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PubMed1981

[The influence of oxygen and bicarbonate administration to the parturient on maternal and fetal blood gases and acid base balance (author's transl)].

The effects of oxygen and bicarbonate administration to parturients were studied by analysis of maternal and fetal blood gas parameters. Oxygen inhalation resulted in a significant increase of the fetal pO2 and appears to be a practicable mean of intrauterine reanimation of hypoxic fetuses. Intravenous bicarbonate was unable to raise the fetal pH. Simultaneous bicarbonate and oxygen administration had no desirable effects on the fetal acid-base-balance.

Acid-Base Equilibrium↗

PubMedDate not supplied

[Correction of the acid-base balance in the newborn asphyxia. The use of sodium bicarbonate].

The treatment of neonatal respiratory distress associates the improvement of lung ventilation with the correction of acid-base equilibrium (metabolic acidosis). In such a context we have considered 10 newborns with respiratory distress and we monitored pH, PCO2, B.E. and standard bicarbonate in capillary blood at 1, 5, 10, 25 hours after birth. The sodium bicarbonate doses given as a result of the emogasanalisis are above those usually recommended. We then give suggestions on how to use the sodium bicarbonate required to correct the acidosis without the aid of an emogasanaliser in order to avoid the iatrogenic alcalosis danger.

Acidosis, Respiratory↗

PubMed1984

[Effect of IV hydration with sodium bicarbonate on high-dose methotrexate disposition kinetics].

Following two-compartment kinetic analysis, the effect of loading of transfusion with sodium bicarbonate on methotrexate disposition was investigated in 13 cases with malignant tumor, being treated with high-dose methotrexate. The mean values of total body clearance, when administered at doses 50 mg and 100 mg per kg body weight, were 0.369 and 0.402 (l/h) per kg, respectively. No significant relationship was observed between alpha value and total amount of transfusion, of urine or dosage of sodium bicarbonate. The other kinetic parameters on elimination, beta value, K10 and total body clearance, did not also correlate with those values described above. These results suggest that the elimination profile of methotrexate show linear kinetics, and that massive administration of transfusion with sodium bicarbonate be not necessary if pH value of urine exceeds 7.0.

Adolescent↗

PubMed1984

Use of sodium bicarbonate to treat tricyclic antidepressant-induced arrhythmias in a patient with alkalosis.

Sodium bicarbonate has been recommended for the treatment of arrhythmias induced by tricyclic antidepressants. It is unclear, however, whether this therapy is effective only in the presence of acidosis. A case is presented in which there was an immediate response to sodium bicarbonate in three episodes of ventricular tachycardia despite the presence of alkalosis on two of the three occasions. Given the poor response to conventional therapy of arrhythmias induced by tricyclic antidepressants the use of sodium bicarbonate may be reasonable even in the presence of alkalosis. However, in the presence of pre-existing respiratory or metabolic alkalosis, such therapy is not without risk, and it is suggested that it be reserved for life-threatening situations when the arrhythmia has failed to respond to hyperventilation or antiarrhythmics or both.

Adult↗

PubMed1993

[Should bicarbonates still be administered in lactic acidosis?].

Bicarbonate administration during lactic acidosis seems logical in view of the myocardial depression associated with the decrease in intracellular pH. This treatment has been recently challenged on the basis of observations showing an increase in the veno-arterial gradient for CO2 during acute circulatory failure. The partial transformation of bicarbonate in CO2 carries the risk of aggravating the phenomenon and thereby decreasing intracellular pH. Alternatives to sodium bicarbonate--carbicarb, THAM and dichloroacetate--are discussed.

Acidosis, Lactic↗

PubMed1996

Does the administration of carbicarb lead acutely to back-titration of non-bicarbonate buffers?

OBJECTIVE: We have recently demonstrated in a model of acute metabolic acidosis in rats that the administration of NaHCO3 does not lead acutely to back-titration of non-bicarbonate buffers. Carbicarb is a new alkalinizing agent that has been proposed as a replacement for NaHCO3 in the treatment of metabolic acidosis. Hence, the purpose of this study was to examine the impact of carbicarb on back-titration of non-bicarbonate buffers. METHODS: Rats were anaesthetized, intubated and ventilated to a PCO2 of approximately 30 mmHg. Acute metabolic acidosis was induced by the infusion over 1 hour of 3.5 mmol of hydrochloric acid. After a 20 min equilibration period, 3 groups of rats (n = 7 in each group) were examined. Rats in groups I received 0.75 meq of Na from 1 M carbicarb solution as an intravenous bolus, rats in group II received equimolar NaCl, while rats in group III were used as time controls. Calculations were performed to quantitate the amount of HCO3- that was retained in the ECF volume and the amount that was titrated with H+ and excreted as "acid-base" CO2. "Acid-base" CO2 was considered as the amount of CO2 that was excreted in excess of what would be produced during metabolism. RESULTS: As compared to the NaCl and the time control groups, the administration of carbicarb led to significant alkalinization of the ECF, pH rose from 7.23 +/- 0.02 to 7.34 +/- 0.03. Of the 0.75 mmol of carbicarb that was administered, 0.61 +/- 0.05 mmol (70%) was retained in ECF. There was virtually no "acid-base" CO2 produced. CONCLUSIONS: The administration of carbicarb does not lead acutely to back-titration of non-bicarbonate buffers especially under conditions of fixed ventilation.

Acidosis↗

PubMed1996

Bicarbonate absorption in eel intestine: evidence for the presence of membrane-bound carbonic anhydrase on the brush border membranes of the enterocyte.

Bicarbonate absorptive fluxes through the isolated intestine of the European eel (Anguilla anguilla) were evaluated by the pH-stat method under short-circuited conditions. It was found that bicarbonate absorptive flux was dependent on the luminal Na+ and was inhibited by luminal 4-acetamido-4' stilbene-2-2' disulfonic acid (SITS; 2.5 x 10(-4) M) and luminal acetazolamide (10(-4) M), while luminal amiloride (1 mM) was without effect. Furthermore, by using brush border membrane vesicles (BBMV) isolated from eel intestine, the existence of two carbonic anhydrase (CA) isoforms, one tightly associated to the brush border membrane (BBM) and the other soluble in the cytosol, was demonstrated. The membrane-bound CA differs from the cytoplasmic isoform in that 1) it is relatively resistant to treatment with 0.045% lauryl sulfate sodium salt (SDS); 2) it is less inhibitable by ethoxzolamide and sulfanilamide; and 3) its Kmapp is significantly lower than that of the cytoplasmic isoform. These results suggest that a BBM-bound CA isozyme would play an important role in bicarbonate absorption from the lumen, facilitating the HCO3- transfer through the luminal membrane of the eel enterocyte most likely via a Na+ (HCO3-) or (OH-) cotransport system.

Anguilla↗

PubMed2006

Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger.

Canalicular bile is modified along bile ducts through reabsorptive and secretory processes regulated by nerves, bile salts, and hormones such as secretin. Secretin stimulates ductular cystic fibrosis transmembrane conductance regulator (CFTR)-dependent Cl- efflux and subsequent biliary HCO3- secretion, possibly via Cl-/HCO3- anion exchange (AE). However, the contribution of secretin to bile regulation in the normal rat, the significance of choleretic bile salts in secretin effects, and the role of Cl-/HCO3- exchange in secretin-stimulated HCO3- secretion all remain unclear. Here, secretin was administered to normal rats with maintained bile acid pool via continuous taurocholate infusion. Bile flow and biliary HCO3- and Cl- excretion were monitored following intrabiliary retrograde fluxes of saline solutions with and without the Cl- channel inhibitor 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) or the Cl-/HCO3- exchange inhibitor 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). Secretin increased bile flow and biliary excretion of HCO3- and Cl-. Interestingly, secretin effects were not observed in the absence of taurocholate. Whereas secretin effects were all blocked by intrabiliary NPPB, DIDS only inhibited secretin-induced increases in bile flow and HCO3- excretion but not the increased Cl- excretion, revealing a role of biliary Cl-/HCO3- exchange in secretin-induced, bicarbonate-rich choleresis in normal rats. Finally, small hairpin RNA adenoviral constructs were used to demonstrate the involvement of the Na+-independent anion exchanger 2 (AE2) through gene silencing in normal rat cholangiocytes. AE2 gene silencing caused a marked inhibition of unstimulated and secretin-stimulated Cl-/HCO3- exchange. In conclusion, maintenance of the bile acid pool is crucial for secretin to induce bicarbonate-rich choleresis in the normal rat and that this occurs via a chloride-bicarbonate exchange process consistent with AE2 function.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1976

Regulation of glucose transport in chick fibroblasts: bicarbonate, lactate and ascorbic acid.

The rate at which chick embryo fibroblasts in primary or secondary culture transport glucose or 3-O-methyl glucose is strongly influenced by the presence of bicarbonate ion in the culture medium. Cells growing or maintained on glucose at physiologic concentration (5.5 mM) have an 8 to 10 fold higher rate of glucose uptake than their counterparts cultivated without bicarbonate. These cells also produce more lactate as a consequence of their more rapid intake of glucose. The hydrogen acceptors, methylene blue and dehydroascorbate added to the culture medium reduce the cell capacity to transport glucose and 3-O-methyl glucose to levels obtaining in the bicarbonate-free medium. There is a concomitant reduction in glucose utilized by cells during 24 hours and further reduction in lactate formed per molecule of glucose metabolized.

Animals↗

PubMed1992

Phenylephrine and ATP enhance an amiloride insensitive bicarbonate-dependent alkalinizing mechanism in rat single cardiomyocytes.

To expel the excess protons generated during a cellular acidification and to fully recover basal intracellular pH (pHi), cardiac cells rely on the amiloride-sensitive Na/H antiport. We report that rat single ventricular cardiomyocytes, loaded with the fluorescent pH indicator Snarf-1 and treated with inhibitors of the Na/H antiport, amiloride or its analogues, partially restored their pHi through a bicarbonate-dependent mechanism following an acidosis (imposed by the ammonia-pulse technique). In the presence of ethylisopropylamiloride (10 microM) or amiloride (1 mM) and 25 mM bicarbonate in the extracellular solution, the average time that cells needed to recover half of their pHi, following the removal of 20 mM NH4Cl, was 3.4 min, while the rate of proton efflux was calculated to be 2.0 mM/min. The stilbene derivative, 4-4'-di-isothiocyanostilbene-2,2'-disulphonate (DIDS 200 microM), a known blocker of anion transporters, inhibited this recovery. Both phenylephrine (100 microM, 3 microM propranolol present), an alpha 1-adrenoceptor agonist, and ATP (10 microM), a purinergic agonist, significantly enhanced the rate of proton efflux that was due to this HCO3-dependent alkalinizing mechanism. Phenylephrine and ATP also shortened by three-fold the time that a myocyte needed to recover half of its initial pHi. This bicarbonate-dependent alkalinizing mechanism could provide an additional means by which cardiac cells recover their pHi from acidosis, especially under conditions in which the Na/H antiport is inhibited. Furthermore, catecholamines and ATP, which are released under various pathophysiological conditions often associated with intracellular acidosis, could play an important role in the modulation of pHi under these conditions.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1991

Influence of the bicarbonate pool and on the occurrence of 13CO2 in exhaled air.

In 13CO2 breath tests, based on 13C:12C ratio measurements, the appearance of 13C in exhaled CO2 was monitored after the administration of a 13C-labelled compound. Independently of the substrate used, the existence of a bicarbonate pool into which the CO2 produced enters before being exhaled, imposes a delay on the appearance of changes in the 13C:12C ratio. To estimate the nature and magnitude of this delay, we applied a two-compartment model to describe the kinetics of the body bicarbonate pool and we evaluated the 13C:12C ratio of CO2 entering that pool from the measured 13C:12C ratio in the exhaled CO2 after an oral intake of "naturally labelled" 13C-glucose. Our results demonstrated that discrepancies between total and exogenous glucose oxidation in relation to the peak occurrence time, as well as the absolute quantities, could be adequately explained by the interference of the bicarbonate stores.

Bicarbonates↗

PubMed1992

Bicarbonate-dependent changes of intracellular sodium and pH in identified leech glial cells.

A new triple-barrelled ion-sensitive microelectrode was used to investigate the importance of bicarbonate for the regulation of intracellular Na+ and pH (Nai and pHi, respectively) of neuropile glial cells in the central nervous system of the leech Hirudo medicinalis. Addition of CO2/HCO3- produced an increase of the Nai activity and an intracellular alkalinization, indicating bicarbonate accumulation in the glial cells. Changes of external pH (from 7.4 to 7.0 and 7.8) produced large and rapid shifts of pHi and Nai and of the membrane potential in the presence, but not in the absence, of bicarbonate. Thus, acid/base transport and Na+ movements across the glial membrane into and out of the cells were accelerated severalfold in CO2/HCO3(-)-buffered saline as compared to a CO2/HCO3(-)-free, HEPES-buffered saline. The results suggest that the electrogenic, reversible, cotransport of Na+ and HCO3- in the glial cell membrane [3,9] can produce significant changes in intraglial pH and Na activity, and can carry a significant fraction of the total Na+ flux across the cell membrane.

Animals↗

PubMed1976

Arterial and mixed venous PCO2 and hydrogen ion, bicarbonate and base excess concentrations in water-depleted dogs.

The arterial (a), mixed venous (v), and arterial-mixed venous differences (A-V) of hydrogen ion concentration ([H+]), PCO2, HCO-3 and base excess (BE) were measured during 3 h in control (C), water-depleted (WD) and water- and salt-depleted (WSD) dogs. In WD animals the difference in hydrogen ion concentration between venous and arterial blood increased because the [H+] increased more in venous than in arterial blood. In WSD animals (A-V) [H+] remained unchanged since both [H+]a and [H+]v increases were parallel. [H+] variations seem to represent the changes in fixed-acid concentration of blood. The difference between both groups of animals in (A-V) [H+] changes could be ascribed to PCO2 variations. [HCO-3] values changed inconsistently. Arterial samples from the experimental groups showed a continuous decrease at the same rate of change. The mean values in WSD were lower than in WD. [HCO-3]v of WSD decreased slowly during the experiment. The rate of decrease of (A-V) [HCO-3] was higher in WD than in WSD. The different behavior of of [HCO-3] between both arterial and mixed venous samples and among experimental groups disappeared if [HCO-3] changes were corrected for bicarbonate generation due to PCO2 variation (respiratory bicarbonate). Thus [HCO-3] corrected for PCO2 variation represents metabolic changes, in good agreement with both [H+] and BE variations. The metabolic acidosis cannot be explained only on the basis of the increase in blood lactate; it is suggested that other fixed acids might contribute to the decrease in blood bicarbonate. In both experimental groups PvCO2 increased continuously. The (A-V) PCO2 showed the same rate of change. There is a good relationship between this increase and the degree of plasma volume change. It therefore might be that PvCO2 increase is a direct consequence of hemodynamic impairment. In WD and WSD, BE decreased progressively in both arterial and mixed venous samples. BEa values were lower than BEv values after the experiment began. (A-V) BE decreased in an exponential manner in both experimental groups; this change could be ascribed to the increased level of deoxygenated hemoglobin in mixed venous blood, thus giving rise to a decrease in fixed acid concentration.

Acid-Base Equilibrium↗

PubMed1997

Validation of the labeled bicarbonate technique for measurement of short-term energy expenditure in the mouse.

The energy expenditure of free-living animals has been studied extensively by the doubly-labeled water (DLW) technique. This method provides a reasonably accurate estimate of daily energy needs. However, there is considerable interest in the energy demands of animals over much shorter timescales, for which the DLW technique is less useful. We examined the possibility of measuring the expenditure of small animals over these shorter timescales from the washout kinetics of a bolus dose of 13C labeled bicarbonate. The study involved 19 laboratory mice which were injected either i.p. or s.c. with 0.2 ml of 13C labeled bicarbonate in water. Mice were placed in a standard respirometry system, maintained at different temperatures to precipitate a 3 fold variation in metabolism. Samples of breath were collected from the chamber into vacutainers at one minute intervals for approximately 40 minutes to an hour. Samples were analyzed by admission to a mass spectrometer (VG Optima) via a GC interface which identified and admitted the CO2 peak. The log converted isotope elimination was linear (r2 > 98% in all cases) indicating a single pool was involved. We evaluated the pool size from a dilution series of the injectate in equilibrium with CO2 gas. Conventional compartmental analysis produced an estimate which on average across the 19 individuals provided a reasonable estimate of the CO2 production. Individual estimates were however imprecise and the overall correlation between isotope and calorimeter estimates had an r2 of only 15%. Reasons for this discrepancy are unclear. Nevertheless an empirical model, using the elimination gradient, pool size and route of isotope administration as predictors explained 86% of the variation in CO2 production. Elimination of a bolus dose of 13C labeled bicarbonate provides a useful tool for estimating the energy metabolism of mice over intervals between 15 and 40 minutes.

Animals↗

PubMed1990

Ammonium and bicarbonate homeostasis in chronic liver disease.

Whereas traditionally in acid-base physiology one considers just two organs (lungs and kidneys) to be involved in the regulation of systemic acid-base homeostasis, recent developments indicate that also the liver must be viewed as an important organ for pH regulation. This is because urea synthesis is a quantitatively important bicarbonate-consuming process, which in turn underlies a feedback control by the acid-base status at least in vitro. Consequently, renal ammoniagenesis, generally accepted to be a direct bicarbonate-generating process, can be viewed as a pH-controlled ammonium homeostatic response. In view of the controversies regarding the roles of ureogenesis and renal ammoniagenesis in acid-base regulation, their relationships were studied in 28 patients with normal renal functions, but varying degrees of a well-compensated chronic liver disease. Progressive loss of urea cycle capacity (as determined by in vitro incubations of human liver tissue) was parallelled by increasing in vivo plasma bicarbonate levels (and metabolic alkalosis) and an increasing NH4+ excretion into the urine. Accordingly, renal ammoniagenesis rose with the extent of metabolic alkalosis. Neither hypokalemia, hyperaldosteronism, diuretic treatment, or volume contraction were present, and a satisfactory explanation for this unusual behavior of renal ammoniagenesis in terms of traditional acid-base physiology cannot be given. Here, it seems that renal ammoniagenesis is governed rather by the need to eliminate ammonia than by the acid-base status.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1990

Changes in membrane conductances and areas associated with bicarbonate secretion in turtle bladder.

Transepithelial impedance-analysis studies were performed in turtle bladder epithelium in order to measure changes in the different epithelial membranes resulting from stimulation of electrogenic bicarbonate secretion. Changes in membrane conductance relate to changes in ionic permeability, whereas changes in membrane capacitance relate to changes in membrane area, since most biological membranes exhibit a specific capacitance of approximately 1 muF/cm2. The results of this investigation are summarized as follows: (i) cAMP and carbachol, agents which have been shown previously to stimulate electrogenic bicarbonate secretion, result in increases in apical-membrane conductance and capacitance; (ii) these changes occur concomitantly with the observed change in transport (measured using the short-circuit-current technique), thereby suggesting that bicarbonate secretion may be regulated in part by changes in the chloride conductance of the apical membrane; (iii) the increase in conductance does not reflect an increase in the membrane's specific conductance, thereby indicating that it results from the addition of membrane possessing similar ionic permeability as the existing apical membrane; (iv) the magnitude of the changes in capacitance indicate that a minor cell population (beta-type carbonic-anhydrase-rich cells) increase their apical-membrane area by several-fold; (v) a lack of transport-associated changes in the basolateral-membrane parameters suggest that transport is not regulated by alterations in basolateral-membrane ionic conductance or area; (vi) a lack of colchicine sensitivity, coupled with the magnitude of the changes in apical-membrane capacitance, indicate that the membrane remodeling processes are different from those involved in the regulation of proton secretion in a different cell population (alpha-type carbonic-anhydrase-rich cells).

1-Methyl-3-isobutylxanthine↗

PubMed1979

Further evidence for the existence of an intrinsic bicarbonate-stimulated Mg2+-ATPase in brush border membranes isolated from rat kidney cortex.

The aim of this study was to provide further evidence for the existence of a nonmitochondrial becarbonate-stimulated Mg2+-ATPase in brush border membranes derived from rat kidney cortex. A plasma membrane fraction rich in brush border microvilli and a mitochondrial fraction were isolated by differential centrifugation. Both fractions contain a Mg2+-ATPase activity which can be stimulated by bicarbonate. The two Mg2+-ATPases are stimulated likewise by chloride, bicarbonate, and sulfite or inhibited by oligomycin and aurovertin, though to different degrees. In contrast to these similarities, only the Mg2+-ATPase activity of the mitochondrial fraction is inhibited by atractyloside, a substance which blocks an adenine nucleotide translocator in the inner mitochondrial membrane. On the other hand, filipin, an antibiotic that complexes with cholesterol in the membranes inhibits exclusively the Mg2+-ATPase of the cholesterol-rich brush border membranes. Furthermore it could be demonstrated by the use of bromotetramisole, an inhibitor of alkaline phosphatase activity, that the Mg2+-ATPase activity in the membrane fraction is not due to the presence of the highly active alkaline phosphatase in these membranes. These results support the assumption that an intrinsic bicarbonate-stimulated Mg2+-ATPase is present in rat kidney brush border membranes.

Adenosine Triphosphatases↗

PubMed1984

Sympathetic activity, plasma renin activity (PRA) and kininogen levels in patients haemodialysed with acetate and bicarbonate.

Sympathetic, renin and kinin responses to an acetic and bicarbonate fluid in haemodialysed patients were investigated. Increases in dopamine-beta-hydroxylase (DBH) activity, PRA and kininogen levels were found during single dialysis but there was no difference in acetate and bicarbonate haemodialysis. The present results suggest that changes in sympathetic renin and kinin activity were similar in patients treated with either acetate or bicarbonate fluid.

Acetates↗