicarbonate transport occurs in collecting ducts but not in proximal straight tubules or in cortical thick ascending limbs in the same experimental situation.

Ammonium Chloride↗
PubMed1987

Effect of proximal gastric vagotomy on basal and vagally stimulated gastric bicarbonate secretion in duodenal ulcer patients.

Basal gastric bicarbonate secretion and the response to vagal stimulation accomplished by sham feeding were investigated in duodenal ulcer patients before and after proximal gastric vagotomy. Gastric bicarbonate secretion was measured with a computer-based system, which continuously recorded the pH and PCO2 of the gastric perfusate. Preoperatively, basal bicarbonate secretion was 414 +/- 57 mumol/h (mean +/- SEM, n = 9), and the secretory response to vagal stimulation 691 +/- 83 mumol/h (p less than 0.01). About 2 months after proximal gastric vagotomy the basal gastric bicarbonate secretion was 539 +/- 74 mumol/h, and the response to vagal stimulation 693 +/- 72 mumol/h (p less than 0.01). The basal bicarbonate secretion thus increased by 30% after vagotomy (p less than 0.01) but about 1 year later was not significantly different from the basal preoperative value. In the early postoperative period anticholinergics significantly reduced the enhanced basal bicarbonate secretion to a preoperative level. When tested 1 year after the operation anticholinergics did not affect basal bicarbonate secretion but abolished the response to sham feeding. The findings of the study suggest the existence of cholinergic vagal nerve fibres stimulating human gastric bicarbonate secretion and indicate that inhibitory nerve fibres may modulate gastric bicarbonate secretion.

Adult↗
PubMed1987

Basal and stimulated human gastric bicarbonate secretion.

The mucus-bicarbonate barrier on the gastric mucosa is regarded as a first-line of defence against acid. Both mucus and bicarbonate originate from the mucus cells in the gastric mucosa. Bicarbonate is secreted actively by Cl-/HCO3- exchange at the luminal cell membrane. A computer based system with continuous measurement of pH and PCO2 in a gastric perfusion system was used to determine human gastric bicarbonate secretion. The rate of basal gastric bicarbonate secretion in 24 healthy subjects was 386 +/- 31 mumol/h (mean +/- SEM). The 95% confidence interval for basal bicarbonate output was 103-669 mumol/h. Vagal stimulation by sham feeding increased the bicarbonate output by 63% and instillation of 16,16 dimethyl prostaglandin E2 increased the bicarbonate output by 214%. The response to vagal stimulation was independent of intragastric pH. The sham feeding response was abolished by premedication with anticholinergics. Basal and vagally stimulated bicarbonate secretion was unaffected by prostaglandin biosynthesis blockade.

16,16-Dimethylprostaglandin E2↗
PubMed1997

Acute therapy for hyperkalemia with the combined regimen of bicarbonate and beta(2)-adrenergic agonist (salbutamol) in chronic renal failure patients.

This study was aimed to evaluate the efficacy of combination therapy of bicarbonate and salbutamol for hyperkalemia in 9 hemodialysis patients. Simultaneous administration of 8.4% sodium bicarbonate (i.v., 2 mEq/kg) for 1/2 hour and salbutamol (15 mg) in nebulized form for 10 min was compared with treatment modality of either bicarbonate or salbutamol alone. Infusion of sodium bicarbonate induced a significant rise in plasma bicarbonate from 17.3 +/- 3.2 to 22.1 +/- 2.4 mEq/L (p < 0.01), but was ineffective in lowering plasma potassium (-0.13 +/- 0.06 mEq/L). As expected, salbutamol significantly lowered plasma potassium (-0.57 +/0 0.03 mEq/L, p < 0.02 vs. basal value) in all except 2 patients. The combined regimen of bicarbonate and salbutamol to a total 9 patients including 2 patients without hypokalemic effect to salbutamol alone revealed a substantially greater fall in plasma potassium (-0.96 +/- 0.08 mEq/L, p = 0.000 vs. either drug alone) accompanied with significant increase in plasma bicarbonate and blood pH. Treatment with salbutamol or the combined regimen produced slight increases in heart rate but not in blood pressure. It is concluded that the combined regimen of bicarbonate and beta(2)-adrenergic agonist (salbutamol) could be recommended as an efficient alternative for severe hyperkalemia in uremic patients, and is suggested that the enhanced transcellular hypokalemic effects of salbutamol in this combined regimen with bicarbonate would be related to the activation of Na-K pump with acute correction of underlying metabolic acidosis.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Hypercapnia and resultant bicarbonate transfer processes in an elasmobranch fish (Scyliorhinus stellaris).

In order to test the effects of hypercapnia on the acid-base status of fish, larger spotted dogfish were exposed to sudden changes of PCO2 in a closed seawater recirculation system. pH, PCO2 and PO2 were determined in arterial blood and seawater. The exchange of bicarbonate between extracellular space (ECS), intracellular space (ICS), and seawater (SW) was obtained from changes of the total bicarbonate amount in ECS and SW. After fourfold increase of PCO2 arterial pH fell markedly, but started to recover immediately towards control values. This was caused by compensatory accumulation of bicarbonate in the ECS. According to the origin of the extracellular bicarbonate increase three periods could be distinguished: 1.-- Bicarbonate transferred from ICS to both ECS and SW; 2. -- Bicarbonate transferred from both SW and ICS to ECS; 3. -- Bicarbonate transferred from SW to both ECS and ICS. After return to normocapnia similar periods occurred with opposite transfer directions and delayed period transitions. In the first period the ICS was found to be the only source for compensatory bicarbonate increases and even in the second period the ICS contributed to compensation of the extracellular pH. Thus bicarbonate exchange with the ICS appears to be an important regulatory mechanism diminishing the extracellular pH variations after changes in PCO2, before other compensatory mechanisms are initiated.

Animals↗
PubMedDate not supplied

Prevention of hemodialysis associated hypoxemia by use of low-concentration bicarbonate dialysate.

Hypoxemia during acetate dialysis is caused by hypoventilation due to bicarbonate loss across the dialyzer and its regeneration from acetate by a CO2 consuming process. Loss of bicarbonate is prevented by using a bicarbonate containing dialysate, but hypoxemia is still found by many authors. In the current study, ten patients were dialyzed twice against acetate dialysate, high concentration bicarbonate (36 mmol/L), and low concentration bicarbonate (29 mmol/L) dialysates. A significant decrease in PO2 was found during both acetate and high concentration bicarbonate dialysis. Hypoxemia was prevented by low concentration bicarbonate dialysate. A possible explanation for the hypoxemia in high concentration bicarbonate dialysis may be hypoventilation induced by alkalosis. It was concluded that low concentration bicarbonate dialysate prevents hypoxemia during hemodialysis.

Bicarbonates↗
PubMed1989

Characterization of bicarbonate-dependent potassium uptake in cultured corneal endothelial cells.

Bovine corneal endothelial (BCE) cells in culture demonstrated 86Rb+ uptake which was mostly ouabain-sensitive with some (15 to 50%) ouabain-insensitive uptake that was dependent on the presence of bicarbonate in the incubation medium. Bovine smooth muscle (SM) cells demonstrated ouabain-sensitive 86Rb+ uptake but the ouabain-insensitive 86Rb+ uptake was not bicarbonate-dependent. Although omission of bicarbonate from the incubation buffer resulted in some reduction in the pH, this change was not responsible for the reduction in the ouabain-insensitive 86Rb+ uptake. Furthermore, the removal of bicarbonate decreased the 86Rb+ influx but not its efflux. This ouabain-insensitive and bicarbonate-dependent 86Rb+ influx in BCE cells proceeded at a linear rate for at least 60 min and increased as a function of bicarbonate concentration such that almost maximal uptake was observed at a concentration of about 10 to 15 mM. Saturation of the bicarbonate-dependent 86Rb+ pump in BCE cells occurred at a concentration of 2 mM Rb+ in the incubation buffer, similar to the previously observed value for the Na+, K+-ATPase. Competition experiments with both unlabeled Rb+ and K+ demonstrated that likewise in the Na+, K+-ATPase the 86Rb+ influx represented physiological influx of K+. Furthermore, the energy requirements of the bicarbonate-dependent 86Rb+ uptake were similar to those of the 86Rb+ uptake via the Na+, K+-ATPase. The results described in this work demonstrated a novel bicarbonate-dependent K+ pump in addition to the Na+, K+-ATPase pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Which bicarbonate concentration is adequate to lactate-buffered substitution fluids in maintenance hemofiltration?

We investigated the metabolic and hemodynamic effects of a lactate- and a bicarbonate-buffered (bicarbonate concentration 31.4 mmol/l, type I) hemofiltration substitution fluid in a prospective crossover study of 3 weeks each in 11 patients on maintenance hemofiltration. The lactate-buffered hemofiltration (lactate concentration 34-44.5 mmol/l) lead to hyperlactatemia in all patients without signs of overt lactic acidosis but showed a better control of acid-base balance (pH, base excess, standard bicarbonate) than the type I bicarbonate-buffered fluid (p < 0.01). In 6 patients a higher concentration of bicarbonate- (39.7 mmol/l, type II) buffered fluid was tested. The parameters of acid-base balance showed a better control during type II than during type I bicarbonate hemofiltration and were similar to the lactate-buffered phase. Plasma lactate levels between type I and type II bicarbonate hemofiltration were not different. Also in the steady state phase of the treatment (days 7-9 [week 3]) parameters of acid-base balance rose more to normal values during type II than during lactate-buffered hemofiltration. Hemodynamic parameters showed no differences between the three types of buffers used. Furthermore, also the type II bicarbonate fluid was well tolerated. Bicarbonate in a higher concentration (39.7 mmol/l) proved to be a safe and practical alternative to lactate-buffered hemofiltration.

Acid-Base Equilibrium↗