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PubMed1993

Short-term clinical study with bicarbonate-containing peritoneal dialysis solution.

OBJECTIVE: The evaluation of the efficacy, adequacy, clinical tolerance, and safety of a new bicarbonate continuous ambulatory peritoneal dialysis (CAPD) solution. DESIGN AND PATIENTS: A 6-week cross-over clinical study in 6 stable CAPD patients was performed. After a control period (2 weeks) with a standard CAPD solution (lactate, 35 mmol/L), a two-chamber bag containing 34 mmol/L of bicarbonate was used for 4 weeks. A breakable valve divided the two chambers, one containing bicarbonate and the other calcium. The two solutions were mixed just before use, thus avoiding the calcium and magnesium carbonate precipitation. RESULTS: No differences between control and study periods were found for blood urea nitrogen, creatinine, total proteins, albumin, total and ionized calcium, phosphate, sodium, potassium, chlorine, and hemoglobin. Blood bicarbonate significantly increased from 21.25 +/- 2.02 to 23.36 +/- 1.15 (p < 0.05) during the study. The peritoneal equilibration tests for urea nitrogen, creatinine, proteins, sodium, potassium, and glucose were slightly reduced during bicarbonate dialysate, but this effect was compensated for by a slight increase of ultrafiltration, thus keeping peritoneal clearances constant. Residual renal function did not change during the study. No side effects occurred during the bicarbonate period. CONCLUSION: A CAPD bicarbonate solution is effective in uremic acidosis correction, does not affect dialysis adequacy, is safe, and well tolerated.

Adult↗
PubMed2002

Role of bicarbonate in the regulation of intracellular pH in the mammalian ventricular myocyte.

Bicarbonate is important for pHi control in cardiac cells. It is a major part of the intracellular buffer apparatus, it is a substrate for sarcolemmal acid-equivalent transporters that regulate intracellular pH, and it contributes to the pHo sensitivity of steady-state pHi, a phenomenon that may form part of a whole-body response to acid/base disturbances. Both bicarbonate and H+/OH- transporters participate in the sarcolemmal regulation of pHi, namely Na(+)-HCO3-cotransport (NBC), Cl(-)-HCO3- exchange (i.e., anion exchange, AE), Na(+)-H+ exchange (NHE), and Cl(-)-OH- exchange (CHE). These transporters are coupled functionally through changes of pHi, while pHi is linked to [Ca2+]i through secondary changes in [Na+] mediated by NBC and NHE. Via such coupling, decreases of pHo and pHi can ultimately lead to an elevation of [Ca2+]i, thereby influencing cardiac contractility and electrical rhythm. Bicarbonate is also an essential component of an intracellular carbonic buffer shuttle that diffusively couples cytoplasmic pH to the sarcolemma and minimises the formation of intracellular pH microdomains. The importance of bicarbonate is closely linked to the activity of the enzyme carbonic anhydrase (CA). Without CA activity, intracellular bicarbonate-dependent buffering, membrane bicarbonate transport, and the carbonic shuttle are severely compromised. There is a functional partnership between CA and HCO3- transport. Based on our observations on intracellular acid mobility, we propose that one physiological role for CA is to act as a pH-coupling protein, linking bulk pH to the allosteric H+ control sites on sarcolemmal acid/base transporters.

Acid-Base Equilibrium↗
PubMed1994

[Doppler echocardiographic evaluation of the new mechanical bileaflet Sorin Bicarbon valve prosthesis compared with St. Jude Medical].

BACKGROUND: Despite the Bicarbon valve has been marketed for more than two years, no systematic Doppler evaluation of its normal functioning has yet been published. Therefore, the aims of this study were to establish the normal flow characteristics for the Bicarbon bileaflet prosthetic heart valve and to compare them with those obtained from the St. Jude Medical valve prosthesis. METHODS: Doppler echocardiographic characteristics of normally functioning Bicarbon prostheses were prospectively assessed in 76 consecutive patients (44 males and 32 females, mean age 60 +/- 10 years) with 79 valves in mitral (n = 29) and aortic (n = 50) position whose function was considered normal by clinical and echocardiographic evaluation. In addition, Doppler characteristics of the Bicarbon valves in aortic position were compared to those of 27 normal functioning St. Jude Medical implanted during the same period. RESULTS: For the mitral valve prostheses, we found non significant difference among prosthesis sizes in terms of transprosthetic gradients or pressure half time. Peak and mean gradients were similar in the 27-mm and 31-mm size valves (from 11 +/- 4 to 11 +/- 2 mm Hg and from 5 +/- 2 to 5 +/- 1 mm Hg, respectively; p = NS for both). Similarly, the pressure half time was similar in the 27-mm and in the 31-mm size valve (85 +/- 16 and 76 +/- 13 msec; p = NS). Conversely, for the aortic valve prostheses, there was a significant decrease in transprosthetic gradients and an increase in effective orifice areas as prosthesis size increased. Mean gradient was 13 +/- 1 mm Hg in 19-mm size valves, and it decreased to 6 +/- 2 mm Hg in the 29-mm size. Effective prosthetic valve area calculated using the continuity equation, ranged between 1.0 +/- 0.3 cm2 for 19-mm size valves to 3.5 +/- 0.7 cm2 for 29-mm size. With analysis of variance, effective prosthetic aortic valve area differentiated various valve sizes (F = 23.3; p < 0.0001) better than peak (F = 3.2; p = 0.017) or mean (F = 4.19; p = 0.0035) gradients alone did. Furthermore, effective prosthetic aortic valve area correlated better than peak and mean gradients with prosthetic size (r = 0.87, r = -0.58 and r = -0.57; respectively). In addition, peak and mean transprosthetic gradients and effective prosthetic aortic valve areas did not show any statistically significant difference between the Bicarbon and the St. Jude Medical valves in aortic position, either in 19 and 21 mm (25 +/- 8 mm Hg, 13 +/- 4 mm Hg, 1.3 +/- 0.3 cm2 and 32 +/- 11 mm Hg, 17 +/- 6 mm Hg, 1.2 +/- 0.4 cm2, respectively; p = NS), or in 23 and 25 mm (21 +/- 8 mm Hg, 11 +/- 4 mm Hg, 2.1 +/- 0.5 cm2 and 24 +/- 11 mm Hg, 12 +/- 5 mm Hg, 1.8 +/- 0.4 cm2, respectively; p = NS) or in 27 and 29 mm (12 +/- 2 mm Hg, 7 +/- 1 mm Hg, 2.8 +/- 0.9 cm2 and 16 +/- 5 mm Hg, 7 +/- 2 mm Hg, 2.6 +/- 0.4 cm2, respectively; p = NS). CONCLUSIONS: This study suggest that the Bicarbon valve prosthesis offers relatively little resistance to forward flow except at a small anulus diameter. Furthermore, these is no statistically significant difference between the Bicarbon and the St. Jude Medical in aortic position with regard to early hemodynamic performances.

Aged↗
PubMed1991

Differential effects of sodium bicarbonate and aluminium hydroxide on the absorption and activity of glipizide.

The effects of sodium bicarbonate and aluminium hydroxide on the absorption and activity of glipizide have been studied in healthy volunteers in two randomized cross-over trials. After an overnight fast, 5 mg glipizide was given either with 150 ml water or with water containing 3.0 g sodium bicarbonate or 1.0 g aluminium hydroxide. Sodium bicarbonate significantly increased the AUC of plasma glipizide from 0 to 0.5 h, 0 to 1 h, and from 0 to 2 h (six-, four- and twofold, respectively). The time to peak concentration (tmax) fell from 2.5 h during the control phase to 1.0 h during the sodium bicarbonate phase. The absorption half-life (t1/2a), lag time and mean residence time (MRT) were also significantly decreased. No significant change in peak plasma concentration (Cmax), total AUC or elimination half-life (t1/2) was noted. The decremental plasma glucose areas from 0 to 1 h and 0 to 2 h were significantly larger (80% and 50%, respectively) than during the control phase. The maximal decrease in glucose was 50% greater during the sodium bicarbonate phase, and the time to reach it was reduced by 35 min. Aluminium hydroxide had no significant effects on the rate or extent of absorption of glipizide, and the glucose response also remained unaffected. It is concluded that the concomitant ingestion of sodium bicarbonate and glipizide may result in accelerated absorption of glipizide and an increased effect on glucose. A common dose of aluminium hydroxide did not appear to affect the absorption of glipizide.

Adult↗
PubMed1993

Hemodynamic effects of sodium bicarbonate in critically ill neonates.

OBJECTIVE: To analyze the cardiovascular effects of sodium bicarbonate in neonates with metabolic acidosis. DESIGN: Prospective, open, non-randomized, before-after intervention study with hemodynamic measurements performed before and 1, 5, 10, 20, and 30 min after bicarbonate administration. SETTING: Neonatal intensive care unit, tertiary care center. PATIENTS: Sequential sample of 16 paralysed and mechanically ventilated newborn infants with a metabolic acidosis (pH < 7.25 in premature and < 7.30 in term infants, base deficit > -8). INTERVENTION: An 8.4% sodium bicarbonate solution diluted 1:1 with water (final osmolality of 1000 mOsm/l) was administered in two equal portions at a rate of 0.5 mmol/min. The dose in mmol was calculated using the formula "base deficit x body weight (kg) x 1/3 x 1/2". MEASUREMENTS AND RESULTS: Sodium bicarbonate induced a significant but transient rise in pulsed Doppler cardiac output (CO) (+27.7%), aortic blood flow velocity (+15.3%), systolic blood pressure (BP) (+9.3%), (+14.6%), transcutaneous carbon dioxide pressure (PtcCO2) (+11.8%), and transcutaneous oxygen pressure (PtcO2) (+8%). In spite of the PaCO2 elevation, pH significantly improved (from a mean of 7.24 to 7.30), and the base deficit decreased (-39.3%). Calculated systemic vascular resistance (SVR) (-10.7%) and diastolic BP (-11.7%) decreased significantly, while PaO2 and heart rate (HR) did not change. Central venous pressure (CVP) (+6.5%) increased only slightly. By 30 min after bicarbonate administration all hemodynamic parameters, with the exception of the diastolic BP, had returned to baseline. CONCLUSION: Sodium bicarbonate in neonates with metabolic acidosis induces an increase in contractility and a reduction in afterload.

Acidosis, Lactic↗
PubMed2004

Rabbit corneal hydration and the bicarbonate pump.

Experiments were conducted on the transport properties of the rabbit corneal endothelium at 22 degrees C, at which temperature the endothelium was able to stabilize the hydration of corneal stroma at physiological values. When bicarbonate was omitted from the bathing solution, the cornea swelled at 11 +/- 1 microm x h(-1). The swelling was completely reversible upon the subsequent re-introduction of bicarbonate. Similar swelling rates were observed when the endothelial pump was irreversibly inhibited with ouabain. In an Ussing-type chamber, the endothelium developed an electrical resistance of 25.0 +/- 1.0 ohms x cm2 and a short circuit current (s.c.c.) of 6.0 +/- 1.1 microA x cm(-2). Neither electrical resistance of the corneal endothelium nor its s.c.c. were changed significantly after exposure to 0.5 mM amiloride. Ouabain abolished the s.c.c. but had no significant effect on resistance. When paired preparations were short-circuited, the endothelium developed a net H[14C]O3- flux of 0.24 +/- 0.03 micromoles x cm(-2) x h(-1) into the aqueous humour, which was close in magnitude and direction to the s.c.c. of 0.22 +/- 0.01 microEq x cm(-2) x h(-1). There was no significant net flux of 86Rb (0.04 +/- 0.03 micromoles x cm(-2) x h(-1)). Similar magnitude fluxes for both bicarbonate and rubidium were found with open-circuit preparations. It is suggested that a metabolically driven electrogenic bicarbonate current passing across the corneal endothelium is solely responsible for maintaining corneal hydration at 22 degrees C. Based on these and other studies, a model is proposed for active bicarbonate transport across corneal endothelium consisting of uphill entry into the cell through a baso-lateral membrane sodium/bicarbonate cotransporter (NBC) and downhill exit through an apical membrane anion channel. Studies on the transport properties of the endothelium at 35 degrees C are discussed and reasons suggested for the discrepancy between short circuit current and net bicarbonate flux at this closed eye temperature.

Animals↗
PubMed1990

Paradoxical effect of bicarbonate on cytoplasmic pH.

The effect of an abrupt rise in bicarbonate concentration on cytoplasmic pH was studied in human platelets suspended in a Tyrode's buffer. Addition of bicarbonate raised extracellular pH but simultaneously caused pronounced cytoplasmic acidification. This effect may be due to combination of bicarbonate with hydrogen ions in extracellular fluid to form carbonic acid, which is converted by carbonic anhydrase to water and carbon dioxide. Bicarbonate ions do not diffuse rapidly across cell membranes, whereas carbon dioxide is highly diffusible and can combine with water in the cytoplasm, forming carbonic acid and reducing the intracellular pH. In accord with this explanation cytoplasmic acidification by bicarbonate was antagonised by acetazolamide (an inhibitor of carbonic anhydrase). Cytoplasmic acidification could contribute to adverse effects of intravenous sodium bicarbonate in patients with severe acidaemia. These findings add weight to the body of opinion that such treatment is both illogical and dangerous.

Acetazolamide↗
PubMed1990

Effects of a membrane-bound trypsin-like proteinase and seminal proteinase inhibitors on the bicarbonate-sensitive adenylate cyclase in porcine sperm plasma membranes.

Plasma membranes were purified from flagella of porcine cauda epididymal sperm and proteolytic regulation of bicarbonate-sensitive adenylate cyclase was studied. It was found that the epididymal sperm plasma membrane contained a trypsin-like proteinase which inactivated adenylate cyclase. Bicarbonate activates adenylate cyclase as reported previously, but, at the same time, the anions enhance the inactivation of the enzyme by the membrane-bound trypsin-like proteinase. This phenomenon is not due to the direct activation of the proteinase, but closely related to the activation of adenylate cyclase by bicarbonate. It was also found that seminal proteinase inhibitors blocked the inactivation of adenylate cyclase and maintained the bicarbonate activation of the enzyme at high level. Actually, bicarbonate keeps adenylate cyclase fully active in ejaculated sperm, because membrane-bound proteinase is completely inhibited by the seminal proteinase inhibitors. These results suggest that the interactions between membrane-bound proteinase and seminal proteinase inhibitor are involved in the regulation of the bicarbonate-sensitive adenylate cyclase system.

Adenylyl Cyclase Inhibitors↗
PubMed2006

Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest.

OBJECTIVE: This study evaluates the effect of early administration of an empirical (1 mEq/kg) sodium bicarbonate dose on survival from prehospital cardiac arrest within brief (<5 minutes), moderate (5-15 minutes), and prolonged (>15 minutes) down time. METHODS: Prospective randomized, double-blinded clinical intervention trial that enrolled 874 prehospital cardiopulmonary arrest patients managed by prehospital, suburban, and rural regional emergency medical services. Over a 4-year period, the randomized experimental group received an empirical dose of bicarbonate (1 mEq/kg) after standard advanced cardiac life support interventions. Outcome was measured as survival to emergency department, as this was a prehospital study. RESULTS: The overall survival rate was 13.9% (110/792) for prehospital arrest patients. There was no difference in the amount of sodium bicarbonate administered to nonsurvivors (0.859 +/- 0.284 mEq/kg) and survivors (0.8683 +/- 0.284 mEq/kg) (P = .199). Overall, there was no difference in survival in those who received bicarbonate (7.4% [58/420]), compared with those who received placebo (6.7% [52/372]) (P = .88; risk ratio, 1.0236; 0.142-0.1387). There was, however, a trend toward improved outcome with bicarbonate in prolonged (>15 minute) arrest with a 2-fold increase in survival (32.8% vs 15.4%; P = .007). CONCLUSION: The empirical early administration of sodium bicarbonate (1 mEq/kg) has no effect on the overall outcome in prehospital cardiac arrest. However, a trend toward improvement in prolonged (>15 minutes) arrest outcome was noted.

Advanced Cardiac Life Support↗
PubMed2006

Identification and membrane localization of electrogenic sodium bicarbonate cotransporters in Calu-3 cells.

Cystic fibrosis (CF) is a severely life-shortening genetic disease resulting from mutations in the gene for the cystic fibrosis transmembrane conductance regulator (CFTR). Impaired bicarbonate secretion is a key component of CF-related pancreatic disease, but the role of impaired bicarbonate secretion in CF lung disease is less well understood. The submucosal glands of the conducting airways produce and secrete a complex airway surface liquid that lines the airway epithelium and plays a significant role in mucociliary clearance. The serous cell is the predominant cell type of the submucosal gland and a predominant site of CFTR expression. Calu-3 cells are a model of airway submucosal gland serous cells that demonstrates vectorial bicarbonate secretion in response to elevations in cAMP. Based on previously published measurements of unidirectional ion flux, pharmacological inhibition of short-circuit current and ion substitution studies, one can hypothesize the existence of an electrogenic sodium bicarbonate cotransporter (NBC) in the basolateral membrane of Calu-3 cells that mediates bicarbonate entry from the interstitium. To test this hypothesis, we performed reverse-transcriptase PCR, western blotting, and surface biotinylation to identify and localize electrogenic NBCs in Calu-3 cells. Our data demonstrate that both pNBC1 and NBC4 mRNAs can be identified and that their protein products are expressed at the basolateral membrane of polarized Calu-3 cells. These data suggest that these transporters contribute to regulated bicarbonate secretion across Calu-3 cells and perhaps human airway submucosal glands.

Base Sequence↗
PubMed2002

Intestinal bicarbonate secretion by marine teleost fish--why and how?

Intestinal fluids of most marine teleosts are alkaline (pH 8.4-9.0) and contain high levels of HCO(3)(-) equivalents (40-130 mM) which are excreted at a significant rate (>100 microEq kg(-1) h(-1)). Recent research reveals the following about this substantial HCO(3)(-) secretion: (1) It is not involved in acid-base regulation or neutralisation of stomach acid, but increases in parallel with drinking rate at elevated ambient salinities suggesting a role in osmoregulation; (2) In species examined so far, all sections of the intestine can secrete bicarbonate; (3) The secretion is dependent on mucosal Cl(-), sensitive to mucosal DIDS, and immuno-histochemistry indicates involvement of an apical Cl(-)/HCO(3)(-) exchanger. In addition, hydration of CO(2) via carbonic anhydrase in combination with proton extrusion appears to be essential for bicarbonate secretion. The mode of proton extrusion is currently unknown but potential mechanisms are discussed. One consequence of the luminal alkalinity and high bicarbonate concentrations is precipitation of calcium and magnesium as carbonate complexes. This precipitation is hypothesised to reduce the osmolality of intestinal fluids and thus play a potential role in water absorption and osmoregulation. The present studies on European flounder reveal that elevated luminal calcium (but not magnesium) concentrations stimulate intestinal bicarbonate secretion both acutely and chronically, in vitro and in vivo. At the whole animal level, the result of this elevated bicarbonate secretion was increased calcium precipitation with an associated reduction in the osmolality of rectal fluids and plasma. These observations suggest direct functional links between intestinal bicarbonate secretion, divalent cation precipitation and osmoregulation in marine teleost fish.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1986

Lowered levels of bicarbonate in seminal plasma cause the poor sperm motility in human infertile patients.

Both the adenylate cyclase activity and the motility of human sperm were stimulated by bicarbonate with the same concentration dependency. The correlation between bicarbonate levels in semen and the motility of sperm from the patients with male infertility was investigated. Bicarbonate in semen was found to originate mainly from the seminal vesicles, and a significant positive correlation was observed between bicarbonate levels and volume of semen. The motility of infertile sperm was also found to correlate positively to the seminal levels of bicarbonate. These results suggest that the lowered levels of bicarbonate in semen are at least in part responsible for the poor sperm motility in infertile patients, as a result of the failure in the activation of sperm adenylate cyclase.

Acid Phosphatase↗
PubMed1987

Effects of bicarbonate on arterial and brain intracellular pH in neonatal rabbits recovering from hypoxic lactic acidosis.

We used 31P spectroscopy to determine whether administration of a neutralizing dose of bicarbonate in rabbits with lactic acidosis caused a paradoxical brain intracellular acidosis. Ten 10- to 16-day-old rabbits were anesthetized with 0.75% halothane/oxygen and their lungs mechanically ventilated. Metabolic acidosis was induced by decreasing PaO2 to 25 to 35 mm Hg for 1 to 2 hours until the base deficit was 10 to 15 mEq/L. Cerebral ischemia was prevented by maintaining arterial blood pressure at +/- 20% of control value with a venous infusion of epinephrine. Hypoxia was then terminated by administration of 100% oxygen, which was continued for the remainder of the study. After 15 minutes 100% oxygen, 5 mEq/kg 4.2% bicarbonate was administered to five animals; 5 minutes later the same dose was repeated. Control rabbits were given equal volumes of saline solution. In all animals, arterial pH decreased from 7.43 +/- 0.06 to 7.25 +/- 0.08 (SE) during hypoxia, and brain intracellular pH from 7.22 +/- 0.06 to 7.09 +/- 0.09 (SE). Both pH values remained low during reoxygenation. Bicarbonate administration normalized arterial pH (7.41 +/- 0.03), whereas treatment with saline solution did not (7.23 +/- 0.01, P less than 0.05). PaCO2 rapidly increased by 10 mm Hg in the bicarbonate group, and remained elevated; it was unaffected by saline solution administration. Brain intracellular pH in the bicarbonate group increased by 0.12 U over 40 minutes, but intracellular pH in the saline solution group decreased 0.05 pH U (P less than 0.05) over the same period. We conclude that administering a total dose of 10 mEq/kg sodium bicarbonate to neonatal rabbits recovering from hypoxic lactic acidosis increases arterial pH, brain intracellular pH, and PaCO2; it does not produce paradoxical intracellular acidosis in the brain.

Acidosis, Lactic↗
PubMed1986

Effects of pyruvate salts, pyruvic acid, and bicarbonate salts in preventing experimental oxalate urolithiasis in rats.

Sodium pyruvate, potassium pyruvate, pyruvic acid, sodium bicarbonate and potassium bicarbonate were added to a calcium-oxalate lithogenic diet (a glycolic-acid diet) in order to determine their effects in preventing lithogenicity. Male Wistar-strain rats who had been fed the glycolic-acid diet developed marked urinary calculi within four weeks. Rats in the sodium and potassium pyruvate groups had, however, almost no stones in the urinary system. Rats in the bicarbonate and pyruvic-acid groups showed slightly less effect than those in the pyruvate groups. Urinary oxalate excretion was high in all the groups during the experiment. The urinary oxalate concentration was relatively higher in the sodium-pyruvate group, and significantly higher in the potassium-pyruvate group, than in the glycolic-acid group. Urinary citrate excretion was high both in the pyruvate and bicarbonate groups; the urinary citrate concentration was, however, significantly higher in the pyruvate groups than in the bicarbonate groups at the fourth experimental week. The urinary calcium and magnesium concentrations were irrelevant to the diets administered. Therefore, it can be concluded that pyruvate salts inhibit urinary calculi formation, not by decreasing oxalate synthesis, but by increasing the urinary citrate concentration; bicarbonate salts work in the same manner, but a little less effectively.

Animals↗
PubMed1991

Correction of metabolic acidosis in experimental CPR: a comparative study of sodium bicarbonate, carbicarb, and dextrose.

STUDY OBJECTIVE: Carbicarb, sodium bicarbonate, and 5% dextrose were compared for effects on resuscitability in a canine model of electromechanical dissociation after ventricular fibrillation. DESIGN/INTERVENTIONS: 21 healthy mongrel dogs were anesthetized with pentobarbital, intubated, and mechanically supported. They were instrumented to measure heart rate, arterial pressure, pulmonary artery pressure, right atrial pressure, cardiac output, and arterial and mixed venous blood gases. The dogs were then subjected to a protocol that consisted of three successive CPR episodes. During each episode they were treated with repeated injections of one of the three substances, randomly chosen. After two minutes of ventricular fibrillation and four minutes of electromechanical dissociation, CPR was started with a thumper (rate, 60; duty cycle, 50%). If recovery was not obtained after five minutes of CPR, 1 mEq/kg carbicarb or sodium bicarbonate or 5 mL D5W was injected in the right atrium. Half the dose of the same substance was injected every five minutes thereafter; 1 mg epinephrine was also injected every five minutes until recovery. Hemodynamic and gasometric evaluations were performed five and 20 minutes after recovery. This later evaluation served as baseline for the next CPR episode. MEASUREMENTS AND MAIN RESULTS: The duration and success rates of CPR are similar in the three CPR groups. Hemodynamic parameters were also similar during recovery. Bicarbicarb and sodium bicarbonate increased bicarbonate levels and corrected pH in the arterial and mixed venous blood. There was no difference in the blood gas values after carbicarb and sodium bicarbonate. CONCLUSION: In this model of cardiac arrest, carbicarb was not superior to sodium bicarbonate in the correction of metabolic acidosis during CPR.

Acidosis, Lactic↗
PubMed1983

Effects of acetate and bicarbonate hemodialysis on cardiac function in chronic dialysis patients.

Previous studies have suggested that acetate hemodialysis causes myocardial depression. This study examines the acute effects of hemodialysis using, alternately, bicarbonate and acetate in the dialysate, on cardiac function in ten patients. These patients were also studied during acetate dialysis using a large surface area (SA) dialyzer. Each patient was dialyzed for 4 hr with: (1) 1.0 m2 SA dialyzer and bicarbonate dialysate; (2) 1.0 m2 SA dialyzer and acetate bath, and; (3) 2.5 m2 SA dialyzer and acetate dialysate. All studies were performed during isovolemic dialysis to separate the effects of changes in cardiac filling volume with hemodialysis, from changes in myocardial contractility. Myocardial function, as assessed by pre- and postdialysis echocardiographically derived fractional shortening (Fs) and mean velocity of circumferential shortening (VCF), improved (P less than 0.05) to the same extent, after all three dialysis treatments. This occurred despite greater increases (P less than 0.002) in pH and bicarbonate after bicarbonate dialysis and decreases (P less than 0.05) in PO2, PCO2 and bicarbonate after acetate dialysis with 2.5 m2 SA dialyzer. These results indicate that diffusive dialysis with both acetate and bicarbonate dialysate improves myocardial function and do not support the view that acetate influx during dialysis can lead to myocardial depression.

Acetates↗
PubMed1990

Reclamation of filtered bicarbonate.

Approximately 85% of the filtered bicarbonate load is reabsorbed in the proximal convoluted tubule. Transport in this segment displays saturation kinetics, and exhibits a higher capacity for reabsorption in the earliest portion. Reclamation of bicarbonate is highly regulated in the proximal tubule: an increase in luminal [HCO3-], flow rate and arterial PCO2 increase, while alkalinization of the peritubular surface inhibits bicarbonate absorption. Angiotensin II also appears to regulate bicarbonate transport, especially in the S1 segment. The majority of the filtered bicarbonate load which escapes reabsorption in the proximal tubule is reabsorbed in the thick ascending limb of Henle's loop. Bicarbonate reclamation in this segment is enhanced by luminal [HCO3-] and furosemide, and by chronic metabolic acidosis and increased dietary sodium intake. Amiloride, AVP and glucagon inhibit absorption in the thick ascending limb.

Acid-Base Equilibrium↗
PubMed1992

Sodium bicarbonate ingestion and its effects on anaerobic exercise of various durations.

Four groups of male subjects participated in anaerobic testing on a Repco EX10 cycle ergometer to determine the effectiveness of sodium bicarbonate (0.3 g kg-1 body mass) as an ergogenic aid during exercise of 10, 30, 120 and 240 s duration. Blood was collected 90 min prior to ingestion of sodium bicarbonate (NaHCO3), after ingestion of NaHCO3 and immediately post-exercise from a heated (43-46 degrees C) fingertip and analysed immediately post-collection for pH, base excess, bicarbonate and lactate. The total work undertaken (kJ) and peak power achieved during the tests were also obtained via a Repco Work Monitor Unit. Blood bicarbonate levels were again increased above the control and placebo conditions (P < 0.001) and blood lactate levels were also increased following the bicarbonate trials. The pH levels fell significantly (P < 0.05) below the control and placebo conditions in all trials. The results indicate that NaHCO3 at this dosage has no ergogenic benefit for work of either 10 or 30 s duration, even though blood bicarbonate levels were significantly increased (P < 0.05) following ingestion of NaHCO3. For work periods of 120 and 240 s, performance was significantly increased (P < 0.05) above the control and placebo conditions following NaHCO3 ingestion.

Adult↗