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PubMed2005

Comparison of sodium bicarbonate and carbicarb for the treatment of metabolic acidosis in newborn calves.

Carbicarb (an equimolar mixture of sodium bicarbonate and sodium carbonate) was compared with sodium bicarbonate alone for the treatment of acidosis in newborn calves: 25 of 49 calves with a blood pH at birth of less than 7-2 and a base deficit of less than -3 mmol/litre were treated intravenously with sodium bicarbonate and 24 were treated with carbicarb. The doses were calculated on the basis of the base deficit in a blood sample taken 10 minutes after birth, and further blood samples were taken immediately after the treatment and 30 and 60 minutes after the treatment for the determination of acid-base status, blood gases and haematological and biochemical variables. Both treatments resulted in a significant increase in blood pH, but there was no difference between them. The mean (sd) blood pH before treatment was 7.09 (0.02) and after treatment it was 7.28 (0.01). There was no increase in the partial pressure of carbon dioxide after treatment with either sodium bicarbonate or carbicarb. Both treatments were associated with an increase in sodium concentration and decreases in the total erythrocyte count, haematocrit and haemoglobin concentration.

Acidosis↗
PubMed1987

Bicarbonate and ammonia changes in brain during spreading depression.

An alkaline, followed by an acid-going transient, characterizes acid-base changes in the interstitial space during spreading depression in a variety of brain structures. In rat, such changes are associated with a significant rise in brain lactate content. How brain proton buffers behave during spreading depression is unknown. Techniques to significantly improve the response time of gas permeable membrane semimicroelectrodes for carbon dioxide and ammonia are reported. Measurements with such electrodes, when coupled to measurements of hydrogen ion concentration (from microelectrodes), permit rapid changes to be determined in bicarbonate concentration or ammonia and ammonium ion concentration, respectively. Bicarbonate concentration fell from 30 +/- 1 (n = 16) to 14 +/- 1 mM (n = 16) during spreading depression. On the other hand, ammonia concentration rose from 2.3 +/- 0.1 to 4.4 +/- 0.3 microM (n = 17) while ammonium ion concentration rose from 116 +/- 11 (n = 17) to 382 +/- 30 microM (n = 17) during spreading depression. Bicarbonate changes probably reflect titration of brain bicarbonate stores by accumulated lactic acid. Similar physicochemical changes do not explain the rise in ammonia and ammonium ion concentrations. Instead, elevation of the latter can only result from an increase in ammonia content of the interstitial space.

Ammonia↗
PubMed1994

Effect of adrenergic and cholinergic agents on esophageal bicarbonate secretion in opossums.

The effects of cholinergic and adrenergic agonists and antagonists on esophageal bicarbonate secretion in the opossum were studied in vivo using a recirculated unbuffered saline solution and pH stat technique. The basal rate of secretion was 0.28 +/- 0.02 mumol.h-1.cm-2, and this increased in a dose-dependent manner by intravenous administration of carbachol (maximal increase 0.74 +/- 0.07 mumol.h-1.cm-2 at 6 micrograms/kg). Furthermore, like carbachol, the acetylcholinesterase inhibitor edrophonium also increased bicarbonate secretion, whereas atropine and pirenzepine, which had no effect on basal secretion, abolished the increase in secretion produced by carbachol. Intravenous administration of either adrenergic agonists or antagonists had no significant effect on secretion. These data indicate that basal bicarbonate secretion in the opossum esophagus is independent of intrinsic adrenergic or cholinergic activity, and so not under autonomic nervous system control, but that endogenous release of acetylcholine, presumably from parasympathetic nervous fibers, can stimulate bicarbonate secretion through activation of cholinergic M1 receptors.

Animals↗
PubMed1996

Intracerebral adrenoceptor agonists influence rat duodenal mucosal bicarbonate secretion.

We have studied the effects of intracerebral administration of selective alpha-adrenergic agonists on duodenal bicarbonate secretion. Duodenum free of Brunner's glands was cannulated in situ in anesthetized rats, and bicarbonate secretion into the luminal reperfusate was continuously titrated by pH stat. Infusion of the alpha 1-selective adrenoceptor agonist, phenylephrine (1,000-2,500 micrograms.kg-1.h-1), into a lateral brain ventricle increased (P < 0.01) duodenal bicarbonate secretion. Pretreatment with prazosin, an alpha 1-antagonist, significantly (P < 0.01) reduced the stimulatory effect when infused into the lateral ventricle (30 micrograms.kg-1.h-1), but not when administered intravenously (1,000 micrograms.kg-1.h-1). Hexamethonium (10 mg.kg-1.h-1 iv) abolished stimulation, whereas cervical vagotomy, epidural blockade, and naloxone were each without effect. Vasopressin, vasopressin antagonists, ts, and oxytocin did not affect basal secretion. Intracerebro-ventricular administration of the alpha 2-adrenoceptor agonist, clonidine (1,000 micrograms.kg-1.h-1), in contrast to alpha 1-receptor activation, decreased (P < 0.01) the secretion. Thus central nervous adrenoceptors influence duodenal mucosal bicarbonate te secretion, and alpha 1-adrenoceptor stimulation may provide protection against luminal acid. This potent stimulation was not mediated by the vagal nerves, spinal cord pathways, or the release of beta-endorphin but involves nicotinic, possibly enteric nervous transmission.

Adrenergic alpha-Agonists↗
PubMed1976

Compensatory adaptation of sodium and bicarbonate excretion: effect of diuretics.

Complete clamping of the contralateral kidney results in a rapid and significant increase in the fractional excretion of Na, K, and bicarbonate by the remaining kidney during bicarbonate loading. Similar studies were performed in dogs after administration of diuretics with different major sites of action to localize the adaptive excretory response to acute reduction in renal mass. Volume expansion was carefully avoided. In experiments with the loop inhibitor, furosemide, contralateral kidney clamping rapidly and significantly increased fractional excretion of Na and bicarbonate. A more delayed and smaller response was observed in dogs given hydrochlorothiazide. Acetazolamide, a potent inhibitor of proximal Na bicarbonate reabsorption, completely blocked the excretory response to contralateral kidney clamping. The enhanced response with furosemide and its blockade with acetazolamide indicates a proximal site of adaptation to acute contralateral kidney exclusion. The overall natriuretic response depends on the level of inhibition of loop reabsorption.

Acetazolamide↗
PubMed1976

Glucose and bicarbonate reabsorption in edematous dogs.

Glucose and bicarbonate reabsorption were studied in dogs made edematour by aortocaval fistula (A-V dogs) and in sham-operated dogs. Following construction of the A-V fistula, there was a significant increase in body weight; glomerular filtration rate, renal plasma flow, hematocrit, and sodium excretion decreased significantly. Bicarbonate reabosorption was significantly higher in A-V than in sham dogs both during control and volume expansion. Volume expansion depressed bicarbonate reabsorption significantly in both groups. Glucose reabsorption fell following volume expansion in both groups; glucose reabsorption was significantly higher in A-V dogs than in sham dogs during control and volume expansion. Volume expansion led to a minimal increase in sodium excretion in A-V dogs when compared to the increase in the sham dogs. These data demonsttate that chronic sodium retention is associated with enhanced reabsorption of glucose and bicarbonate. The site in the neophron responsible for the increase in reabsorption of these substances cannot be determined with certainty based on these clearance studies although it is possible that proximal reabsorption may be enhanced in this model.

Acid-Base Equilibrium↗
PubMed1977

Bicarbonate ions in active sodium transport across toad bladder.

The conductance, ga, and electromotive force, E, of active ion transport across toad bladders mounted as sacs were estimated from electrical measurements made before and after addition of sufficient ouabain (1.89 X 10(-3) M) to eliminate spontaneous potential. The ratio of net sodium transport (estimated from bidirectional fluxes) to external current in bladders voltage clamped to 0 mV was significantly less than unity in a normal medium containing HCO3- and Cl- ions, and also when Cl- was replaced with SO42-. However, when acetazolamide was added or when HCO3- was replaced by phosphate, short-circuit current and net sodium transport became equal. Spontaneous potential, E, and ga were all reduced about 20% by these maneuvers. The response of bidirectional sodium fluxes to voltage clamping at 0 mV or 120 mV in a bicarbonate-free medium was otherwise similar to that observed in a normal medium: net flux varied linearly with potential and calculated fluxes in the active transport path indicated a value significantly greater than unity for the empirical constant Q in the equation for change in the flux ratio, f, with change in potential, psi, viz., delta ln f = Q(ZF/RT)delta psi, similar to the high value for this constant that we have found in a bicarbonate-containing medium. We conclude that bicarbonate ions facilitate active sodium transport and also may be actively transported from serosa to mucosa in Dominican toads. However, coupling between bicarbonate and sodium fluxes does not account for the high value for Q for sodium in the active transport path.

Animals↗
PubMed1979

Carbonic anhydrase-dependent bicarbonate reabsorption in the rat proximal tubule.

The extent to which bicarbonate reabsorption in the rat proximal convoluted tubule depends on carbonic anhydrase has been examined by in vivo microperfusion and the measurement of total CO2 concentration by microcalorimetry. Tubules were perfused with an ultrafiltrate-like solution at 13 nl/min, and volume reabsorptive rate (JV) was measured using [14C]inulin. Addition of either 800 or 100 microM acetazolamide to the perfusion solution completely inhibited the reabsorption of total CO2. The control total CO2 reabsorptive rate (JtCO2) was 147 +/- 23 pmol/mm.min, and acetazolamide reduced JtCO2 to -3 +/- 5 pmol/mm.min. Acetazolamide reduced JV by 65% from a control of 2.3 +/- 0.4 to 0.8 +/- 0.1 nl/mm.min. The dose-response curve for acetazolamide showed that the I50 for inhibition of JtCO2 was 4 microM. The inactive congener of acetazolamide, t-butyl acetazolamide, did not reduce JV or inhibit bicarbonate reabsorption, indicating that the effect of acetazolamide on JtCO2 was specific for carbonic anhydrase inhibition. Since bicarbonate reabsorption was completely blocked by carbonic anhydrase inhibition, there is no need to postulate either carbonic acid recycling or carbonic anhydrase-independent bicarbonate reabsorption.

Acetazolamide↗
PubMed1982

Effects of lysine on bicarbonate and fluid absorption in the rat proximal tubule.

The effects of lysine on bicarbonate and fluid reabsorption in the rat proximal tubule were studied by luminal and capillary perfusion in situ. The proximal tubule and peritubular capillaries were perfused with bicarbonate Ringer solution containing [14C]inulin. The rate of bicarbonate reabsorption (JHCO3) was estimated to be 124 +/- 9.5 peq.min-1.mm-1 using a pH membrane glass electrode. The rate of net fluid reabsorption (Jv) was 2.6 +/- 0.21 nl.min-1.mm-1. When 10 mM L-lysine was added to the luminal perfusate, a 35% reduction in JHCO3 and no change in Jv were observed. Increase of L-lysine concentration in the luminal perfusate to 20 mM did not reduce JHCO3 further nor did it influence Jv.l When 10 mM L-lysine was added to the capillary perfusate, a 13% reduction in JHCO3 was observed (NS). Increase of lysine concentration in the capillary perfusate to 20 mM significantly reduced JHCO3 by 26% (P less than 0.01). There was no significant change in Jv under both conditions. The effect of L-lysine in the lumen was related to its reabsorption kinetics, D-Lysine, which was not reabsorbed significantly, did not affect bicarbonate reabsorption in the proximal tubule. These results indicate that the inhibitory effect of L-lysine is related to the entry of lysine into the cell from the lumen.

Absorption↗
PubMed1982

Bicarbonate reabsorption and potassium handling in isolated perfused kidneys of Bufo marinus.

Average rates of bicarbonate reabsorption, normalized for glomerular filtration rates, rose linearly with perfusate [HCO3-] of 6-21 mM with a constant bicarbonate/creatinine clearance ratio of 0.06, similar to the in vivo value. Maximal rates of bicarbonate reabsorption occurred at 20-25 mM HCO3- perfusate. At 3 mM perfusate [K+], normalized rates of potassium reabsorption were constant from filtered perfusates mimicking metabolic acidosis, and from control perfusates; during perfusion with alkalotic Ringer solutions net potassium secretion was observed. Elevation of perfusate [K+] to 10 mM in alkalotic Ringer significantly decreased maximal rates of bicarbonate reabsorption. Overall, the pattern of bicarbonate reabsorption in toad kidneys perfused at 6-21 mM HCO3- was similar to that observed in acid-base disturbances of metabolic origin in mammals, while the pattern of potassium excretion showed significant differences in these two vertebrate classes.

Animals↗
PubMed1983

Passive driving forces of proximal tubular fluid and bicarbonate transport: gradient dependence of H+ secretion.

The effect of oncotic pressure changes on fluid (Jv) and net bicarbonate transport (JHCO-3) and the transepithelial bicarbonate permeability (PHCO-3) were measured by an improved luminal and capillary microperfusion method that allows paired experiments on the same tubule. Rat proximal tubules were pump-perfused and Jv and [HCO-3] measured with [14C]inulin and a pH glass electrode. Raising peritubular protein (0-8-15 g/100 ml bovine serum albumin) stimulated Jv and HCO-3 reabsorption. The response to oncotic pressure changes was asymmetrical since changes of the luminal protein concentration had no significant effects. Whereas transepithelial solvent drag effects on HCO-3 must be minimal, peritubular protein most likely stimulates translocation of fluid and bicarbonate from intercellular spaces into peritubular capillaries. PHCO-3 was measured from HCO-3 net flux along a lumen-to-capillary-directed electrochemical potential gradient. In these experiments active H+ transport and Jv were minimized by 10(-4) M acetazolamide and luminal raffinose. PHCO-3 was 1.77 X 10(-5) cm X s-1 and was unaffected by increasing luminal flow rate from 10 to 45 nl X min-1. Since bicarbonate backflux is only a small fraction of physiological rates of JHCO-3, net transport alterations at varying [HCO-3] in the lumen must be due to changes in active HCO-3 (H+) transport. Thus, active H+ ion secretion across the luminal membrane of the proximal tubule is gradient dependent.

Acetazolamide↗
PubMed1984

Regulation of proximal bicarbonate reabsorption.

Under free-flow conditions, alterations in acid-base and extracellular volume status affect absolute proximal bicarbonate reabsorption. Microperfusion studies have characterized the individual determinants of the active and passive components of proximal acidification. These determinants include luminal bicarbonate concentration, luminal flow rate, peritubular bicarbonate concentration, PCO2, extracellular volume status, and solute-solvent interactions. When these individual determinants are integrated into a computer-simulated model of absolute proximal bicarbonate reabsorption, the results agree well with the in vivo free-flow data.

Absorption↗
PubMed1987

Bicarbonate transport by initial collecting tubule of aquatic- and land-phase amphibia.

The rate of bicarbonate reabsorption (JHCO3) by in vitro initial collecting tubules (ICT) from aquatic- and land-phase Ambystoma tigrinum was measured. These animals intrinsically have different levels of plasma bicarbonate, 17.6 and 27.1 mM, respectively. ICT from both phases reabsorbed bicarbonate at 11 pmol X mm-1 X min-1 when perfused in solutions equilibrated with 3% CO2. The induction of metabolic acidosis or alkalosis had no effect on JHCO3 by in vitro ICT. JHCO3 was abolished when ICT from aquatic animals were perfused with solutions equilibrated with 1% CO2 and returned toward the control value when 3% CO2 was reintroduced. The effect of plasma CO2 partial pressure on JHCO3 of the ICT may explain, at least in part, the observed difference in plasma bicarbonate of the aquatic- and land-phase animals. JHCO3 was reduced to 22% of control with amiloride and to 42% of control when a Na+-free perfusate was used, but was insensitive to ethoxzolamide. These data are consistent with the presence of a sodium-proton exchanger on the apical membrane and a carbonic anhydrase-independent mechanism of H+ secretion.

Absorption↗
PubMed1990

Effects of intracellular calcium on proximal bicarbonate absorption.

Using in vivo microperfusion in the proximal convoluted tubule (PCT) of the Munich-Wistar rat, we assessed the impact of raising intracellular calcium concentration on bicarbonate transport and its regulation by angiotensin II. Luminal perfusion with the calcium ionophore A23187 caused a dose-dependent increase in S1 PCT bicarbonate absorption, with a maximal change of 60 peq.mm-1.min-1. Subsequent addition of phorbol ester (PMA) after A23187 further increased transport but to a level no higher than previously shown with PMA alone, and A23187 was nonstimulatory when added after PMA. These results suggest that intracellular calcium affects the same pathway as protein kinase C in stimulating proximal acidification. Pretreatment with A23187 (+/- PMA) attenuated by approximately one-third the bicarbonate absorptive response in the S1 PCT usually observed after angiotensin II administration. A23187 had similar actions, but of smaller magnitude, in the S2 PCT. In conclusion, a rise in intracellular calcium increases bicarbonate absorption in the S1 and S2 PCT in vivo.

Absorption↗
PubMed2000

Effects of ammonia on bicarbonate transport in the cortical collecting duct.

Both acidosis and hypokalemia stimulate renal ammoniagenesis, and both regulate urinary proton and potassium excretion. We hypothesized that ammonia might play an important role in this processing by stimulating H(+)-K(+)-ATPase-mediated ion transport. Rabbit cortical collecting ducts (CCD) were studied using in vitro microperfusion, bicarbonate reabsorption was measured using microcalorimetry, and intracellular pH (pH(i)) was measured using the fluorescent, pH-sensitive dye, 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Ammonia caused a concentration-dependent increase in net bicarbonate reabsorption that was inhibited by luminal addition of either of the H(+)-K(+)-ATPase inhibitors, Sch-28080 or ouabain. The stimulation of net bicarbonate reabsorption was not mediated through apical H(+)-ATPase, basolateral Na(+)-K(+)-ATPase, or luminal electronegativity. Although ammonia caused intracellular acidification, similar changes in pH(i) induced by inhibiting basolateral Na(+)/H(+) exchange did not alter net bicarbonate reabsorption. We conclude that ammonia regulates CCD proton and potassium transport, at least in part, by stimulating apical H(+)-K(+)-ATPase.

Ammonia↗
PubMed2001

Immunolocalization of electrogenic sodium-bicarbonate cotransporters pNBC1 and kNBC1 in the rat eye.

The human NBC1 gene encodes two electrogenic sodium-bicarbonate cotransport proteins, pNBC1 and kNBC1, which are candidate proteins for mediating electrogenic sodium-bicarbonate cotransport in ocular cells. Mutations in the coding region of the human NBC1 gene in exons common to both pNBC1 and kNBC1 result in a syndrome with a severe ocular and renal phenotype (blindness, band keratopathy, glaucoma, cataracts, and proximal renal tubular acidosis). In the present study, we determined the pattern of electrogenic sodium-bicarbonate cotransporter protein expression in rat eye. For this purpose, pNBC1- and kNBC1-specific antibodies were generated and used to detect these NBC1 protein variants by immunoblotting and immunocytochemistry. pNBC1 is expressed in cornea, conjunctiva, lens, ciliary body, and retina, whereas the expression of kNBC1 is restricted to the conjunctiva. These results provide the first evidence for extrarenal kNBC1 protein expression. The data in this study will serve as a basis for understanding the molecular mechanisms responsible for abnormalities in ocular electrogenic sodium-bicarbonate cotransport in patients with mutations in the NBC1 gene.

Animals↗
PubMed2006

Bicarbonate infusion and pH clamp moderately reduce hyperventilation during ramp exercise in humans.

To test the hypothesis that the decrease in plasma pH contributes to the hyperventilation observed in humans in response to exercise at high workloads, five healthy male subjects performed a ramp exercise [maximal workload: 352 W (SD 35)] in a control situation and when arterialized plasma pH was maintained at the resting level (pH clamp) by intravenous infusion of sodium bicarbonate [129 mmol (SD 23), beginning at 59% maximal workload (SD 5)]. Bicarbonate infusion did not modify O(2) consumption (Vo(2)) but significantly (P < 0.05) increased arterial Pco(2), plasma bicarbonate concentration, and respiratory exchange ratio (P < 0.05). At the three highest workloads, pulmonary ventilation (Ve) and Ve/Vo(2) were approximately 5-10% lower (P < 0.05) when bicarbonate was infused than in the control situation, and hyperventilation was reduced by 15-30%. These data suggest that the decrease in plasma pH is one of the factors that contribute to the hyperventilation observed at high workloads.

Acid-Base Equilibrium↗
PubMed1995

Simultaneous measurement of pH and membrane potential in rat dorsal vagal motoneurons during normoxia and hypoxia: a comparison in bicarbonate and HEPES buffers.

1. The effects of oxygenated and hypoxic bicarbonate/CO2, 10 and 25 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered artificial cerebrospinal fluid (ACSF) have been studied in a rat brain slice preparation. Double-barreled pH-selective microelectrodes were used to measure intracellular pH (pHi) and membrane potential in dorsal vagal motoneurons (DVMs) and to measure extracellular pH (pHe) in the dorsal vagal motonucleus. 2. In bicarbonate ACSF, pHi averaged 7.24 +/- 0.05 (mean +/- SE, n = 21) and ranged from 6.86 to 7.79 pH units. pHe averaged 7.13 +/- 0.08 (n = 10). 3. On changing from oxygenated bicarbonate ACSF to either 10 or 25 mM HEPES ACSF, pHi decreased by 0.13-0.15 units, and the membrane depolarized by 10-11 mV. pHe also decreased in 10 mM HEPES ACSF (pHe 6.89 +/- 0.02, n = 8) but not in 25 mM HEPES ACSF (pHe 7.15 +/- 0.06, n = 3). In most neurons changes in pHi preceded changes in membrane potential. 4. In bicarbonate ACSF and in 25 mM HEPES ACSF, there was a significant linear relationship between prehypoxic pHi and the direction and amplitude of the hypoxia-induced membrane potential change (either an hyperpolarization or a depolarization). 5. In 10 mM HEPES ACSF, hypoxia always induced a depolarization; there was no correlation between prehypoxic pHi and the membrane potential response. 6. In bicarbonate ACSF and in 10 and 25 mM HEPES ACSF, hypoxia resulted in intracellular and extracellular acidification. However, the extracellular acidification in hypoxic 10 mM HEPES buffer was most pronounced (pH 6.40 +/- 0.11, n = 8), reflecting a preexisting extracellular acidification in oxygenated 10 mM HEPES buffer. 7. Various hypotheses that could give rise to a relationship between changes in membrane potential and pH are discussed; arguments are presented in favor of the concept that modulation of ion channels by either pHi or pHe, or both, is responsible for the observed correlations.

Animals↗