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PubMed1998

Effects of calcium and bicarbonate on head-to-head agglutination in ejaculated boar spermatozoa.

The present study was conducted to reveal the effects of calcium and bicarbonate on the occurrence of head-to-head agglutination in ejaculated boar spermatozoa in vitro. Boar spermatozoa were washed and incubated in a modified Krebs-Ringer bicarbonate (mKRB) in a 37 degrees C CO2 incubator (5% CO2 in air) for 1-5 h. Before and after the incubation, aliquots of each sperm sample were fixed, smeared on glass slides, and stained with a phosphate-buffered solution of Giemsa to assess the percentages of head-to-head agglutinated spermatozoa. Before the incubation, only 5-12% of the spermatozoa were agglutinated. After the 1-h incubation, however, the percentage of head-to-head agglutinated spermatozoa rose to approximately 50%, followed by only minor increases thereafter. This rise was dependent on the concentrations of calcium chloride contained in the mKRB and was attenuated by the addition of 2 mM [ethylenebis(oxyethylenenitrilo)]tetra-acetic acid (EGTA) to the medium. Moreover, the replacement of sodium bicarbonate with 2-[4-(2-hydroxyethyl)-1-piperazinyl]ethanesulfonic acid (Hepes) in the medium and treatment with ruthenium red, which have both been shown previously to inhibit calcium uptake by boar spermatozoa, significantly reduced the rise. Based on these findings, it was concluded that extracellular calcium and bicarbonate are key factors regulating head-to-head agglutination in boar spermatozoa. The possible relationship between agglutinability and the fertilizing ability of boar spermatozoa is also discussed.

Animals↗
PubMed2001

Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion.

Pendrin is an anion transporter encoded by the PDS/Pds gene. In humans, mutations in PDS cause the genetic disorder Pendred syndrome, which is associated with deafness and goiter. Previous studies have shown that this gene has a relatively restricted pattern of expression, with PDS/Pds mRNA detected only in the thyroid, inner ear, and kidney. The present study examined the distribution and function of pendrin in the mammalian kidney. Immunolocalization studies were performed using anti-pendrin polyclonal and monoclonal antibodies. Labeling was detected on the apical surface of a subpopulation of cells within the cortical collecting ducts (CCDs) that also express the H(+)-ATPase but not aquaporin-2, indicating that pendrin is present in intercalated cells of the CCD. Furthermore, pendrin was detected exclusively within the subpopulation of intercalated cells that express the H(+)-ATPase but not the anion exchanger 1 (AE1) and that are thought to mediate bicarbonate secretion. The same distribution of pendrin was observed in mouse, rat, and human kidney. However, pendrin was not detected in kidneys from a Pds-knockout mouse. Perfused CCD tubules isolated from alkali-loaded wild-type mice secreted bicarbonate, whereas tubules from alkali-loaded Pds-knockout mice failed to secrete bicarbonate. Together, these studies indicate that pendrin is an apical anion transporter in intercalated cells of CCDs and has an essential role in renal bicarbonate secretion.

Animals↗
PubMed2003

An alternative mechanism of bicarbonate-mediated peroxidation by copper-zinc superoxide dismutase: rates enhanced via proposed enzyme-associated peroxycarbonate intermediate.

Hydrogen peroxide can interact with the active site of copper-zinc superoxide dismutase (SOD1) to generate a powerful oxidant. This oxidant can either damage amino acid residues at the active site, inactivating the enzyme (the self-oxidative pathway), or oxidize substrates exogenous to the active site, preventing inactivation (the external oxidative pathway). It is well established that the presence of bicarbonate anion dramatically enhances the rate of oxidation of exogenous substrates. Here, we show that bicarbonate also substantially enhances the rate of self-inactivation of human wild type SOD1. Together, these observations suggest that the strong oxidant formed by hydrogen peroxide and SOD1 in the presence of bicarbonate arises from a pathway mechanistically distinct from that producing the oxidant in its absence. Self-inactivation rates are further enhanced in a mutant SOD1 protein (L38V) linked to the fatal neurodegenerative disorder, familial amyotrophic lateral sclerosis. The 1.4 A resolution crystal structure of pathogenic SOD1 mutant D125H reveals the mode of oxyanion binding in the active site channel and implies that phosphate anion attenuates the bicarbonate effect by competing for binding to this site. The orientation of the enzyme-associated oxyanion suggests that both the self-oxidative and external oxidative pathways can proceed through an enzyme-associated peroxycarbonate intermediate.

Amyotrophic Lateral Sclerosis↗
PubMed1999

Effects of gamma-aminobutyric acid and peripheral benzodiazepine ligands on duodenal bicarbonate secretion.

BACKGROUND: The effects of gamma-aminobutyric (GABA(A))-receptor ligands and peripheral-type benzodiazepine (BZ) ligands on duodenal mucosal bicarbonate secretion (DBS) were studied in thiobarbiturate-anesthetized rats. METHODS: A segment of proximal duodenum was perfused, and bicarbonate secretion was continuously titrated by pH-stat. In some experiments the vagus nerves were dissected free and cut at the neck level. RESULTS: Luminal GABA (10(-8) to 10(-6) M) increased (P < 0.01) DBS dose-dependently, and the GABA(A) antagonist (+)-bicuculline (0.1-2.5 mg/kg intravenously) caused a similar increase (P < 0.01) in DBS. Vagotomy abolished the latter response, suggesting a centrally elicited nervous action of bicuculline mediated by the vagal nerves. This was supported by the absence of an effect of bicuculline administered intra-arterially close to the duodenum. The GABA(A) agonist muscimol had no effect on DBS when administered intravenously (0.01-0.25 mg/kg) or into a lateral brain ventricle (2 microg/kg/h) but counteracted any stimulation by subsequent intravenous bicuculline. The 'peripheral-type' BZ agonist 4'-chlorodiazepam increased DBS when infused close intra-arterially but had no effect when administered intravenously. CONCLUSIONS: Inhibition of GABA(A) receptors related to cholinergic excitatory pathways in the central nervous system stimulates duodenal mucosal bicarbonate secretion and may increase the local mucosal defense. The stimulation by luminal GABA may reflect modulation of the local mucosal control of duodenal bicarbonate secretion.

Analysis of Variance↗
PubMed2005

Effects of iron on Vitamin C/copper-induced hydroxyl radical generation in bicarbonate-rich water.

The aim of this study was to evaluate whether iron, like copper, could support Vitamin C mediated hydroxyl radical formation in bicarbonate-rich water. By using the hydroxyl radical indicator coumarin-3-carboxylic acid, we found that iron, in contrast to copper, was not capable to support Vitamin C induced hydroxyl radical formation. However, when 0.2 mg/l iron and 0.1 mg/l copper were both added to bicarbonate supplemented Milli-Q water, the Vitamin C induced formation of 7-hydroxycoumarin, as measured by HPLC analysis, was inhibited by 47.5%. The inhibition of hydroxyl radical formation by iron was also evident in the experiments performed on copper contaminated bicarbonate-rich household drinking water samples. In the presence of 0.2 mg/l of ferric iron the ascorbic acid induced hydroxyl radical formation was inhibited by 36.0-44.6%. This inhibition was even more significant, 47.0-59.2%, when 0.8 mg/l of ferric iron was present. None of the other redox-active metals, e.g. manganese, nickel or cobalt, could support ascorbic acid induced hydroxyl radical formation and did not have any impact on the ascorbic acid/copper-induced hydroxyl radical generation. Our results show, that iron cannot by itself produce hydroxyl radicals in bicarbonate rich water but can significantly reduce Vitamin C/copper-induced hydroxyl radical formation. These findings might partly explain the mechanism for the iron-induced protective effect on various copper related degenerative disorders that earlier has been observed in animal model systems.

Ascorbic Acid↗
PubMed1999

Acebutolol-induced ventricular tachycardia reversed with sodium bicarbonate.

BACKGROUND: Acebutolol is a unique beta blocker that possesses cardioselectivity, partial agonist activity, and membrane stabilizing activity. Sodium bicarbonate is used to reverse the cardiotoxic effects of other drugs with membrane stabilizing activity. There have been no reported cases of acebutolol-induced ventricular dysrhythmias treated successfully with bolus sodium bicarbonate. CASE PRESENTATION: A 48-year-old man ingested approximately 6.4 g of acebutolol with ethanol (blood ethanol 61 mmol/L). There were no other coingestants identified. One hour after presentation, the patient had a cardiac arrest with the monitor showing ventricular tachycardia. Sodium bicarbonate 50 mEq intravenous push converted the patient to sinus rhythm and the blood pressure improved to 129/90 mm Hg. CONCLUSION: This case demonstrates a temporal relationship between bolus sodium bicarbonate administration and the termination of acebutolol-induced ventricular tachycardia.

Acebutolol↗
PubMed1976

Effects of halides and bicarbonate on chloride transport in human red blood cells.

Chloride self-exchange was determined by measuring the rate of 36Cl efflux from human red blood cells at pH 7.2 (0 degrees C) in the presence of fluoride, bromide, iodide, and bicarbonate. The chloride concentration was varied between 10--400 mM and the concentration of other halides and bicarbonate between 10--300 mM. Chloride equilibrium flux showed saturation kinetics. The half-saturation constant increased and the maximum flux decreased in the presence of halides and bicarbonate: the inhibition kinetics were both competitive and noncompetitive. The competitive and the noncompetitive effects increased proportionately in the sequence: fluoride less than bromide less than iodide. The inhibitory action of bicarbonate was predominantly competitive. The noncompetitive effect of chloride (chloride self-inhibition) on chloride transport was less dominant at high inhibitor concentrations. Similarly, the noncompetitive action of the inhibitors was less dominant at high chloride concentrations. The results can be described by a carrier model with two anion binding sites: a transport site, and a second site which modifies the maximum transport rate. Binding to both types of sites increases proportionately in the sequence: fluoride less than chloride less than bromide less than iodide.

Bicarbonates↗
PubMed1996

Normovolaemic haemodilution attenuates cardiac depression induced by sodium bicarbonate in canine metabolic acidosis.

This study was designed to determine if coexisting metabolic acidosis or normovolaemic haemodilution, or both, modifies the acute cardiodepressant effect of i.v. sodium bicarbonate. Thirty-one mongrel dogs were anaesthetized with halothane, and the lungs ventilated mechanically; dogs were allocated randomly to one of four groups: control group (pHa 7.39 (SD 0.03), base excess -1.0 (1.6) mmol litre-1, haemoglobin 13.9 (2.5) g dl-1 (n = 8)), metabolic acidosis group (pHa 7.21 (0.05), base excess -11.2 (2.1) mmol litre1, haemoglobin 13.4 (2.6) g dl-1 (n = 8)), anaemia group (pHa 7.40 (0.04), base excess 0.1 (2.0) mmol litre-1, haemoglobin 7.2 (1.1) g dl-1 (n = 8)) or anaemia acidosis group (pHa 7.22 (0.04), base excess -11.0 (2.2) mmol litre-1, haemoglobin 7.4 (0.3) g dl-1 (n = 7)). Metabolic acidosis was induced by continuous i.v. infusion of hydrochloric acid 2 mol litre-1. Normovolaemic haemodilution was undertaken by phlebotomy and simultaneous exchange with lactated Ringer's solution at 37 degrees C. Mean arterial pressure (MAP), pulmonary artery pressure, right atrial pressure (RAP), maximum rate of change of pressure in the right ventricle (RV dP/dtmax) and pulmonary blood flow (PBF) were measured at 30 s, 1 and 3 min after administration of 7% sodium bicarbonate solution 1 mmol kg-1 given into the right atrium over 5 s. Sodium bicarbonate produced significant decreases in MAP and RV dP/dtmax at 30 s in all groups except for the anaemia acidosis group (P < 0.05). There was a significant decrease in right ventricular stroke volume in the metabolic acidosis group from baseline values (P < 0.05), and compared with the three other groups (P < 0.05). These results indicate that the cardiodepressant effect of sodium bicarbonate 1 mmol kg-1 i.v. during metabolic acidosis was more pronounced than without acidosis, but was attenuated in the presence of normovolaemic haemodilution.

Acidosis↗
PubMed1997

High bicarbonate dialysate in haemodialysis patients: effects on acidosis and nutritional status.

BACKGROUND: Metabolic acidosis adversely affects both protein and bone metabolism in patients with chronic renal failure, and could also affect morbidity and mortality. This trial aimed to investigate the effects of different dialysate bicarbonate concentrations on control of acid base balance, and nutritional status. METHODS: Forty-six stable haemodialysis patients were dialysed using LowBic. (30 mmol/l) or HighBic. (40 mmol/l) bicarbonate dialysate in a single blind double crossover trial, of two consecutive six-month periods. Blood gas analysis, anthropometric indices and dialysis dose were measured, in addition to biochemical indices. RESULTS: Predialysis 'arterial' plasma pH values were significantly higher when using the HighBic. dialysate (LowBic. 7.38 +/- 0.05, HighBic. 7.43 +/- 0.04, P < 0.001), as was predialysis serum total CO2 at all times during the study (P < 0.01). Kt/V, (LowBic. 1.27 +/- 0.19, HighBic. 1.27 +/- 0.25), urea generation rates (UGR) (LowBic. 1.99 +/- 0.77, HighBic. 1.92 +/- 0.77 mmol/min), and normalized protein catabolic rate (NPCR) (LowBic. 1.04 +/- 0.26, HighBic. 0.99 +/- 0.28 g/kg/day) did not differ, and values of parathroid hormone (PTH) were comparable. Triceps skinfold thickness (TSF) showed a significant change (LowBic. 14.8 +/- 6.9-11.8 +/- 5.5, HighBic. 14.9 +/- 6.3-15.8 +/- 6.4 mm, P < 0.05) which was reversed following dialysate change (HighBic. 11.8 +/- 5.5-13.3 +/- 7.2, LowBic. 15.8 +/- 6.4-13.8 +/- 6.7 mm, P < 0.05). No differences in mid upper arm circumference were found. CONCLUSIONS: Bicarbonate dialysate concentrations of 40 mmol/l were safe, well tolerated, and produced better control of acidosis, with an increase in TSF, compared to a bicarbonate concentration of 30 mmol/l.

Acidosis↗
PubMed1990

Acetate or bicarbonate for haemodialysis: a randomised, double-blind controlled trial.

In a prospective, randomised, double blind controlled trial the adverse reactions, food consumption, changes in blood chemistry including acid-base balance, and anthropometry were studied during two consecutive dialysis periods of 3 months, using either acetate- or bicarbonate-based dialysis fluids. Sixteen chronic, stable patients were included. The dialysis fluid sodium content was fixed at 140 mmol/l during all treatments. Patient complaints and adverse reactions were identical using the two dialysis fluids. No differences were observed regarding blood chemistry except for a less pronounced metabolic acidosis present during bicarbonate dialysis compared to acetate dialysis. A slight but insignificant increment in food consumption and nutritional status was noticed during bicarbonate dialysis. In conclusion, the use of a bicarbonate-based haemodialysis fluid offered no significant advantages compared to an acetate-based one in the haemodialysis of chronic, stable patients.

Acetates↗
PubMed2003

Unexpected haemodynamic instability associated with standard bicarbonate haemodialysis.

BACKGROUND: The bicarbonate concentration in dialysis fluids for intermittent haemodialysis usually is between 32 and 35 mmol/l. The severity of chronic metabolic acidosis secondary to end-stage renal failure is very variable, however, so that in some patients pre-dialysis acidosis is overcorrected. This study aimed to analyse haemodynamic tolerances to metabolic alkalosis during intermittent haemodialysis. METHODS: In this randomized controlled trial with a single blind, cross-over design, we used dialysis liquids with two different bicarbonate concentrations, 32 (modality A) and 26 (modality B) mmol/l, and in 26 patients, 468 dialysis sessions, compared blood pressure, heart rate, incidence of hypotension and the frequency of corrections required with saline or hypertonic glucose infusions. RESULTS: The results of intradialytic haemodynamic monitoring for modalities A and B, respectively, were: lowest systolic blood pressure 120.8+/-20.8 vs 124.3+/-20.6 mmHg (P < 0.01); mean systolic blood pressure 138.5+/-23.8 vs 144.6+/-24.8 mmHg (P < 0.001); and highest heart rate 73.5+/-12.0 vs 75.8 +/- 12.9 (NS); with modality A, patients had more dialysis sessions with hypotensive episodes (5.55 vs 1.7%, P < 0.05) and required more saline or hypertonic glucose infusions (20.9 vs 13.7% of the dialysis sessions, P < 0.05). CONCLUSIONS: Mild metabolic alkalosis resulting from standard bicarbonate haemodialysis (32 mmol/l) may induce symptomatic hypotension. While normalizing chronic metabolic acidosis is desirable, reducing bicarbonate concentrations should be considered in cases of significant alkalaemia or otherwise untreatable haemodynamic instability.

Adult↗
PubMed2005

The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients.

BACKGROUND: Hyperkalaemia is common in patients with advanced renal disease. In this double-blind, randomized, three-sequence, crossover study, we compared the effect of three dialysate bicarbonate concentrations ([HCO3-]) on the kinetics of serum potassium (K+) reduction during a conventional haemodialysis (HD) session in chronic HD patients. METHODS: We studied eight stable HD patients. The choice of dialysate [HCO3-] followed a previously assigned treatment protocol and the [HCO3-] used were low bicarbonate (LB; 27 mmol/l), standard bicarbonate (SB; 35 mmol/l) and high bicarbonate (HB; 39 mmol/l). Polysulphone dialysers and automated machines provided blood flow rates of 300 ml/min and dialysis flow rates of 500 ml/min for each HD session. Blood samples were drawn at 0 (baseline), 15, 30, 60 and 240 min from the arterial extracorporeal line to assess blood gases and serum electrolytes. In three of the eight patients, we measured serum K+ 1 h post-dialysis as well as K+ removal by the dialysis. The same procedures were followed until the completion of the three arms of the study, with a 1 week interval between each experimental arm. RESULTS: Serum K+ decreased from 5.4+/-0.26 (baseline) to 4.96+/-0.20, 4.90+/-0.19, 4.68+/-0.13 and 4.24+/-0.15 mmol/l at 15, 30, 60 and 240 min, respectively, with LB; from 5.38+/-0.21 to 5.01+/-0.23, 4.70+/-0.25, 4.3+/-0.15 and 3.8+/-0.19 mmol/l, respectively, with SB; and from 5.45+/-0.25 to 4.79+/-0.17, 4.48+/-0.17, 3.86+/-0.16 and 3.34+/-0.11 mmol/l, respectively, with HB (P<0.05 for high vs standard and low [HCO3-] at 60 and 240 min). The decrease in serum K+ correlated with the rise in serum [HCO3-] in all but LB (P<0.05). Potassium rebound was 3.9+/-10.2%, 5.2+/-6.6% and 8.9+/-4.9% for LB, SB and HB dialysates, respectively (P=NS), while total K+ removal (mmol/dialysis) was 116.4+/-21.6 for LB, 73.2+/-12.8 for SB and 80.9+/-15.4 for HB (P=NS). CONCLUSIONS: High dialysate [HCO3-] was associated with a faster decrease in serum K+. Our results strongly suggest that this reduction was due to the enhanced shifting of K+ from the extracellular to the intracellular fluid compartment rather than its removal by dialysis. This finding could have an impact for those patients with life-threatening pre-HD hyperkalaemia.

Acid-Base Equilibrium↗
PubMed1998

Research notes: Sodium bicarbonate supplementation in diets for guinea fowl raised at high environmental temperatures.

An experiment was designed to verify the effect of dietary NaHCO3 supplementation on performance of guinea fowl raised under high environmental temperatures (23.8 to 33.9 C) and average relative humidity of 78.7%. One hundred and forty guinea fowl in their final period of growth (56 to 84 d of age) were allotted to individual wire cages. Five isocaloric (3,000 kcal ME/kg) 16% CP diets based on corn and soybean meal and containing 0, 0.6, 1.2, 1.8, and 2.4% sodium bicarbonate were fed to the birds. The experiment followed a randomized block design with 28 birds per treatment (14 of each sex) with each bird being considered as one repetition. Results showed that weight gain, feed intake, feed conversion, mortality, blood pH, carcass yield, and carcass composition were not affected (P > 0.05) by dietary sodium bicarbonate supplementation. Weight gain, feed intake, feed conversion, carcass moisture, and fat content, however, were significantly (P < 0.05) affected by sex. Females showed 17.49% better weight gain, 7.16% greater feed intake, and 9.6% better feed conversion than males. These differences were exacerbated at supplementation levels of 1.2 and 1.8% sodium bicarbonate in the diet. Male birds showed carcass moisture values significantly (P < 0.05) greater than those of female birds; the opposite occurred with carcass fat levels. The use of sodium bicarbonate in levels up to 2.4% of the diet did not affect the performance of guinea fowl raised under the environmental conditions registered in this study.

Animals↗
PubMed2004

Bicarbonate is required for migration of sperm epididymal protein DE (CRISP-1) to the equatorial segment and expression of rat sperm fusion ability.

Numerous studies have demonstrated that sperm capacitation is a bicarbonate-dependent process. In the rat, capacitation has not been studied as much as in other species, mainly because of the difficulties in carrying out functional assays with this animal model. In the present study, we have examined the influence of bicarbonate in the overall rat sperm capacitation process by analyzing involvement of the anion in 1) protein tyrosine phosphorylation, 2) migration of epididymal protein DE (also known as CRISP-1) from the dorsal region to the equatorial segment of the sperm head that occurs during capacitation, and 3) ability of sperm to fuse with the egg. Incubation of sperm under capacitating conditions produced a time-dependent increase in protein tyrosine phosphorylation. This phosphorylation did not occur in the absence of HCO3- and rapidly increased by either exposure of sperm to HCO3- or replacement of the anion by a cAMP analog (dibutyryl-cAMP) and a phosphodiesterase inhibitor (pentoxifylline). The absence of HCO3- also produced a significant decrease in the percentage of cells showing migration of DE to the equatorial segment. This parameter was completely restored by addition of the anion, but dibutyryl-cAMP and pentoxifylline were not sufficient to overcome the decrease in DE migration. Sperm capacitated in the absence of HCO3- were unable to penetrate zona-free eggs independent of the presence of the anion during gamete coincubation. Exposure of these sperm to bicarbonate, or replacement of the anion by dibutyryl-cAMP and pentoxifylline, only partially restored the sperm fusion ability. Altogether, these results indicate that, in addition to its influence on protein tyrosine phosphorylation, bicarbonate is required to support other rat sperm capacitation- associated events, such as migration of DE to the equatorial segment, and expression of the ability of sperm to fuse with the egg.

Animals↗
PubMed1998

On the cellular mechanisms by which the bicarbonate ion mediates the extragenomic action of progesterone on human spermatozoa.

Progesterone exerts an extragenomic action on human spermatozoa, inducing a rapid calcium transient in the acrosomal domain of these cells and enhancing their potential for fertilization. This response is known to exhibit an absolute dependence on the presence of extracellular bicarbonate, although the mechanisms underlying this interaction are not understood. In this study, bicarbonate was found to exert a dose-dependent impact on the ability of progesterone to promote sperm-oocyte fusion in the absence of any collateral effect on sperm motility. The loss of sperm function in bicarbonate-free medium was associated with a failure to produce reactive oxygen species, an impaired capacity to exhibit redox-associated changes in tyrosine phosphorylation, and an apparent incapacity to generate normal calcium transients on exposure to progesterone. These defects were not related to a cAMP deficiency but were associated with a significant fall in intracellular pH. If cytosolic pH was chemically buffered into the normal range, then the spermatozoa regained every element of their response to progesterone. These results emphasize the importance of an alkaline intracellular milieu for the extragenomic action of progesterone on human spermatozoa and stress the fundamental difference between intracellular and extracellular sources of bicarbonate in maintaining the proton balance within such cells.

Acrosome↗
PubMedDate not supplied

Effect of varying dialysate bicarbonate concentration on serum phosphate.

Hyperphosphatemia is practically a universal problem in patients with chronic renal failure. Conventional treatment of hyperphosphatemia in this situation is either only partially effective or may be associated with potentially serious adverse effects. The authors examined the effect of inducing a metabolic alkalosis on serum phosphate in chronic hemodialysis patients by increasing the concentration of bicarbonate in dialysate. Seven patients participated in the study. Each patient was on dialysis for 2 weeks with each of 2 dialysate regimens. Regimen A contained a bicarbonate concentration of 25 mEq/L and Regimen B a bicarbonate concentration of 40 mEq/L. Despite Regimen B resulting in a significant increase in predialysis and postdialysis serum bicarbonate concentration and arterial pH, no significant difference in serum phosphate was demonstrated after 2 weeks of therapy.

Bicarbonates↗
PubMed1999

Accuracy of intramucosal pH calculated from arterial bicarbonate and the Henderson-Hasselbalch equation: assessment using simulated ischemia.

OBJECTIVES: To determine the accuracy of intramucosal pH (pHi) calculated using arterial bicarbonate instead of mucosal capillary bicarbonate in the Henderson-Hasselbalch equation. DESIGN: Simulation of progressive ischemia in mucosal capillary blood. SETTING: University research laboratory. SUBJECTS: Normal human blood diluted with plasma. INTERVENTIONS: Three venous blood specimens were heparinized and diluted to a mean hemoglobin concentration of 5.0 (+/-0.9) g/dL by addition of plasma (2:1, vol:vol). Mucosal capillary aerobic flow stagnation was simulated by multiple exposures of each cooled specimen to a gas mixture containing 90% nitrogen and 10% CO2. When PCO2 measured at 37 degrees C (98.6 degrees F) was approximately 120 torr (16 kPa), the assigned anaerobic threshold, subsequent anaerobic flow stagnation was simulated by mixing the hypercapnic specimens in sealed syringes with five to six successive small aliquots (<100 microL) of lactic acid (10 g/L). MEASUREMENTS AND MAIN RESULTS: The relationship between Pco2 and pH in the specimens was compared with the relationship between the same PCO2 values and pHi calculated by substituting bicarbonate concentrations of 22 and 26 mmol/L in the Henderson-Hasselbalch equation. As PCO2 rose from 50 torr (8 kPa), conventionally calculated pHi increasingly underestimated simulated mucosal capillary pH, with bias >0.1 pH unit at the simulated anaerobic threshold of 120 torr (16 kPa). As PCO2 rose further the values converged, becoming equivalent at PCO2 approximately 150 torr (20 kPa). From PCO2 > or =200 torr (26.7 kPa), conventional pHi progressively overestimated simulated mucosal pH. The difference was >0.3 pH units at PCO2 = 250 torr (33.3 kPa). CONCLUSIONS: In the mucosal PCO2 range usually encountered clinically, the arterial bicarbonate substitution causes underestimation of mucosal capillary pH. With moderate mucosal capillary lactic acidosis the error becomes small, and in severe regional ischemia there is significant overestimation of mucosal capillary pH.

Anaerobic Threshold↗
PubMed1993

Bicarbonate and citrate in oral rehydration therapy: studies in a model of secretory diarrhea.

In situ perfusion of the rat jejunum and ileum was used to study the effect of inclusion of bicarbonate or citrate on the ability of four oral rehydration solutions to promote small-intestinal absorption of water and sodium. Solutions varied in their sodium (60-90 mM) and glucose (111-140 mM) content and osmolality (281-331 mosmol/kg). They were studied before and after exclusion of base both in normal intestine and in secreting intestine after exposure to cholera toxin. All solutions promoted net water absorption in the normal intestine and reversed net water secretion to absorption in the cholera toxin-treated intestine to varying degrees. Net sodium movement was directly related to the sodium content of oral rehydration solutions. Inclusion of bicarbonate or citrate did not promote significantly greater absorption of water or sodium than did solutions without base, in normal or secreting intestine. In the secreting intestine, inclusion of bicarbonate in two solutions actually resulted in greater sodium secretion than did identical solutions from which bicarbonate was omitted. These studies suggest that the inclusion of base or base precursors in oral rehydration solutions to enhance water and sodium absorption is unjustified in both normal and secreting small intestine.

Animals↗