Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bicarbonates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1990

Inhibition of bicarbonate absorption by peptide hormones and cyclic adenosine monophosphate in rat medullary thick ascending limb.

In vitro microperfusion experiments were performed to examine the effects of peptide hormones on bicarbonate and ammonium transport by the medullary thick ascending limb (MTAL) of the rat. Arginine vasopressin (AVP; 2.8 X 10(-10) M in the bath) reduced bicarbonate absorption by 50% (from 7.8 to 3.7 pmol/min per mm). AVP caused a similar reduction in bicarbonate absorption in tubules perfused with 10(-4) M furosemide to inhibit net NaCl absorption. Glucagon (2 X 10(-9) M in the bath) also reduced bicarbonate absorption (from 11.7 to 7.6 pmol/min per mm). The inhibition of bicarbonate absorption could be reproduced with either exogenous 8-bromo-cAMP or forskolin. With 8-bromo-cAMP (10(-3) M) in the bath, addition of vasopressin to the bath did not significantly affect bicarbonate absorption. PTH significantly inhibited bicarbonate absorption, but the extent of inhibition was less than that observed with either AVP or glucagon. Vasopressin had no effect on net ammonium absorption in MTAL perfused and bathed with 4 mM NH4Cl. These findings indicate that: (a) vasopressin, glucagon, and PTH directly inhibit bicarbonate absorption in the MTAL of the rat; (b) this inhibition occurs independent of effects on net NaCl absorption and appears to be mediated in part by cAMP; and (c) HCO3- and NH4+ absorption can be regulated independently in the MTAL.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Bicarbonate secretion in vivo by rat distal tubules during alkalosis induced by dietary chloride restriction and alkali loading.

To examine in vivo the separate effects on distal tubule JtCO2, of dietary chloride restriction, bicarbonate loading, and changes in luminal chloride concentration, we microperfused distal tubules at a physiologic flow rate (8 nl/min) with solutions containing either 45 or 0 mM chloride (after gluconate substitution). Rats were fed a diet containing zero, minimal, or normal amounts of chloride, while drinking either water or a solution of 0.15 M sodium bicarbonate. Neither extracellular fluid volume contraction nor negative chloride balance ensued. Analysis of covariance with repeated measures demonstrated that dietary chloride, drinking sodium bicarbonate, and perfusion with either 45 mM or zero chloride, each have separate and significant modulating effects on distal tubule bicarbonate secretion. During mild alkalemia, there is modest bicarbonate secretion which is significantly different from zero (-9.9 +/- 3.2 pmol.min-1.mm-1, P less than 0.01), and which is suppressed after perfusion with zero chloride. In contrast, during more pronounced metabolic alkalosis after supplemental bicarbonate drinking, the bicarbonate secretory flux is brisk (-26 +/- 3 pmol.min-1.mm-1) and significantly different from zero and persists (-11 +/- 3 pmol.min-1.mm-1) even during perfusion with zero luminal chloride. Accordingly, in this two-day model of alkalosis induced by dietary chloride restriction, there is regulatory secretion of bicarbonate by distal tubules in vivo which is modulated by luminal chloride concentration.

Absorption↗
PubMed1991

Bicarbonate transport along the loop of Henle. I. Microperfusion studies of load and inhibitor sensitivity.

We microperfused the loop of Henle (LOH) to assess its contribution to urine acidification in vivo. Under control conditions (Na HCO3- = 13 mM, perfusion rate approximately 17 nl/min-1) net bicarbonate transport (JHCO3-) was unsaturated, flow- and concentration-dependent, and increased linearly until a bicarbonate load of 1,400 pmol.min-1 was reached. Methazolamide (2 x 10(-4) M) reduced JHCO3 by 70%; the amiloride analogue ethylisopropylamiloride (EIPA) (2 x 10(-4) M) reduced JHCO3 by 40%; neither methazolamide nor EIPA affected net water flux (Jv). The H(+)-ATPase inhibitor bafilomycin A1 (10(-5) M) reduced JHCO3 by 20%; the Cl- channel inhibitor 5-nitro-2'-(3-phenylpropylamino)-benzoate (2 x 10(-4) M) and the Cl(-)-base exchange inhibitor diisothiocyanato-2,2'-stilbenedisulfonate (5 x 10(-5) M), had no effect on fractional bicarbonate reabsorption. Bumetanide (10(-6) M) stimulated bicarbonate transport (net and fractional JHCO3-) by 20%, whereas furosemide (10(-4) M) had no effect on bicarbonate reabsorption; both diuretics reduced Jv. In summary: (a) the LOH contributes significantly to urine acidification. It normally reabsorbs an amount equivalent to 15% of filtered bicarbonate; (b) bicarbonate reabsorption is not saturated; (c) Na(+)-H+ exchange and an ATP-dependent proton pump are largely responsible for the bulk of LOH bicarbonate transport.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2004

Effects of ingestion of bicarbonate, citrate, lactate, and chloride on sprint running.

PURPOSE: Ingestion of sodium bicarbonate is known to enhance sprint performance, probably via increased buffering of intracellular acidity. The goal was to compare the effect of ingestion of sodium bicarbonate with that of other potential buffering agents (sodium citrate and sodium lactate) and of a placebo (sodium chloride) on sprinting. METHODS: In a double-blind randomized crossover trial, 15 competitive male endurance runners performed a run to exhaustion 90 min after ingestion of each of the agents in the same osmolar dose relative to body mass (3.6 mosmol x kg) on separate days. The agents were packed in gelatin capsules and ingested with 750 mL of water over 90 min. During each treatment we assayed serial finger-prick blood samples for lactate and bicarbonate. A familiarization trial was used to set a treadmill speed for each runner's set of runs. We converted changes in run time between treatments into changes in a time trial of similar duration using the critical-power model, and we estimated likelihood of practical benefit using 0.5% as the smallest worthwhile change in time-trial performance. RESULTS: The mean run times to exhaustion for each treatment were: bicarbonate 82.3 s, lactate 80.2 s, citrate 78.2 s, and chloride 77.4 s. Relative to bicarbonate, the effects on equivalent time-trial time were lactate 1.0%, citrate 2.2%, and chloride 2.7% (90% likely limits +/- 2.1%). Ingested lactate and citrate both appeared to be converted to bicarbonate before the run. There were no substantial differences in gut discomfort between the buffer treatments. CONCLUSION: Bicarbonate is possibly more beneficial to sprint performance than lactate and probably more beneficial than citrate or chloride. We recommend ingestion of sodium bicarbonate to enhance sprint performance.

Adult↗
PubMed2004

Effects of sodium bicarbonate on VO2 kinetics during heavy exercise.

PURPOSE: Sodium bicarbonate was used to investigate the effect of blood pH on VO2 kinetics during heavy exercise. METHODS: On separate days, 10 active subjects performed two 6-min cycling bouts (208 +/- 12 W) at 25 W above their ventilatory threshold. Each subject ingested 0.3 g x kg(-1) of sodium bicarbonate with approximately 1 L of water or water alone 1 h before exercise. VO2 kinetics were examined by means of a three-component mono-exponential model. RESULTS: Bicarbonate ingestion caused a significant increase in the preexercise blood pH (7.512 +/- 0.009 vs 7.425 +/- 0.007; P < 0.001). In the bicarbonate trial, the time constant for the rapid component (27.9 +/- 3.5 s) was slower than the control trial (20.8 +/- 2.4 s; P = 0.017). The higher blood pH after bicarbonate ingestion would have diminished local blood flow and caused a leftward shift of the oxygen-hemoglobin dissociation curve both of which would slow oxygen delivery to working muscle. In addition, bicarbonate ingestion diminished the amplitude of the slow component 29% (463 +/- 43 vs 649 +/- 53 mL x min(-1); P = 0.040). The primary cause of the slow component during heavy exercise is fatigue of working fibers and an accompanying increase of motor unit recruitment. Elevated plasma bicarbonate concentration is reported to stimulate the efflux of H from muscle fibers and to increase intramuscular pH. CONCLUSIONS: The slower time constant during the rapid component suggested that oxygen delivery is a limiting factor of VO2 kinetics during the onset of heavy exercise. Also, these results imply that bicarbonate ingestion diminished fatigue in working fibers during the slow component.

Acid-Base Imbalance↗
PubMed1986

Cholinergic influence on duodenal bicarbonate response to hydrochloric acid perfusion in the conscious rat.

Present information suggests that endogenous prostaglandins, hormonal factors, and neuropeptides participate in the regulation of duodenal bicarbonate secretion in response to luminal hydrochloric acid. The purpose of this study was to examine the effects of cholinergic antagonists and agonists on basal and acid-stimulated bicarbonate secretion in the proximal duodenum of the conscious rat. The basal bicarbonate secretion, 9 mumol X cm-1 X h-1, increased to 21 +/- 3 mumol X cm-1 X h-1 after 5 min of exposure to 150 mM HCl and remained significantly elevated for more than 3.5 h. The muscarinic blocker atropine, 0.5 mg X kg-1, reduced the acid-stimulated bicarbonate response by a third, and higher doses did not increase the inhibition. The ganglionic blocker hexamethonium, 10-20 mg X kg-1, suppressed in a dose-related manner the alkaline response by maximally one half. The opioid inhibitor naloxone was also an effective inhibitor. Hexamethonium, but not atropine, inhibited the basal duodenal bicarbonate secretion, which was unaffected by graded doses of the cholinergic agonists bethanechol and carbachol. We conclude that cholinergic nicotinic activity participates in maintaining basal duodenal bicarbonate secretion in the conscious rat. The bicarbonate response to luminal 150 mM HCl is partially dependent on cholinergic sites, but activation of such sites is not a single final step, since cholinergic agonists failed to elevate bicarbonate secretion from basal.

Animals↗
PubMed1989

The effect of vasoactive intestinal peptide, secretin, and glucagon on human duodenal bicarbonate secretion.

Duodenal luminal acidification increases duodenal mucosal bicarbonate production and also releases both secretin and vasoactive intestinal peptide (VIP). The effect of these two structurally similar peptides on human duodenal bicarbonate production has not been examined in humans. Our purpose was therefore to assess the effect of VIP and secretin and also glucagon, a homologous hormone, on human duodenal bicarbonate secretion. A 4-cm portion of either proximal or distal duodenum was isolated and perfused with iso-osmolar NaCl. Pure porcine VIP (200 and 400 pmol/kg-h intravenously) significantly increased proximal duodenal bicarbonate secretion. Although secretin (0.01 to 0.18 CU/kg-h intravenously) markedly increased pancreatic bicarbonate secretion, it failed to alter duodenal mucosal bicarbonate output in either the proximal or the distal duodenum. Glucagon (1 to 8 micrograms/kg-h intravenously) did not affect proximal duodenal mucosal bicarbonate output. It is concluded that VIP, but neither secretin nor glucagon, significantly stimulates human duodenal mucosal bicarbonate secretion.

Adult↗
PubMed1979

Control of renal bicarbonate transport.

Single rabbit renal tubules were perfused in vitro to elucidate the factors that control bicarbonate transport. One factor studied was the preexisting acid-base status of the rabbits. Cortical collecting ducts from acidotic rabbits (given ammonium chloride) transported bicarbonate from lumen to bath. Collecting ducts from alkalotic rabbits (given sodium bicarbonate) transported bicarbonate in the opposite direction. Thus, bicarbonate transport by collecting ducts in vitro was conditioned by the preexisting state of the rabbit in vivo. In contrast, bicarbonate transport by proximal straight tubules and cortical thick ascending limbs was not affected by ammonium chloride or sodium bicarbonate given to the rabbits. Parathyroid hormone, the second factor studied, strongly inhibited bicarbonate absorption by proximal straight tubules.

Absorption↗
PubMed1998

Laboratory assessment of tooth whitening by sodium bicarbonate dentifrices.

The increasing emphasis on dental aesthetics has made tooth whitening an important function of a dentifrice. This laboratory study investigated the whitening effect of toothbrushing with sodium bicarbonate-based dentifrices compared with standard dentifrices that do not contain sodium bicarbonate. Six dentifrices and a distilled water control were tested for their ability to whiten teeth with intrinsic stain. The dentifrices contained different abrasive systems: (1) 45% NaHCO3; (2) 65% NaHCO3 (Arm and Hammer Dental Care); (3) 94% NaHCO3; (4) 94% NaHCO3 + 1.5% H2O2; (5) silica (Crest Regular Toothpaste); and (6) dicalcium phosphate (Colgate Regular Toothpaste). After a thorough rubber cup cleaning with a pumice slurry, the intrinsic color of the test teeth with a Vita shade of A3 or darker was measured with a spectrophotometer using the standard L*a*b* color scale. Measurements were taken on a total of 12 teeth per test dentifrice before treatment, and after 30, 60, 90 and 120 minutes of mechanical toothbrushing. No changes in L* (lightness/brightness) or a* (red-green hue) occurred, but significant differences in b* (yellow-blue hue) were observed over time. Compared to baseline tooth color, all four sodium bicarbonate-based dentifrices were significantly effective in removing the yellow intrinsic tooth stain, while the water control, silica dentifrice, and dicalcium phosphate dentifrice demonstrated no significant change. Between-group comparisons showed that the four dentifrices containing sodium bicarbonate were significantly more effective than the water and dicalcium phosphate dentifrice groups. The commercial dentifrice containing 65% sodium bicarbonate was also more effective than the commercial silica dentifrice. Although continued toothbrushing from 30 to 120 minutes resulted in additional stain removal, most of the tooth whitening by the sodium bicarbonate-based dentifrices occurred in the first 30 minutes of brushing. In the studies conducted, dentifrices containing high concentrations of sodium bicarbonate were more effective at removing intrinsic tooth stain than dentifrices that do not contain sodium bicarbonate.

Dentifrices↗
PubMed1996

Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial.

OBJECTIVE: To examine the effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and parameters of glucose and lipid metabolism in elderly normotensive individuals. METHODS: We examined 21 healthy men and women aged 60-72 years in a randomized, placebo-controlled, double-blind crossover trial. After reducing dietary salt intake to below 100 mmol/day, study participants were randomly assigned to drink 1.5 l daily of a sodium chloride-rich (sodium 84.5 mmol/l, chloride 63.7 mmol/l, bicarbonate 21.9 mmol/l), a sodium bicarbonate-rich (sodium 39.3 mmol/l, chloride 6.5 mmol/l, bicarbonate 48.8 mmol/l) and a low-sodium (placebo: sodium, chloride and bicarbonate < 0.02 mmol/l) mineral water for 4 weeks each in a three-phase crossover order. Each phase was separated by a 2-week washout period in which the study participants remained on a low-salt diet. Compliance was assessed by biweekly urinary electrolyte excretion and five study participants were excluded from analysis for failing to complete the trial or to fulfil the compliance criteria. RESULTS: Mean arterial blood pressure was significantly lower during the periods of consuming low-sodium -7.0 +/- 7.2 mmHg, P < 0.001) or sodium bicarbonate-rich (-5.7 +/- 6.4 mmHg, P < 0.05) water than at baseline. In contrast, blood pressure during the phase of drinking sodium chloride-rich water was identical to that at baseline. Ambulatory 24 h blood pressure, oral glucose tolerance and plasma lipids were not affected by the different regimens. Urinary calcium excretion was significantly reduced by drinking low-sodium or sodium bicarbonate-rich water but was unchanged under the sodium chloride-rich water. CONCLUSION: Consumption of sodium chloride-rich mineral water can abolish the blood pressure reduction induced by dietary salt restriction in elderly individuals. Sodium bicarbonate-rich mineral water in conjunction with a low-salt diet may have a beneficial effect on calcium homeostasis.

Aged↗
PubMedDate not supplied

Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation.

The loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.

Absorption↗
PubMed2002

Relationship between bicarbonate and cyclic nucleotide in the promoting effects on head-to-head agglutination in boar spermatozoa.

AIM: To clarify the relationship between bicarbonate and cAMP in the promoting effects on the sperm agglutination. METHODS: Spermatozoa were collected from mature boars, washed and resuspended in a modified Krebs-Ringer HEPES lacking calcium chloride (mKRH). The sperm suspensions were incubated in a water bath (38.5 degrees C) for 60 min and then the percentage of head-to-head agglutinated spermatozoa was determined. RESULTS: Supplementation of the mKRH with sodium bicarbonate (5-10 mM) significantly raised the percentage of head-to-head agglutinated spermatozoa in the samples. The addition of selective inhibitors for calcium/calmodulin-dependent phosphodiesterases (type 1: 8-methoxymethyl-IBMX and vinpocetine, 25-50 micro M) or for cAMP-specific phosphodiesterases (type 4: Ro20-1724 and rolipram, 25-50 microM) enhanced the effect of bicarbonate on sperm agglutination as highly as did the addition of non-selective inhibitors for phosphodiesterases (IBMX and papaverine, 25-50 microM). A calmodulin antagonist (W-7, 2 microM), that potentially blocks the stimulator of the calcium/calmodulin-dependent phosphodiesterases, significantly enhanced the effect of bicarbonate on sperm agglutination. Moreover, a phosphodiesterase-resistant cAMP analogue (cBiMPS, 0.1 mM) markedly induced agglutination in more spermatozoa (76%) after the incubation without bicarbonate and phosphodiesterase inhibitors than did a less potent cAMP analogue (dibutyryl cAMP, 1 mM) (21%), while three kinds of cGMP analogues (0.1-1 mM) had no effect on sperm agglutination. In addition, a cAMP antagonist (Rp-cAMPS, 1 mM) significantly reduced the sperm agglutination resulting from the actions of bicarbonate and IBMX. On the other hand, the effect of bicarbonate was abolished by a change of incubation temperature from 38.5 degrees C to 25 degrees C. CONCLUSION: These findings demonstrate that the bicarbonate-induced agglutination of boar spermatozoa is controlled via the cAMP-mediated, temperature-dependent signaling cascade. This cascade is suppressed by the action of the phosphodiesterase (at least types 1 and 4).

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Disordered breathing patterns during bicarbonate hemodialysis in COPD. Effect of cuprophane versus polysulfone membranes.

This study explored the breathing patterns and arterial blood gases before and during cuprophane (CU) bicarbonate and polysulfone (PS) bicarbonate dialysis in six chronic dialysis patients with mild chronic obstructive pulmonary disease (COPD). The studies were performed in random order during two consecutive dialyses. Breathing patterns were monitored by respiratory impedance plethysmography. Apneic episodes, defined as a decrease in tidal volume of 75% lasting 10 sec, were present before and during hemodialysis. In these patients with COPD a high number of apneic episodes (17 +/- 6 [SE]) were observed during CU bicarbonate hemodialysis. Most of these episodes were central rather than obstructive in character. There were fewer events when the same patients were dialyzed with PS membranes (10 +/- 5; p = 0.05). The decrement in PO2 (baseline to 60 min) was 17 +/- 7 during CU and 4 +/- 5 mmHg during PS dialysis (p = 0.10). Minute ventilation decreased in four of six patients on CU bicarbonate and increased in all six patients on PS bicarbonate. It was concluded that bicarbonate hemodialysis does not completely prevent hypoxemia or apnea during dialysis in patients with COPD. Apneic episodes and hypoxemia appear to be less severe during PS bicarbonate than during CU bicarbonate hemodialysis.

Adult↗
PubMed2004

Association of predialysis serum bicarbonate levels with risk of mortality and hospitalization in the Dialysis Outcomes and Practice Patterns Study (DOPPS).

BACKGROUND: Experimental and some clinical data suggest that metabolic acidosis contributes to poor nutritional status, a strong predictor for mortality in hemodialysis patients. However, recent cross-sectional studies indicate that severe predialysis metabolic acidosis is associated with a greater normalized protein catabolic rate (nPCR) and greater serum albumin levels. Given this controversy, we analyzed data from the Dialysis Outcomes and Practice Pattern Study (DOPPS) for associations between predialysis serum bicarbonate and albumin concentrations, nPCR, and patient risk for mortality and hospitalization. METHODS: Data from more than 7,000 representative and randomly selected hemodialysis DOPPS patients from France, Germany, Italy, Japan, Spain, the United Kingdom, and the United States were analyzed. Serum bicarbonate (total CO2 ) levels predialysis were corrected to the midweek interdialytic interval. RESULTS: The midweek predialysis serum bicarbonate level averaged 21.9 mEq/L (mmol/L) and correlated inversely with nPCR, serum albumin, and serum phosphorus values. Before and after adjusting for 15 comorbidities, nutrition, and equilibrated Kt/V, a U-curve best represented the association between predialysis serum bicarbonate level and risk for mortality or hospitalization. Patients with midweek predialysis serum bicarbonate levels of 20.1 to 21.0 mEq/L (mmol/L) faced the lowest risk for mortality, whereas those with bicarbonate levels of 21.1 to 22.0 mEq/L faced the lowest risk for hospitalization. Both high (>27 mEq/L) and low (< or =17 mEq/L) serum bicarbonate levels were associated with increased risk for mortality and hospitalization. CONCLUSION: Moderate predialysis acidosis seems to be associated with better nutritional status and lower relative risk for mortality or hospitalization than is observed in patients with normal ranges of midweek predialysis serum bicarbonate concentration (approximately 24 mEq/L) or severe acidosis (<16 mEq/L).

Acidosis↗
PubMed2004

Gastric acid and salivary bicarbonate. Is there a relationship in duodenal ulcer patients?

PURPOSE: Since saliva protects the oesophageal and oral mucosa against hydrogen ions, the aim of the study was to establish the relationship between the secretion of gastric acid and salivary bicarbonate. MATERIAL AND METHODS: The study involved 43 Helicobacter pylori positive duodenal ulcer patients receiving: 1. omeprazole alone (O), 2. omeprazole and amoxicillin (OA) or 3. omeprazole, amoxicillin and tinidazole (OAT). In each study group the examination was performed twice, before and at the end of a two-week treatment, both under basal conditions and during a gastric secretory test with pentagastrin. Concentrations of gastric hydrogen ions and salivary bicarbonate were evaluated by the titration method. RESULTS: In all therapeutic groups analysed separately, the secretion of gastric acid as well as salivary bicarbonate decreased at the end of the treatment, however only in OA and OAT groups the differences in bicarbonate reached statistical significance. As the changes in the concentration and output of both salivary bicarbonate and gastric acid had the same direction, the three therapeutic groups (O, OA, OAT) were subjected to combined analysis. It showed that under basal conditions and during stimulation with a gastric catheter or catheter and pentagastrin, bicarbonate concentration and output were higher before than at the end of the treatment. However, no direct correlation between gastric acid secretion and salivary bicarbonate was found in groups subjected to either separate or combined analysis. CONCLUSIONS: The results of our study provide evidence for the partial involvement of hydrogen ions of gastric origin in the regulation of salivary bicarbonate secretion in duodenal ulcer patients.

Adult↗
PubMedDate not supplied

Long-term clinical experience with pure bicarbonate peritoneal dialysis solutions.

OBJECTIVES: The aim of this prospective study was to collect long-term experience in incident peritoneal dialysis (PD) patients treated with pure bicarbonate-buffered PD fluids. METHODS: The metabolic parameters acidosis, acid-base status, adequacy, fluid balance, nutritional markers, calcium, phosphorus, parathyroid hormone (PTH), and general laboratory work and medication were compared between incident PD patients in two groups: one treated with a 34 mmol/L bicarbonate-buffered PD fluid (BIC), the other with a 35 mmol/L lactate-buffered PD fluid (LAC). The observation period included 5 visits from 1 month (visit 1) until 12 months (visit 5) after the start of dialysis treatment. For the descriptive analysis, means and standard deviations were calculated. Student's t-test and linear mixed models were used to compare the two treatment groups. RESULTS: 36 patients were followed for 12 months, 18 in the BIC group and 18 in the LAC group. Statistically significant differences between the groups (at the end of study) were found. In BIC group, venous plasma bicarbonate was 27.4 +/- 2.3 mmol/L, base excess 0.8 +/- 2.2 mmol/L, and pH 7.31 +/- 0.05; in LAC group, venous bicarbonate was 25.9 +/- 2.4 mmol/L, base excess -0.6 +/- 2.1 mmol/L, and pH 7.30 +/- 0.04. No patient from the BIC group needed oral bicarbonate, in contrast to 4 patients in the LAC group. Whereas peritoneal urea and creatinine clearances did not differ between the groups, there was better renal solute clearance in the BIC group, accompanied by better-preserved diuresis at 12 months (1333 +/- 935 mL with BIC vs 839 +/- 556 mL with LAC). The reverse was true for ultrafiltration. CONCLUSIONS: Pure bicarbonate-buffered PD solutions were superior in correcting metabolic acidosis and they allowed omission of oral bicarbonate. The minor ultrafiltration with bicarbonate-buffered PD solutions was counterbalanced by better-preserved residual renal function with these solutions.

Acidosis↗
PubMed1985

[Infantile transitory distal renal tubular acidosis with bicarbonate loss].

Apart from the classic distal renal tubular acidosis (RTA), the proximal RTA, and a few cases of distal RTA and renal bicarbonate wasting we know only 2 cases of infantile transient distal RTA with bicarbonate wasting. A 3 month-old male patient is admitted because of deficient suction, vomiting and dehydration. Despite a strong metabolic acidosis (pH 7,09, bicarbonate 8,6 mMol/l, chloride 110 meq/l) the urine is constantly alkaline; clinically the disease manifests itself in the form of an alkali-resistant RTA. Accompanying troubles such as inner ear deafness, G6PDH deficiency, hyperparathyroidism and vitamin D intoxication are to be excluded. A bicarbonate study carried out with care so as to prevent extracellular fluid expansion reveals the lack of excretion of titratable acid (-2.4 to +4.7 mueq/min/1.73 m2), an reduced excretion of ammonium (5 to 24.8 mueq/min/1.73 m2) with regard to GFR (42.4 ml/min/1.73 m2), and a constant loss of bicarbonate (FE HCO3- about 10%) covering most of the bicarbonate plasma concentration, which results in a constantly negative net acid excretion. Even with alkalosis there is no urine minus blood pCO2 increase. The renal excretion of gamma GT is significantly reduced. On substitution with high quantities of bicarbonate (10 meq/kg BW/day) the defect heals up at the age of 13 months. The pathogenesis of this disease is not quite clear, but is similar to that of the Lightwood infantile RTA. The acidification defect may be explained by a deficient hydrogen ions--secretion in the distal tubule; as for kinetics, it is not in the proximal tubule that the bicarbonate wasting occurs but it may be due to increased sodium delivery to the distal nephron.

Acidosis, Renal Tubular↗
PubMed1977

Regulation of citrate transport and pyruvate dehydrogenase in rat kidney cortex mitochondria by bicarbonate.

1. Bicarbonate increased citrate and 2-oxoglutarate accumulation when rat kidney cortex mitochondria were incubated with pyruvate or L(-)-palmitoyl carnitine in the presence of L-malate. 2. Bicarbonate stimulated the exit of citrate from mitochondria. The Km for bicarbonate was 13.5 mM and the Vmax was 0.59 nmol/min/mg of protein at 10 degrees. 3. The bicarbonate-stimulated exit of citrate from the mitochondria was prevented by inhibitors of the tricarboxylate, dicarboxylate, and phosphate transport systems. 4. The activity of pyruvate dehydrogenase was significantly increased by preincubation of rat kidney mitochondria with bicarbonate. This bicarbonate-induced activation was not observed in presence of inhibitors of citrate transport. Bicarbonate did not activate pyruvate dehydrogenase in rat heart mitochondria. Bicarbonate had no effect on pyruvate dehydrogenase activity in either broken mitochondria or whole tissue preparations. 5. The mechanism of this activation is discussed in the light of the known regulatory properties of pyruvate dehydrogenase, pyruvate carboxylase, and citrate synthase.

Animals↗