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PubMed1998

Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis.

STUDY OBJECTIVE: Although adjunctive intravenous bicarbonate therapy is commonly recommended for children with severe diabetic ketoacidosis (DKA), no studies assessing clinical outcome with this therapy have ever been performed. Our objective was to determine whether bicarbonate therapy influenced outcome for pediatric DKA. METHODS: The study was a retrospective consecutive case series of 147 admissions for severe DKA (initial pH < or = 7.15 and glucose concentration > or = 300 mg/dL [16.7 mmol/L]) in 106 children during a 16-year period at a tertiary university medical center. Descriptive statistics were applied to the 147 admissions. The first patient admitted with DKA was then selected for each of the 106 children, and clinical and laboratory data were compared between subjects who did and did not receive bicarbonate. Multivariate and matched pair analyses were performed to control potentially confounding variables. RESULTS: Fifty-seven of the 147 patients admitted with DKA (39%) were successfully treated without bicarbonate, including 9 with a pH of 7.00 or less and one with a pH of 6.73. The frequency of complications was comparable between bicarbonate and nonbicarbonate groups (4% versus 2%, P = 1.00). The mean duration of hospitalization for children receiving bicarbonate was 23% (16 hours) longer than children who did not receive bicarbonate in the multivariate analysis (P = .07) and 37% (22 hours) longer in the matched pair analysis (P = .01). The mean rate of metabolic recovery by three distinct measures was similar between groups, and the sample had 80% power to detect differences of 14% to 29% in these measures. CONCLUSION: We found no evidence that adjunctive bicarbonate improved clinical outcome in children with severe DKA. The rate of metabolic recovery and complications were similar in patients treated with and without bicarbonate, and prolonged hospitalizations were noted in the bicarbonate group. We conclude that adjunctive bicarbonate is unnecessary and potentially disadvantageous in severe pediatric DKA.

Adjuvants, Pharmaceutic↗
PubMed1997

Increased gastric bicarbonate secretion in portal hypertensive anesthetized rats: role of prostaglandins and nitric oxide.

Gastric bicarbonate secretion might be modified in portal hypertension as a consequence of the intramucosal increase in prostaglandins and nitric oxide content. Therefore, we studied gastric bicarbonate secretion in control and portal hypertensive rats and investigated the role of prostaglandins and nitric oxide. Basal gastric bicarbonate secretion was studied in rats, using a gastric pH back-titration technique, two weeks after partial portal vein ligation or a sham operation. The effects of the following drugs were investigated: the prostaglandin synthase inhibitor indomethacin (5 mg/kg intravenously), prostaglandin (PGE2) (1 mg/kg intravenously), the nitric oxide synthase inhibitors N(G)-nitro-L-arginine methyl ester (L-NAME, 5 mg/kg intravenously) and N(G)-monomethyl-L-arginine (L-NMMA, 50 mg/kg intravenously), and the nitric oxide donor nitroprusside (5 mmol/liter in the gastric perfusate). Plasma leakage in the gastric wall was also measured after Evans blue dye injection in portal hypertensive and sham-operated rats pretreated by indomethacin (5 mg/kg, intravenously) and L-NAME (5 mg/kg, intravenously). Basal bicarbonate secretion was significantly increased in portal hypertensive rats as compared to controls. After indomethacin, the bicarbonate secretion was significantly reduced to a similar level in both groups. PGE2 increased bicarbonate secretion significantly more in portal hypertensive rats than in sham-operated rats. The NO synthase inhibitor L-NMMA significantly increased bicarbonate secretion in portal hypertensive rats only, while the other inhibitor, L-NAME, increased it significantly more in portal hypertensive than in the sham-operated rats. Plasma leakage in portal hypertensive rats, which was increased in the basal condition as compared to control, was further enhanced by indomethacin but not by L-NAME pretreatment. The nitric oxide donor significantly reduced bicarbonate secretion in portal hypertensive rats to reach a similar level as in sham-operated rats. Basal gastric bicarbonate secretion is increased in portal hypertensive rats. This could be due to an enhanced prostaglandin mucosal level. Nitric oxide, which reduces bicarbonate secretion, may contribute to limiting prostaglandin-induced bicarbonate overproduction.

Anesthesia↗
PubMed2001

Initial effect of sodium bicarbonate on intracellular pH depends on the extracellular nonbicarbonate buffering capacity.

OBJECTIVE: The effect of sodium bicarbonate on intracellular pH under conditions close to those in vivo, with both bicarbonate and nonbicarbonate buffering systems, is unknown. We postulated that this effect depends on the nonbicarbonate buffering capacity because the alkali-induced back-titration of these buffers results in a concentration-dependent release of CO2 in the extracellular space, leading to a decrease in intracellular pH. DESIGN: The study was conducted in two stages. First, human hepatocytes were perfused with pH 7 bicarbonate-buffered medium (5 mM HCO3-, 20 torr Pco2) containing no nonbicarbonate buffer or small amounts (5 mM 4-[2-hydroxyethyl]-1-piperazineethanesulfonic acid [HEPES]) or large amounts (20 mM HEPES) of nonbicarbonate buffer. Second, the changes in intracellular pH of hepatocytes placed in acidotic human blood (pH 7, 5 mM HCO3-, 20 torr Pco2) at three hematocrits (40%, 20%, and 5%) were measured. SETTING: Research laboratory at a medical university. SUBJECTS: Cryopreserved human hepatocytes thawed the day before the experiments. INTERVENTIONS: Sodium bicarbonate was infused for 10 mins to increase the HCO3- concentration from 5 to 30 mM. In the second part, 20 mM sodium bicarbonate was added directly to the blood bathing the cells. MEASUREMENTS AND MAIN RESULTS: The intracellular pH was measured with the pH-sensitive fluorescent dye bis-carboxyethyl carboxy-fluorescein in its esterified form, acetoxy-methyl ester, by using a single-cell imaging technique. Gas analyses were performed before and during the sodium bicarbonate load. Sodium bicarbonate caused a decrease in intracellular pH with all media except the artificial medium containing no HEPES. This decrease was small in media with low nonbicarbonate buffering capacity (5 mM HEPES and 5% hematocrit blood) and large in media with high nonbicarbonate buffering capacity (20 mM HEPES and 40% hematocrit blood). The change in intracellular pH was linked closely to the change in Pco2 caused by the sodium bicarbonate. CONCLUSIONS: The effect of sodium bicarbonate on intracellular pH depends on changes in Pco2 in the medium bathing the cells. The increase in Pco2 is correlated with the extracellular nonbicarbonate buffering capacity because of the release of H+ ions coming from the back-titration of these buffers. We conclude that sodium bicarbonate may exacerbate cell acidosis under buffering conditions close to those in vivo and that the initial changes in cell pH caused by sodium bicarbonate depend on the extracellular nonbicarbonate buffering capacity.

Blood↗
PubMed1976

Compensatory adaptation of bicarbonate excretion following acute contralateral kidney exclusion in the dog.

Changes in the excretion of bicarbonate, sodium and potassium in one kidney after exclusion (complete sudden ligation of renal pedicle) of its partner have been studied in 16 dogs undergoing bicarbonate diuresis. Fluid balance, haematocrit, plasma electrolyte and protein concentrations were maintained constant throughout the experiment. Acute contralateral renal pedicle ligation lead to an immediate increase in bicarbonate as well as water, sodium and potassium excretion by the remaining kidney. The rapid and immediate increase in the fractional and absolute rates of bicarbonate excretion was observed at varying levels of bicarbonate loading, with the greatest response occurring at the highest infusion rate. Sodium, potassium and water excretion also increased in parallel with urinary bicarbonate loss. The increase in bicarbonate exposition, glomerular filtration rate, effective renal plasma flow, aldosterone and vasopressin. In 8 sham-operated animals, no abrupt increase in sodium and bicarbonate excretion occurred despite similar continued infusion of sodium bicarbonate. It was concluded that exclusion of one kidney induces immediate adaptive excretory changes for sodium and bicarbonate in the remaining kidney, and that these changes are not accounted for by any of the known factors normally regulating sodium and bicarbonate excretion.

Adaptation, Physiological↗
PubMed1987

Bicarbonate-dependence of responses to ethylenediamine in the guinea-pig isolated ileum: involvement of ethylenediamine-monocarbamate.

gamma-Aminobutyric-acid (GABA)-mimetic responses were induced by ethylenediamine (EDA) in the isolated ileum of the guinea-pig maintained in bicarbonate buffered Krebs-Henseleit (KBC) solution, pH 7.4, 37 degrees C, the responses consisting of a contraction followed by a relaxation. There were no such responses to EDA in bicarbonate-free phosphate buffered (KPO) or HEPES buffered (KHO) Krebs solution, gassed with 100% O2, pH 7.4, 37 degrees C, yet the ileum responded to GABA in bicarbonate-free Krebs solution. Similar GABA-mimetic responses were induced by EDA in the isolated ileum maintained in bicarbonate-free KPO or KHO modified Krebs solution, gassed with O2, if HCO3- (5mM) was first added immediately before the test dose of EDA (0.1-1 mM), the threshold [HCO3-]being 2 mM for EDA-induced responses in these preparations. However, ileal GABA-mimetic responses were induced in bicarbonate-free KPO or KHO solutions by EDA that had been pretreated with carbon dioxide, where the final [HCO3-]in the bath did not exceed 25 microM. Ethylenediamine monocarbamate (synthetic EDAC) released [3H]-GABA from preloaded segments of ileum maintained in bicarbonate-free KPO or KHO solution containing amino-oxyacetic acid and beta-alanine, the release being sensitive to 3-mercaptopropionic acid which prevents GABA release. EDA itself did not evoke any such release in the absence of bicarbonate, but released [3H]-GABA from segments maintained in KBC solution. 4 GABA-mimetic responses were induced by EDAC in the isolated ileum maintained in bicarbonate-free KPO solution, as was a delta-aminovalerate-sensitive depression of ileal twitch responses elicited by transmural stimulation, all of which were also sensitive to 3-mercaptopropionic acid. 5 It is concluded that GABA-mimetic responses to EDA in the isolated ileum of the guinea-pig, maintained in normal Krebs bicarbonate medium, result from the release of endogenous GABA by ethylenediamine monocarbamate formed through the rapid reaction of EDA with the carbon dioxide of bicarbonate buffered Krebs solution. Furthermore, in the ileum, HCO3 ions per se are not necessary for this GABA-releasing property of EDA if the latter is first converted to the monocarbamate, since syntheticethylenediamine monocarbamate elicits ileal GABA-mimetic responses in the total absence of bicarbonate.

Animals↗
PubMed1975

Glomerular-tubular balance for bicarbonate in the dog.

Previous work that apparently showed a functional relationship between GFR and maximum bicarbonate reabsorption was done at a time when the effects on the latter of several factors (PCO2, plasma potassium concentration, and extracellular fluid volume expansion) were not recognized. The present study re-examines this relationship, while controlling these factors. In 14 hydropenic dogs, bicarbonate reabsorption per unt GFR increased linearly with increases in plasma bicarbonate concentration. At any level of plasma bicarbonate concentration,the absolute rate of bicarbonate reabsorption was functionally related to the GFR. In six volume-expanded dogs, bicarbonate reabsorption remained stable at 20-22 mmol/liter GFR as plasma bicarbonate was raised to greater than 40mM. The absolute rate of bicarbonate reabsorption increased with large increases in GFR induced by methylprednisolone and high-protein diet. In a third group of dogs, bicarbonate reabsorption varied directly with increases in GFR, while plasma bicarbonate concentration was held relatively constant above the threshold. We conclude there is a close functional relationship between the absolute rate of bicarbonate reabsorption and GFR in individual dogs.

Animals↗
PubMed1985

A model of proximal tubular bicarbonate absorption.

A model is presented that utilizes determinants of acidification defined from microperfusion studies in the rat to stimulate the effect on absolute bicarbonate absorption along the entire proximal convoluted tubule. Net bicarbonate absorption is considered to consist of active transcellular proton secretion in parallel with passive paracellular bicarbonate diffusion. The rate of proton secretion is calculated as a function of luminal bicarbonate concentration using Michaelis-Menten kinetics. The K1/2 is modified by luminal flow rate and the Vmax by peritubular bicarbonate concentration. Solute-solvent interactions and axial heterogeneity are also included as determinants of proton secretion rate. The model demonstrates that a given percentage stimulation or inhibition of active proton secretion leads to a much smaller effect on absolute proximal bicarbonate absorption along the entire tubular length. This blunting of the stimulation or inhibition is greatest when filtered bicarbonate load is limited by decreases in glomerular filtration rate or plasma bicarbonate concentration. In addition, the model shows that flow dependence is greater at low plasma bicarbonate concentrations, whereas the effect of extracellular fluid volume expansion is greater at high plasma bicarbonate concentrations. Agreement between the model predictions and the results of free-flow micropuncture studies from our laboratory is good with the exception of the effect of raising plasma bicarbonate concentration. This discrepancy is resolvable by allowing the effect of peritubular pH to increase along the length of the tubule, a hypothesis that requires verification.

Absorption↗
PubMed1987

Kinetics of bicarbonate transport in the early proximal convoluted tubule.

Bicarbonate permeability and bicarbonate transport kinetics in the S1 segment of the proximal convoluted tubule (PCT) have not been previously studied. In vivo microperfusion at a rate of 30 nl/min was performed in early and late PCT of Munich-Wistar rats. Bicarbonate permeability was first defined, using a bicarbonate-free, acetazolamide-containing perfusate, and was over fourfold higher in the early compared with the late PCT (20.4 +/- 1.8 vs. 4.6 +/- 0.4 X 10(-7) cm2/s, P less than 0.001). Net bicarbonate absorption was then measured using perfusate bicarbonate concentrations of 15, 25, 40, and 100 mM at 30 nl/min perfusion rate. Proton secretory rate was calculated for each group by subtracting the passive bicarbonate transport component from the net flux. Saturation kinetics of acidification were observed in both the early and late PCT. The maximal proton secretory rate at the highest luminal bicarbonate concentration (Vmax) in the early PCT was about twice that in the late PCT (504 +/- 37 vs. 265 +/- 15 peq.mm-1.min-1, P less than 0.001). However, the luminal bicarbonate concentration eliciting half-maximal proton secretion (apparent Km) was approximately the same (11 mM) in the early and late PCT. In conclusion, the early PCT has a higher bicarbonate permeability and proton secretory capacity than the late PCT. Increased Vmax but axial constancy of Km suggests that there is amplification of similar transport mechanism(s) affecting bicarbonate absorption in S1 compared with S2 cells.

Absorption↗
PubMed1975

CSF bicarbonate regulation in respiratory acidosis and alkalosis.

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.

Acetazolamide↗
PubMed1987

Reduced glomerular filtration rate can maintain a rise in plasma bicarbonate concentration in humans.

In humans, deficiency of chloride and potassium were found to perpetuate the hyperbicarbonatemia that attends metabolic alkalosis induced by gastric aspiration partly by increasing renal bicarbonate reabsorption, commensurate with the attendant increase in filtered bicarbonate load, and partly by decreasing glomerular filtration rate (GFR), which minimizes the degree of which the filtered bicarbonate load increases and thereby minimizes the requisite increase in bicarbonate reabsorption. The relative contribution of stimulated renal bicarbonate reabsorption might increase, however, if the supply of extrarenal bicarbonate is increased, in which case a greater degree of hyperbicarbonatemia would be sustained. To investigate that possibility, we reexamined the mechanism of perpetuation of gastric alkalosis in normal subjects eating a low NaCl diet supplemented with bicarbonate salts. Prior to gastric aspiration, plasma bicarbonate concentration ([HCO3]p) and pH were higher than in similarly studied subjects not receiving bicarbonate: 29.9 +/- 0.6 vs. 25.3 +/- 0.1 and 7.43 +/- 0.008 vs. 7.41 +/- 0.002 mEq/l, respectively. With continued bicarbonate supplementation, gastric aspiration induced a further significant increase (p less than 0.05) in [HCO3]p of 10.8%, to values not significantly different from those in nonbicarbonate-loaded subjects with gastric alkalosis: 33.2 +/- 1.2 mEq/l. GFR decreased significantly by 8.4% (from 98 +/- 4 to 90 +/- 3 ml/min, p less than 0.025), offsetting nearly commensurately the increase in [HCO3]p so that total bicarbonate reabsorption was not significantly increased (2.90 +/- 0.12 vs. 2.97 +/- 0.19 mEq/min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Faecal excretion of bicarbonate in ulcerative colitis.

The normal colon absorbs water, sodium and chloride and secretes potassium and bicarbonate. In ulcerative colitis (UC), modifications occur in the absorption of water, sodium and chloride, whereas the secretion of potassium remains unchanged. There appear to be no data in the literature on bicarbonate secretion. Since some 25% of chloride absorption is coupled with bicarbonate secretion by an anion exchange mechanism, the impairment in chloride absorption should be accompanied by modifications in bicarbonate secretion. Faecal bicarbonate was therefore measured in 20 patients with active UC and 15 normal control subjects. Faecal pH, pCO2 and electrolytes (Na+, K+, Cl-, HCO3-), blood acid-base balance, urinary pH and bicarbonate were determined on the same day in all patients. Faecal pH and bicarbonate were significantly reduced in UC versus controls: pH 6.06 +/- 0.39 versus 6.52 +/- 0.43; HCO3- 8.4 +/- 5.2 versus 34.6 +/- 12.3 mEq/l (mean +/- SD), whereas sodium and chloride were increased. Faecal potassium concentration was normal, but potassium output was increased. Metabolic alkalosis was observed in 8 patients and a normal acid-base balance in the remaining 12. Urinary pH was acid and urinary bicarbonate negligible in all patients. No correlation was observed between plasma, faecal and urinary bicarbonate. Data emerging from this study show that the faecal excretion of bicarbonate is reduced in patients with active UC. A possible explanation for this finding may be impairment of the colonic anion exchange mechanism induced by inflammation of the mucosa. The role of organic anions is also hypothesized. The acid-base balance does not seem to be directly affected by the decrease in faecal bicarbonate loss.

Acid-Base Equilibrium↗
PubMed1983

Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.

Maintenance of chronic metabolic alkalosis might occur by a reduction in glomerular filtration rate (GFR) without increased bicarbonate reabsorption or, alternatively, by augmentation of bicarbonate reabsorption with a normal GFR. To differentiate these possibilities, free-flow micropuncture was performed in alkalotic Munich-Wistar rats with a glomerular ultrafiltrate total CO2 concentration of 46.5 +/- 0.9 mM (vs. 27.7 +/- 0.9 mM in controls). Alkalotic animals had a markedly reduced single nephron GFR compared with controls (27.4 +/- 1.5 vs. 51.6 +/- 1.6 nl/min) and consequently unchanged filtered load of bicarbonate. Absolute proximal bicarbonate reabsorption in alkalotic animals was similar to controls (981 +/- 49 vs. 1,081 +/- 57 pmol/min), despite a higher luminal bicarbonate concentration, contracted extracellular volume, and potassium depletion. When single nephron GFR during alkalosis was increased toward normal by isohydric volume expansion or in another group by isotonic bicarbonate loading, absolute proximal bicarbonate reabsorption was not substantially augmented and bicarbonaturia developed. To confirm that a fall in GFR occurs during metabolic alkalosis, additional clearance studies were performed. Awake rats were studied before and after induction of metabolic alkalosis associated with varying amounts of potassium and chloride depletion. In all cases, the rise in blood bicarbonate concentration was inversely proportional to a reduction in GFR; filtered bicarbonate load remained normal. In conclusion, a reduction in GFR is proposed as being critical for maintaining chronic metabolic alkalosis in the rat. Constancy of the filtered bicarbonate load allows normal rates of renal bicarbonate reabsorption to maintain the alkalotic state.

Absorption↗
PubMed1985

Bicarbonate secretion and chloride absorption by rabbit cortical collecting ducts. Role of chloride/bicarbonate exchange.

Cortical collecting ducts (CCD) from rabbits treated with deoxycorticosterone (DOC) actively secrete bicarbonate at high rates. To investigate the mechanism of bicarbonate secretion, we measured bicarbonate and chloride transport in CCD from rabbits treated with DOC for 9-24 d. Removal of chloride (replaced with gluconate) from both perfusate and bath inhibited bicarbonate secretion without changing transepithelial voltage. Removal of chloride only from the bath increased bicarbonate secretion, while removal of chloride only from the perfusate inhibited secretion. In contrast to the effect of removing chloride, removal of sodium from both the perfusate and bath (replacement with N-methyl-D-glucamine) did not change the rate of bicarbonate secretion. The rate of bicarbonate secretion equaled the rate of chloride absorption in tubules bathed with 0.1 mM ouabain to inhibit any cation-dependent chloride transport. Under these conditions, chloride absorption occurred against an electrochemical gradient. Removal of bicarbonate from both the perfusate and bath inhibited chloride absorption. Removal of bicarbonate only from the bath inhibited chloride absorption, while removal of bicarbonate from the lumen stimulated chloride absorption. We conclude that CCD from DOC-treated rabbits actively secrete bicarbonate and actively absorb chloride by an electroneutral mechanism involving 1:1 chloride/bicarbonate exchange. The process is independent of sodium.

Absorption↗
PubMed1977

Influence of fetal extracellular volume contraction on renal reabsorption of bicarbonate in fetal lambs.

In order to determine the renal threshold for bicarbonate in the fetal lamb and factors that may influence renal reabsorption of bicarbonate in the fetus, 18 acute fetal lamb preparations (110-140 days of gestation) were studied. In the first series of experiments involving nine fetuses, the renal bicarbonate threshold of normal fetuses varied from 12.0 to 23.5 mM/liter with a mean value of 17.7 +/- 1.37 mM/liter. This is significantly lower (P less than 0.005) than the value measured in five adult sheep of 28.7 +/- 1.68 mM/liter. There was a significant and positive correlation between the fetal plasma bicarbonate at threshold level and the fetal kidney weight, as well as fetal age. In a second series of experiments, the excretion of bicarbonate and sodium was studied in nine fetuses before and after dehydration by peritoneal dialysis. After peritoneal dialysis there was a significant decrease in urinary pH (P less than 0.025), bicarbonate excretion (P less than 0.001), sodium excretion (P less than 0.001), fractional excretion of sodium (P less than 0.01). When glucose was replaced by mannitol in the peritoneal dialysis fluid the effects on bicarbonate reabsorption paralleled those when glucose was present in dialysis fluid. It was also shown that when glucose was given intravenously to the fetus, up to a plasma concentration of 200 mg/100 ml, there was no effect on the fetal renal reabsorption of bicarbonate. These data indicate that the low threshold for bicarbonate reabsorption by the fetal kidney is not due to a limited capacity to increase bicarbonate or sodium reabsorption and suggest that the fetal kidney is able to respond to volume depletion by increasing its reabsorption in bicarbonate and electrolytes.

Absorption↗
PubMed2002

Circadian changes in urinary bicarbonate, nitric oxide metabolites and pH in female player during handball camp involved in an exercise, rest and sleep cycle.

Bicarbonate and nitric oxide levels are important humoral factors in the blood and are affected by the human body's physical condition. There are few reports, however, on changes in blood bicarbonate and nitric oxide levels during exercise and rest. Since urinary bicarbonate and nitric oxide metabolites reflect the levels of bicarbonate and nitric oxide in the blood, we studied circadian changes in 6 female athletes by monitoring their urinary pH and their levels of urinary bicarbonate and nitric oxide metabolites. Measurements were taken during exercise, rest and sleep. Six female athletes participated in a 3-day team handball training camp where they followed a schedule of exercise, rest and sleep. Urinary samples were collected immediately before and after handball training, at bed-time and upon waking. The urinary pH and levels of urinary bicarbonate and nitric oxide metabolites, including nitrite and nitrate, were examined with a blood gas analyzer and a NOx analyzer. The samples collected after handball training, as compared to the samples taken before exercise, showed a decreased pH, a decrease in levels of bicarbonate and little change in NO metabolites. During rest, urinary bicarbonate, NO metabolites and pH increased markedly in all 6 subjects. The levels of urinary bicarbonate, NO metabolites and pH significantly decreased upon waking. This study took into account the subjects' various physiological conditions when considering the significance of their changes in urinary bicarbonate, NO metabolites and pH during the 3 day handball training program. There were significant circadian changes in the urinary pH, and in the levels of urinary bicarbonate and nitric oxide metabolites, in the athletes involved in the exercise, rest and sleep program at team handball camp.

Activity Cycles↗
PubMed1994

Duodenal mucosal bicarbonate secretion in pigs is accompanied by compensatory changes in pancreatic and biliary HCO3- secretion.

BACKGROUND: The purpose of the study was to examine the effect of stimulation and inhibition of duodenal mucosal bicarbonate secretion on pancreatic and hepatic bicarbonate secretion in response to acid. METHODS: The effect of inhibition (indomethacin) or stimulation (misoprostol) of duodenal mucosal bicarbonate secretion on pancreatic and biliary bicarbonate secretion in response to intraduodenal infusion of HCl or intravenous infusion of secretin was studied in anaesthetized pigs. RESULTS: The hepatic and pancreatic response to exogenous secretin was not significantly altered by stimulation/inhibition of duodenal bicarbonate secretion. However, pancreatic and biliary bicarbonate secretion in response to duodenal acidification was significantly augmented by inhibition of duodenal mucosal bicarbonate secretion; conversely, it was reduced by stimulation of duodenal bicarbonate secretion. The increase in plasma secretin levels in response to duodenal acidification was reduced by stimulation and augmented by inhibition of duodenal mucosal bicarbonate secretion. CONCLUSIONS: Duodenal mucosal bicarbonate secretion can serve as a modulator of both pancreatic and biliary bicarbonate secretion in response to luminal acidification, possibly through regulation of the release of secretin.

Acid-Base Equilibrium↗
PubMed1999

In vivo analysis of amantadine renal clearance in the uninephrectomized rat: functional significance of in vitro bicarbonate-dependent amantadine renal tubule transport.

Amantadine transport into renal proximal and distal tubules is bicarbonate dependent. In the present study, we addressed the effects of bicarbonate on renal clearance and urinary excretion of amantadine. Renal clearance of kynurenic acid was also studied to determine whether bicarbonate effects are specific for organic base transport by the kidney. After a moderate diuresis was established, animals received i.v. [(3)H]amantadine or [(3)H]kynurenic acid followed by an acute dose of sodium bicarbonate or physiological saline. Urine and blood samples were analyzed for [(3)H]amantadine or [(3)H]kynurenic acid, blood gases, and pH. Amantadine and kynurenic acid were excreted by the kidneys, and both compounds underwent renal tubular secretion. Amantadine metabolism occurred, and one metabolite was detected in the urine. In the bicarbonate-treated rats, the total amount of amantadine excreted in the urine was decreased, whereas the amount of metabolite recovered was similar in both groups. Bicarbonate treatment caused a sustained increase in blood bicarbonate levels, a mild increase in blood pH, and a decrease in amantadine renal clearance and in the amantadine/creatinine clearance ratio. Only a transient decrease in the renal clearance of kynurenic acid and the kynurenic acid/creatinine clearance ratio was observed. This study demonstrates that short-term changes in bicarbonate concentration may have significant effects on renal organic cation elimination. Coupled with our previous in vitro demonstration of bicarbonate-dependent organic cation transport, the present study suggests that bicarbonate inhibition of renal tubule organic cation secretion may explain the previous observation that bicarbonate dosing decreases amantadine excretion by the kidney.

Amantadine↗
PubMed2000

[Changes in acid-base equilibrium and CO2 output induced by bicarbonate infusion].

BACKGROUND: Bicarbonate therapy for metabolic acidosis can cause tissue hypercapnia. We tested the hypothesis that CO2 retention is initially confined to blood and that tissue hypercapnia is consequent to blood hypercapnia. METHODS DESIGN: prospective study. SETTING: general Intensive Care Unit in an University Hospital. PATIENTS: ten patients, aged 34-84, undergoing fixed mechanical ventilation for stroke, respiratory failure, polytrauma, or coma and presenting fairly stabilized circulatory condition were included in the study providing that definite exclusion criteria were absent. Sodium bicarbonate, 0.08, 0.17, and 0.25 mEq/kg, was infused in 5 minutes during stages A, B, and C. During each stage, before and after bicarbonate infusion, heart rate, arterial pressure, central venous pressure, and PetCO2 were registered and arterial and central venous haemogasanalysis were performed. CO2 output was measured during and after bicarbonate infusion and total CO2 output over basal values was calculated. RESULTS: Heart rate, arterial pressure, central venous pressure did not change in any stage, while PetCO2 increased in all. Following bicarbonate infusion, pH increased more in venous than in arterial blood and was significantly affected by the amount of bicarbonate infused. In arterial blood both PCO2 and total CO2 content (TCO2) increased. In venous blood PCO2 did not change while TCO2 increased so that arterial-venous rl CO2 difference was unaffected. CO2 output changed in no patient but two during stage A, and increased by 0.54 +/- 0.16 mL/kg during stage B and by 1.18 +/- 0.26 mL/kg during stage C so that 14.5 +/- 4.3 and 21.2 +/- 4.7% of given bicarbonate was released as CO2 through the lungs. CO2 output increased after a latency that was significantly shorter during stage C (145 +/- 51 sec) than during stage B (226 +/- 53 sec). CONCLUSIONS: Since arterial-venous TCO2 difference was unaffected and haemodynamic parameters were stable, the conclusion is drawn that CO2 and bicarbonate did not diffuse out of vascular compartment during this study. However CO2 and bicarbonate diffusion out of blood would have occurred if bicarbonate infusion had continued, because CO2 excess was released through the lungs after a latency and extended after the infusion. Consequently, tissue hypercapnia during bicarbonate infusion could probably be prevented by improving CO2 release through the lungs, i.e. by hyperventilating the patient.

Acid-Base Equilibrium↗