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PubMed1991

Effects of bicarbonate supplementation on urinary mineral excretion during very low energy diets.

Metabolic acidosis is associated with increased calciuria and ammoniagenesis. This study evaluated the effects of oral sodium bicarbonate (NaHCO3) or combined potassium bicarbonate-calcium carbonate supplementation on urinary mineral excretion during the ketoacidosis of a very-low-energy protein diet. Seventeen healthy obese subjects (BMI: 37.5 +/- 3.2 kg/m2, weight: 100 +/- 3 kg) were given a 1.72 MJ all protein (93 g) liquid formula and a multivitamin-mineral supplement daily for 3 weeks. Subjects in groups 1 (n = 6) and 2 (n = 5) received 16 mmol KCl. In addition, subjects in group 1 received 60 mmol Na+ daily as sodium chloride, subjects in group 2, 60 mmol Na+ as NaHCO3. The subjects in group 3 (n = 6) were given 32 mmol K+ as bicarbonate and 16 mmol Ca++ as carbonate daily. Metabolic acidosis was prevented in groups 2 and 3 with bicarbonate and bicarbonate-carbonate administration. This was reflected in significant curtailment of the augmented ammonium nitrogen excretion found in group 1. The additional oral K+ in group 3 improved K+ balance and probably also inhibited ammoniagenesis. Urine calcium was greater (p less than 0.04) in group 1 subjects, but similar in groups 2 and 3, despite higher calcium intake in group 3. Urinary phosphorus decreased with time in all groups, but more so in the group 2 subjects who received NaHCO3. Acidosis was associated with the reverse effect on urinary magnesium, which decreased in group 1 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1998

The effects of extracellular pH with and without bicarbonate on intracellular procaine concentrations and anesthetic effects in crayfish giant axons.

BACKGROUND: The potentiating effect of sodium bicarbonate on local anesthetic action is attributed to two mechanisms: (1) an increase in the un-ionized local anesthetic due to extracellular alkalinization, and (2) an accelerated conversion of local anesthetic from un-ionized to ionized form with intracellular acidification caused by bicarbonate. To evaluate these hypotheses, the intracellular pH, intracellular ionized procaine concentration, and evoked action potentials were measured in crayfish giant axons. METHODS: In all measurements, axon preparations from crayfish were perfused extracellularly for 15 min with either bicarbonate-containing solution at pH 7.6 (bicarb/7.6) or bicarbonate-free solution at pH 7.6 (nonbicarb/7.6) or pH 8.0 (nonbicarb/8.0). Intracellular pH was measured using a pH-sensitive microelectrode. Intracellular anesthetic concentration was measured using a specially designed procaine-sensitive microelectrode with each of three solutions containing 1 mM procaine hydrochloride. Membrane potential was measured and, as an index of anesthetic action, the dV/dt of evoked action potential was calculated during perfusion with procaine. RESULTS: Mean intracellular pH was significantly lower in the bicarb/7.6 (7.16+/-0.07) group than in the nonbicarb/7.6 (7.33+/-0.09) and nonbicarb/8.0 (7.33+/-0.12) groups (P < 0.01). The mean intracellular ionized procaine concentration was significantly higher in the bicarb/7.6 (0.53+/-0.08 mM; P < 0.05) and nonbicarb/8.0 (0.58+/-0.13 mM; P < 0.01) than in nonbicarb/7.6 (0.32+/-0.14 mM) group but did not differ between the bicarb/7.6 and nonbicarb/8.0 groups. The mean percentage decrease in dV/dtmax was approximately coincident with the mean intracellular procaine concentration in each solution. CONCLUSION: The presence of bicarbonate or extracellular alkalinization increased the intracellular concentration of ionized procaine and the anesthetic effect.

Action Potentials↗
PubMed1990

Effects of cigarette smoke and nicotine on duodenal bicarbonate secretion in the rabbit and the rat.

The effects of short-time exposure to cigarette smoke on duodenal mucosal bicarbonate secretion were studied in anesthetized rabbits and rats. The bicarbonate secretion was measured by continuous titration of recirculating luminal perfusate. In artificially ventilated rabbits, intermittent exposure to cigarette smoke during two 10-min periods caused a marked (approximately 40%) decrease (p less than 0.01) in duodenal bicarbonate secretion. After the exposures, secretion gradually recovered and had returned to the pre-exposure rate after 50 min. The decrease in secretion was associated with decreases in heart rate (approximately 15%) and blood pressure (approximately 30%) that, however, were of shorter duration. Neither reduced amounts of smoke (1/6 or 1/3) nor nicotine (25-1,000 micrograms/kg, intravenously) had any major effect on the bicarbonate secretion. In the spontaneously breathing rat, smoke was administered for 1-2 breaths every 30 s during a 5-min period. This exposure resulted in a significant (p less than 0.05) decrease in bicarbonate secretion and some increase in the blood pressure. Exposure to smoke had no effect on the secretion in rats with both splanchnic nerves cut, suggesting neural sympathetic mediation of the smoke-induced inhibition.

Animals↗
PubMed1994

Potentiation of canine pancreatic bicarbonate output by oleic acid is not neurally dependent.

To study neural involvement in potentiation of acid-induced pancreatic bicarbonate output, six dogs underwent extrapancreatic denervation and pancreatic fistula creation. Pancreatic responses to secretin (16 and 32 ng/kg/h) and cholecystokinin (50 ng/kg/h) were then assessed. The duodenum was then perfused with three sets of perfusates. The first set contained hydrochloric acid with either D- or L-phenylalanine. The second set contained bovine serum albumin and hydrochloric acid with or without oleic acid; the albumin and acid were varied so that each 50 ml contained 1, 2, or 4 meq titratable acid (pH 2.0-4.5). The third set was identical to the second except for initial pH of 3.5. Pancreatic responses predicted upon addition of cholecystokinin to secretin, L-phenylalanine to hydrochloric acid, or oleic acid to bovine serum albumin were compared with observed responses. At both doses, secretin-induced bicarbonate output was increased by cholecystokinin (16 ng/kg/h: 0.88 +/- 0.29 meq/15 min; 32 ng/kg/h: 1.01 +/- 0.23 meq/15 min). The latter significantly exceeded predicted output (16 ng/kg/h: 0.38 +/- 0.10 meq/15 min; 32 ng/kg/h: 0.58 +/- 0.15 meq/15 min), verifying potentiation. L-phenylalanine failed to potentiate bicarbonate output evoked by acidified D-phenylalanine. In contrast, addition of oleic acid to pH 2.0 or 3.5 bovine serum albumin potentiated bicarbonate output. These data suggest that enteropancreatic reflexes mediate potentiation of acid-induced pancreatic bicarbonate output by amino acids, but not by fatty acids.

Animals↗
PubMed2002

Insulin inhibits secretin-induced pancreatic bicarbonate output via cholinergic mechanisms.

INTRODUCTION: Exogenous insulin inhibits secretin-stimulated pancreatic bicarbonate output via a dose-dependent mechanism; this effect is prevented by pancreatic denervation. AIMS: To investigate possible cholinergic mediation, we examined the effect of bethanechol on secretin-stimulated pancreatic secretion during euglycemic, hyperinsulinemic clamp. METHODOLOGY: In four dogs with chronic pancreatic fistulas, euglycemic, hyperinsulinemic clamp (1.25 mU/kg/min) was begun after a 30-minute basal period; computer-assisted glucose administration maintained euglycemia. Control studies were performed with volume-matched and rate-matched vehicle infusion. After 1 hour, secretin infusion was begun at a dosage of 16 ng/kg/h; the dose was doubled every 30 minutes. The studies were then repeated during background bethanechol infusion (90 microg/kg/h) begun 30 minutes after clamp initiation. Pancreatic juice was analyzed for bicarbonate and protein; serum samples were analyzed for glucose and insulin. RESULTS: Exocrine outputs and serum glucose and insulin levels did not differ in the basal period. Insulin levels were significantly elevated during the euglycemic, hyperinsulinemic clamp (62 microU/mL versus 12 microU/mL; p < 0.01); glucose levels did not differ. As before, secretin-induced bicarbonate output was inhibited by euglycemic, hyperinsulinemic clamp. The inhibitory effect of insulin was reversed by bethanechol. Despite the euglycemic, hyperinsulinemic clamp, secretin-induced bicarbonate output was potentiated by bethanechol at higher secretin doses (p < 0.05). CONCLUSION: These data confirm that cholinergic mechanisms mediate insulin's inhibition of secretin-induced pancreatic bicarbonate output.

Animals↗
PubMed2006

Does bicarbonate correct coagulation function impaired by acidosis in swine?

BACKGROUND: Coagulopathy is an important contributor to morbidity and mortality in trauma patients. Acidosis contributes to coagulopathy. Acidosis can be neutralized with intravascular bicarbonate, but it is unclear if the coagulation defect is rapidly reversed. The effects of acidosis and bicarbonate neutralization on coagulation function were investigated in vivo. METHODS: Acidosis was induced in 12 pigs by infusing 0.2 mol/L HCl to pH 7.1. Pigs were then infused with either LR to maintain a pH of 7.1 (A-LR, n = 6) or 0.3 mol/L bicarbonate to a pH of 7.4 (A-Bi, n = 6). Blood samples were taken at baseline, 15 minutes after acidosis induction, and 15 minutes after bicarbonate neutralization. Coagulation function was assessed by prothrombin time (PT), partial thromboplastin time (PTT), thrombin generation, initial clot formation time (R), clotting rapidity (alpha), and clot strength (MA). RESULTS: Compared with baseline values, acidosis reduced fibrinogen concentration to 66% +/- 2% in A-LR and to 71% +/- 3% in A-Bi, and decreased platelet counts to 49% +/- 4% in A-LR and to 53% +/- 4% in A-Bi. Thrombin generation decreased to 60% +/- 4% in A-LR and to 53% +/- 7% in A-Bi. Acidosis prolonged PT and PTT about 20% and decreased alpha and MA. After pH neutralization, fibrinogen and platelet levels remained depleted and no reversal of acidosis-induced changes in thrombin generation, PT, PTT, alpha, and MA were observed. CONCLUSION: Acidosis impaired coagulation by depleting fibrinogen and platelets and by inhibiting clotting kinetics. The deficit associated with acidosis was not reversed with bicarbonate pH neutralization.

Acidosis↗
PubMed1982

Chloride--bicarbonate exchange in red blood cells: physiology of transport and chemical modification of binding sites.

About 80% of the CO2 formed by metabolism is transported from tissues to lungs as bicarbonate ions in the water phases of red cells and plasma. The catalysed hydration of CO2 to bicarbonate takes place in the erythrocytes but most of the bicarbonate thus formed must be exchanged with extracellular chloride to make full use of the carbon dioxide transporting capacity of the blood. The anion transport capacity of the red cell membrane is among the largest ionic transport capacities of any biological membrane. Exchange diffusion of chloride and bicarbonate is nevertheless a rate-limiting step for the transfer of CO2 from tissues to lungs. Measurements of chloride and bicarbonate self-exchange form the basis for calculations that demonstrate that the ionic exchange processes cannot run to complete equilibration at capillary transit times less than 0.5 s. The anion exchange diffusion is mediated by a large transmembrane protein constituting almost 30% of the total membrane protein. The kinetics of exchange diffusion must depend on conformational changes of the protein molecule, associated with the binding and subsequent translocation of the transported anion. We have characterized the nature of anion-binding sites facing the extracellular medium by acid-base titration of the transport function and modification of the transport protein in situ with group-specific amino acid reagents. Anion binding and translocation depend on the integrity and the degree of protonation of two sets of exofacial groups with apparent pK values of 12 and 5, respectively. From the chemical reactivities towards amino acid reagents it appears that the groups whose pK = 12 are guanidino groups of arginyl residues, while the groups whose pK = 5 are likely to be carboxylates of glutamic or aspartic acid. Our studies suggest that the characteristics of anion recognition sites in water-soluble proteins and in the integral transport proteins are closely related.

Amino Acids, Dicarboxylic↗
PubMed1988

Oral rehydration therapy without bicarbonate for prevention and treatment of dehydration: a double-blind controlled trial.

Forty children (less than or equal to 2 years of age) were admitted to hospital with acute gastroenteritis and were randomly assigned to receive either an oral rehydration solution (ORS) containing bicarbonate (Na 35, K 20, Cl 37, HCO3 18, glucose 202 mmol litre-1) or an identical solution in which bicarbonate was replaced by chloride ions. Groups were matched for age, sex, ethnic origin, duration of diarrhoea and nutritional status. On admission, degree of dehydration, biochemical and haematological parameters were similar. The majority had minimal or no dehydration and only 30% had moderate to severe dehydration. All children were treated successfully with no complications. Oral rehydration solution intake by each group was similar. Clinical outcome, as judged by speed of rehydration or maintenance of hydration, duration of diarrhoea, stool frequency and length of hospital stay, was the same in both groups. After 24 h of ORS there was no difference between groups in venous pH, serum bicarbonate, urea and electrolytes. In hospitalized children with acute gastroenteritis in the United Kingdom an ORS without bicarbonate is a safe, effective means to prevent dehydration and maintain hydration and acid-base status where dehydration is not severe. Exclusion of bicarbonate would simplify production, increase stability and reduce the cost of ORS without apparent impairment of efficacy.

Acidosis↗
PubMed1994

Kinetics of 13CO2 elimination after ingestion of 13C bicarbonate: the effects of exercise and acid base balance.

In order to investigate the effects of muscular work and preceding exercise on the retention of exogenous labelled bicarbonate, we studied the effects of oral administration of [13C]bicarbonate (0.1 mg kg-1) in five subjects at rest before exercise and during and after 1 h of treadmill walking at 73% VO2max on three separate occasions. Elimination of CO2 from labelled bicarbonate was 62.6 +/- 8.1% at rest, 103.6 +/- 11.3% during exercise (P < 0.01) and 43.0 +/- 4.7% during recovery from exercise (P = 0.01). During exercise mean residence time (MRT) was shorter than at rest (35 +/- 7 min vs. 54 +/- 9 min, P < 0.02) and CO2 pool size was larger (998 +/- 160 ml CO2 kg-1, vs. 194 +/- 28 ml CO2 kg-1, P < 0.001). Compared to values obtained at rest, during recovery from exercise, MRT and CO2 pool size were reduced (34 +/- 5 min, P < 0.05; 116 +/- 19 ml CO2 kg-1, P < 0.02, respectively). In an additional five subjects acidosis and alkalosis were induced prior to administration of oral [13C]bicarbonate at rest. Elimination of bicarbonate was lower during acidosis (46.1 +/- 5.6%, P < 0.01) but was unaltered (50.9 +/- 5.6%, NS) during alkalosis, compared to the values obtained at resting pH. During acidosis MRT and CO2 pool size decreased (37 +/- 3 min, P < 0.01 and 123 +/- 10 ml CO2 kg-1, P < 0.01, respectively) whereas in alkalosis MRT was unchanged (65 +/- 8 min NS) but CO2 pool size was increased (230 +/- 23 ml CO2 kg-1, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1990

Vagal and sympathetic control of gastric and duodenal bicarbonate secretion.

This report summarizes data concerning the extrinsic neural control of bicarbonate secretion by the gastric and duodenal mucosa. Parasympathetic vagal effects have been studied in experimental animals and in man by means of direct electrical vagal stimulation, sham-feeding procedures and intracerebroventricular peptide injections. The results show that the vagal nerves have a stimulatory effect on gastroduodenal bicarbonate secretion. Furthermore, both conventional nicotinic and muscarinic cholinoceptor, as well as non-cholinergic transmission, mediate the vagal effect. Sympathetic splanchnic nerve effects have been investigated by means of nerve sections, direct electrical stimulation, reflex activation and stereotaxic electrical hypothalamic stimulation. The data show that the splanchnic nerves have a predominantly inhibitory action on gastroduodenal bicarbonate secretion by use of peripheral adrenergic neurones and receptors of the alpha-2 subtype. The role of the adrenal glands is not fully understood. It is concluded that gastroduodenal bicarbonate secretion is under autonomic neural control, mainly in the classical antagonistic fashion; the parasympathetic vagal nerves stimulate bicarbonate output, whereas the sympathetic splanchnic nerves are mainly inhibitory.

Acid-Base Equilibrium↗
PubMed2005

Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate during cardiopulmonary resuscitation.

BACKGROUND: The use of sodium bicarbonate (SB) in cardiopulmonary resuscitation (CPR) is controversial. This study analyzes the effects of SB use on CPR outcome in the Brain Resuscitation Clinical Trial III (BRCT III), which was a multicenter randomized trial comparing high-dose to standard-dose epinephrine during CPR. Sodium bicarbonate use in BRCT III was optional. METHODS: The entire BRCT III database was reviewed. Analysis included only patients who arrested out of the hospital and whose time from collapse to initiation of ACLS was no longer than 30 min (total n = 2122 patients). Sodium bicarbonate use by the 16 participating study sites was analyzed. The study sites were divided according to their SB usage profile: 'low SB user' sites administered SB in less than 50% of CPRs and their first epinephrine to SB time exceeded 10 min; and 'high SB user' sites used SB in over 50% of CPRs and their first epinephrine to SB time was <10 min. RESULTS: Sites' SB usage rates ranged between 3.1% and 98.2% of CPRs. Sodium bicarbonate usage rates correlated inversely with the sites' intervals from collapse (r = - 0.579 P = 0.018) from initiation of ACLS (r = - 0.685 P = 0.003) and from first epinephrine (r = - 0.611 P = 0.012) to SB administration. Mean ROSC rate in the 'high SB user' sites was 33.5% (CI = 30.0-37.0) compared to 25.7% (CI = 23.1-28.4) in the 'low SB user' sites. In the 'high SB user' sites, hospital discharge rate was 5.3% (CI = 3.6-7.0) compared to 3% (CI = 2.0-4.0) in the 'low SB user' sites, and 5.3% (CI = 3.6-7.0) had a favorable neurological outcome compared to 2.1% (CI = 1.2-3.0) in the 'low SB user' sites. Collapse to ACLS interval was 8.5 min (CI = 8.1-9.0) in the 'high SB user' sites compared to 10.2 min (CI = 9.8-10.6) in the 'low SB user' sites, and their ACLS to first epinephrine interval was 7.0 min (CI = 6.5-7.5) compared to 9.7 min (CI = 9.3-10.2). Multivariate regression analysis found that belonging to 'high SB user' sites independently increased the chances for ROSC (OR 1.36, CI 1.08-1.7) and for achieving a good neurological outcome (OR 2.18, CI 1.23-3.86). CONCLUSIONS: Earlier and more frequent use of SB was associated with higher early resuscitability rates and with better long-term outcome. Sodium bicarbonate may be beneficial during CPR, and it should be subjected to a randomized clinical trial.

Acidosis↗
PubMed2001

The stoichiometry of the electrogenic sodium bicarbonate cotransporter NBC1 is cell-type dependent.

1. The pancreatic variant of the sodium bicarbonate cotransporter, pNBC1, mediates basolateral bicarbonate influx in the exocrine pancreas by coupling the transport of bicarbonate to that of sodium, with a 2 HCO3-:1 Na+ stoichiometry. The kidney variant, kNBC1, mediates basolateral bicarbonate efflux in the proximal tubule by coupling the transport of 3 HCO3- to 1 Na+. The molecular basis underlying the different stoichiometries is not known. 2. pNBC1 and kNBC1 are 93 % identical to each other with 41 N-terminal amino acids of kNBC1 replaced by 85 distinct amino acids in pNBC1. In this study we tested the hypothesis that the differences in stoichiometry are related to the difference between the N-termini of the two proteins. 3. Mouse renal proximal tubule and collecting duct cells, deficient in both pNBC1- and kNBC1-mediated electrogenic sodium bicarbonate cotransport function were transfected with either pNBC1 or kNBC1. Cells were grown on a permeable support to confluence, mounted in an Ussing chamber and permeabilized apically with amphotericin B. Current through the cotransporter was isolated as the difference current due to the reversible inhibitor dinitrostilbene disulfonate. The stoichiometry was calculated from the reversal potential by measuring the current-voltage relationships of the cotransporter at different Na+ concentration gradients. 4. Our data indicate that both kNBC1 and pNBC1 can exhibit either a 2:1 or 3:1 stoichiometry depending on the cell type in which each is expressed. In proximal tubule cells, both pNBC1 and kNBC1 exhibit a 3 HCO3-:1 Na+ stoichiometry, whereas in collecting duct cells, they have a 2:1 stoichiometry. These data argue against the hypothesis that the stoichiometric differences are related to the difference between the N-termini of the two proteins. Moreover, the results suggest that as yet unidentified cellular factor(s) may modify the stoichiometry of these cotransporters.

Animals↗
PubMed1989

An economical new process for incenter bicarbonate dialysate production: comparison with acetate in a large dialysis population.

It is generally agreed that bicarbonate dialysate is preferable to acetate dialysate, but the major limiting factors of high cost and technical difficulty in maintaining its stability for prolonged periods preclude its widespread use. The procedure developed by the authors stabilizes bicarbonate dialysate for up to 4 days, rendering bicarbonate dialysate feasible for routine out-patient use. HCO3 dialysate is produced in our dialysis unit after an initial investment of $10,000.00, at a cost per 4-h treatment of $1.22 at a dialysate flow of 500 cc/min. One hundred fifty-one chronic dialysis patients participated in an 18-week study to evaluate clinical symptomatology when bicarbonate was substituted for acetate as the dialysis base buffer. Evaluation of each dialysis treatment (total of 8,183 treatments) consisted of both subjective and objective criteria (vomiting, angina, cramps, hypotension, and frequency of use of mannitol, hypertonic saline, and nitroglycerine). The patients were unaware of the change in dialysate solutions. There was a significant reduction (p less than 0.001) in the incidence of vomiting, cramps, hypotension, nausea, flushing, and the use of mannitol and hypertonic saline during bicarbonate dialysate treatment compared with acetate dialysate. Shortness of breath, angina, mental confusion, and paresthesias were not statistically changed. Although the method of HCO3 dialysate production is associated with occasional higher bacterial count than currently recommended by AAMI standards, no adverse reactions were observed in patients treated with standard efficiency dialyzers. It is concluded that the process for incenter HCO3 production is safe, economical, and better tolerated than acetate dialysate.

Acetates↗
PubMedDate not supplied

Agreement between bicarbonate measured on arterial and venous blood gases.

OBJECTIVE: This study aims to determine the extent of agreement between venous and arterial bicarbonate for a group of emergency department patients with respiratory or metabolic illness requiring blood gas analysis as part of their evaluation. METHODS: This prospective study of patients who were deemed by their treating doctor to require an arterial blood gas analysis to determine their ventilatory or acid-base status, compared bicarbonate on an arterial and a venous sample taken as close to simultaneously as possible. Data were analysed using bias (Bland-Altman) methods. Subgroup analyses were performed for the metabolic, respiratory, chronic obstructive airways disease and acidotic subgroups. RESULTS: Two hundred and forty-six patients were entered into the study; 195 with acute respiratory disease and 51 with suspected metabolic derangement. The values of bicarbonate on arterial and venous samples showed close agreement with an average difference between the samples of 1.20 mmol/L (95% limits of agreement being -2.73 to +5.13 mmol/L). Similar agreement was found for all subgroups. CONCLUSION: Venous bicarbonate estimation shows a high level of agreement with the arterial value, with acceptably narrow 95% limits of agreement. These results suggest that venous bicarbonate estimation may be an acceptable substitute for arterial measurement.

Adult↗
PubMed2006

Effect of sodium bicarbonate in rats acutely poisoned with dichlorvos.

The development of effective antidotes against organophosphates such as dichlorvos has been a persistent challenge over the past decades. Therapy of organophosphate poisoning is based on the administration of atropine and oxime as standard antidotes. The present study was undertaken to evaluate the ability of sodium bicarbonate to improve protective effects of standard antidotes in rats poisoned with dichlorvos. The aim of this experiment was to establish the correlation between protective effects and biochemical parameters relevant for acid-base status. In order to examine the protective effect of both standard antidotes and their combinations, groups of experimental animals were poisoned subcutaneously with increasing doses of dichlorvos. Immediately thereafter, rats were treated with atropine 10 mg/kg intramuscularly, oximes 10 mg/kg intramuscularly and sodium bicarbonate 3 mmol/kg intraperitoneally. These antidotes were administered either as single doses or in combinations. In the biochemical part of the experiments, rats were poisoned with dichlorvos 1.3 LD(50) (10.64 mg/kg) subcutaneously and immediately thereafter treated with atropine 10 mg/kg intramuscularly, oximes (trimedoxime or obidoxime) 10 mg/kg intramuscularly and sodium bicarbonate 3 mmol/kg intraperitoneally either as single doses or in combinations. Parameters relevant for acid-base status were measured 10 minutes after the administration of antidotes. The results of our study indicate that addition of sodium bicarbonate to standard antidotes significantly improves protective effects of atropine, obidoxime and trimedoxime. Correlation between protection and biochemical outcome is clearly evident when sodium bicarbonate is being added to atropine.

Acidosis↗
PubMed1988

Comparative potency of carbachol, sham feeding, fundic distension and 16,16-dimethyl prostaglandin E2 as stimulants of human gastric bicarbonate secretion.

Six healthy subjects in random order underwent gastric bicarbonate secretion investigations, including stimulation with increasing doses of the cholinergic agonist carbachol, sham feeding, fundic distension and gastric instillation of 16,16-dimethyl prostaglandin E2. Bicarbonate secretion was measured by a computer-based system which continuously recorded pH and PCO2 of the effluent in a high-volume gastric perfusion system. The peak 30 min gastric bicarbonate output in response to carbachol, 150 mg subcutaneously, was 114% (P less than 0.05). Vagal stimulation by sham feeding resulted in a corresponding increase of 112% (P less than 0.05), while fundic distension to a volume of 600 ml gave an increase of 114% (P less than 0.05). In comparison, the response to 80 micrograms 16,16-dimethyl prostaglandin E2 was much greater, the peak bicarbonate output being increased by 245% (P less than 0.05). Both sham feeding and fundic distension appear to be either submaximal stimuli of gastric bicarbonate secretion in man or may possess both stimulatory and inhibitory actions.

16,16-Dimethylprostaglandin E2↗
PubMed1988

The effect of DIDS on fluid reabsorption from the proximal convoluted tubule of the rat: dependence on the presence of bicarbonate.

The effects of the anion transport inhibitor DIDS (4,4'-diisothiocyano-stilbene-2,2'-disulphonate) on fluid reabsorption by the rat proximal convoluted tubule were investigated by the stationary microperfusion (split-drop) method. Addition of 10(-5) mol 1-1 DIDS to luminal and capillary perfusates in the presence of peritubular bicarbonate (25 mmol 1-1) increased the reabsorptive half-time (t 1/2) from 35.1 +/- 4.5 to 57.0 +/- 6.2 s, corresponding to a decrease in fluid reabsorption (Jv) from 1.33 +/- 0.06 to 0.89 +/- 0.09 nl min-1 mm-1. Omission of bicarbonate per se from the peritubular capillaries reduced Jv to 0.41 +/- 0.03 nl min-1 mm-1 and this reabsorptive flux was completely inhibited by the addition of 2 mmol 1-1 NaCN to both the luminal and peritubular perfusates. In the absence of bicarbonate, the addition of DIDS at either 10(-4) or 10(-5) mol 1-1 to both lumen and capillary perfusates had no significant effect on either t 1/2 or Jv. These results show that the inhibitory action of DIDS on fluid reabsorption is dependent on the presence of bicarbonate. However, the proximal tubule also reabsorbs water in the absence of bicarbonate by a mechanism that is dependent on cellular metabolism, but is insensitive to DIDS at the concentrations used in this study.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1980

Effect of cimetidine and sodium bicarbonate on pancreatic replacement therapy in cystic fibrosis.

Fifteen patients with cystic fibrosis and pancreatic insufficiency were studied during four randomised seven day treatment periods in which they received only pancreatic supplement (Pancrelipase, 27 capsules per day) or supplement plus cimetidine (20 mg/kg body weight/24 h) or sodium bicarbonate (15 g/m2/24 h) alone or in combination. Dietary intake was not fixed but was restricted to foods of known fat and nitrogen content from which daily intakes could be computed. Faecal fat and nitrogen were calculated as g/24 h and percentage of intake. Addition of either cimetidine or bicarbonate resulted in significant improvement in fat and nitrogen excretion, which was not greater with the combination of both drugs. Cimetidine and sodium bicarbonate in these doses are therefore sufficient to produce maximal improvement in digestive activity of pancreatic supplements. Fat excretion per gram of intake fell with cimetidine and bicarbonate from 12 times the normal level, to normal, in patients consuming less than 120 g fat daily. Above this intake the dose of pancreatic supplement appeared to be inadequate. Faecal nitrogen excretion increased with nitrogen intake in all four periods, but, in contrast with fat excretion, the response to cimetidine and bicarbonate was not affected by the level of intake. Dietary intake appears to be a significant factor in determining the faecal output of fat and nitrogen in patients with pancreatic insufficiency and should be considered when determining the optimum amount of pancreatic supplementation.

Adolescent↗