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At least 973 records · Page 54Linked to original sources
PubMed1986

Bicarbonate therapy in severe diabetic ketoacidosis.

Twenty-one adult patients with severe diabetic ketoacidosis entered a randomized prospective protocol in which variable doses of sodium bicarbonate, based on initial arterial pH (6.9 to 7.14), were administered to 10 patients (treatment group) and were withheld from 11 patients (control group). During treatment, there were no significant differences in the rate of decline of glucose or ketone levels or in the rate of increase in pH or bicarbonate levels in the blood or cerebrospinal fluid in either group. Similarly, there were no significant differences in the time required for the plasma glucose level to reach 250 mg/dL, blood pH to reach 7.3, or bicarbonate level to reach 15 meq/L. We conclude that in severe diabetic ketoacidosis (arterial pH 6.9 to 7.14), the administration of bicarbonate does not affect recovery outcome variables as compared with those in a control group.

Adult↗
PubMed1987

Indomethacin inhibits duodenal mucosal bicarbonate secretion and endogenous prostaglandin E2 output in human subjects.

Nonsteroidal anti-inflammatory drugs are a frequent cause of gastric and duodenal mucosal injury. We examined the effect of indomethacin on duodenal mucosal bicarbonate secretion and prostaglandin output in healthy subjects. Subjects received either 50 mg of indomethacin or placebo orally 13 hours and 1 hour before study. A 4-cm segment of proximal (the duodenal bulb) or distal (10 to 14 cm beyond the pylorus) duodenum was isolated and perfused with 154 mM NaCl containing a nonabsorbable marker. In the proximal duodenum indomethacin reduced both basal and acid-stimulated bicarbonate secretion by approximately 65% (p less than 0.01); in the distal duodenum indomethacin decreased basal and acid-stimulated bicarbonate output by approximately 45% (p less than 0.01). Oral indomethacin inhibited basal and acid-stimulated duodenal prostaglandin E2 output in both the proximal and distal duodenum. We conclude that, by decreasing duodenal mucosal bicarbonate production and prostaglandin output in humans, oral indomethacin, in two doses of 50 mg each, impairs an important duodenal defense mechanism.

Administration, Oral↗
PubMed1999

[Reduction of renal uranium uptake by acetazolamide: the importance of urinary elimination of bicarbonate].

Acetazolamide was compared with bicarbonate for the treatment of contamination with uranium. Uranium was injected peritoneally in rats, and its distribution was investigated. Acetazolamide was three times more efficient than bicarbonate in reducing the renal content of uranium. On the other hand, it had no effect on hepatic or skeletal content. In this study, renal physiology provides the basis for understanding the mode of action of acetazolamide and bicarbonate. In this context, it is of interest to determine the alkalinity of the urine, with the aim of knowing whether bicarbonate is present to mobilize uranium.

Acetazolamide↗
PubMedDate not supplied

An amino acid-based peritoneal dialysis fluid buffered with bicarbonate versus glucose/bicarbonate and glucose/lactate solutions: an intraindividual randomized study.

OBJECTIVE: In order to study acute metabolic changes and peritoneal transport, amino acids as osmotic agent and bicarbonate as buffer were tested as new agents in peritoneal dialysis (PD) solutions. DESIGN: In a prospective, cross-over, randomized, intraindividual study, we investigated the acute metabolic changes following the application of three different PD fluids: (1) a 1% amino acid-based PD solution buffered with bicarbonate (34 mmol/L) (Amino/Bic); (2) a 1.5% glucose anhydrous-containing bicarbonate-buffered solution (34 mmol/L) (Glu/Bic); and (3) a conventional 1.5% glucose anhydrous-based dialysis solution with lactate (35 mmol/L) (Glu/Lac). SETTING: University medical center. PATIENTS: Ten nondiabetic patients stable on continuous ambulatory peritoneal dialysis (time on dialysis, 42.5 +/- 21.5 months) were treated and monitored with the test solutions over a 6-hour dwell. Three different study days followed in a randomized order for each patient (interval of 1-3 weeks). Blood and dialysate samples were taken at 0.25, 0.5, 1, 2, 4, and 6 hours. Immediately after the 1-hr dwell (and after sampling), the patients received a standardized breakfast, thereby simulating usual food intake. RESULTS: Following the application of Amino/Bic a significant increase in plasma amino acids occurred, with peak levels (maximum 250% increase) after either the 1-hr or the 2-hr dwell. Before taking the standard meal (0.5 hr, 1 hr), the mean serum glucose level with Amino/Bic was 8% +/- 13% lower than with Glu/Bic (p = 0.06) and 14% +/- 8% lower than with Glu/Lac (p < 0.01). This difference was still significant after the standard breakfast and also for the whole dwell (average serum glucose 0.5-6 hr: Amino/Bic, 91 +/- 6 mg/dL; Glu/Bic, 100 +/- 8 mg/dL; Glu/Lac, 102 +/- 7 mg/dL; p < 0.01 MANOVA). The serum insulin profiles did not differ between the fluids. A transperitoneal protein- and amino acid-related nitrogen loss of 0.49 +/- 0.18 g and 0.48 +/- 0.12 g per dwell was measured using Glu/Bic and Glu/Lac, while a positive balance of 1.80 +/- 0.43 g was achieved with Amino/Bic. The parameters of acid-base status (pH, HCO3, pCO2) remained nearly unchanged in the blood, irrespective of the solution used, while dialysate values differed markedly. No significant differences with respect to ultrafiltration (Amino/Bic, -68 +/- 199 mL/6 hr; Glu/Bic, -51 +/- 89 mL/6 hr; Glu/ Lac, -2 +/- 134 mL/6 hr) and peritoneal creatinine clearance (Amino/Bic, 4.9 +/- 0.6 mL/min; Glu/Bic, 5.1 +/- 0.6 mL/min; Glu/ Lac, 4.8 +/- 0.5 mL/min) were measured. CONCLUSIONS: Our results demonstrate that ultrafiltration and small solute clearance over a 6-hour dwell with a 1% Amino/Bic solution were comparable to those of 1.5% Glu/Bic and 1.5% Glu/Lac. Reduced serum glucose concentrations were found with Amino/Bic and this fluid compensated the transperitoneal protein-nitrogen loss of about three glucose dwells. Bicarbonate buffering (34 mmol/L) did not change blood acid-base status combined with either glucose or amino acids.

Adult↗
PubMed1996

Effects of a high-bicarbonate dentifrice on intraoral demineralization.

Dentifrices available on the market today contain sodium bicarbonate in a wide range of concentrations. Anticaries efficacy has been demonstrated for these dentifrices in a variety of tests. New insights were gained in the present study in which the effect of a high-bicarbonate dentifrice on the sucrose-induced demineralization of tooth enamel in situ was examined. With the intraoral Delta Ip system it is possible to follow the minute changes in tooth enamel that essentially model the daily episodes of demineralization accompanying the ingestion of various foods. The results revealed a pronounced effect on the pH of the test plaque and a considerable reduction in mineral loss from the enamel. The effect persisted from more than 1 hour and, during that time, appeared to predominate over the effect of fluoride. These findings suggest that bicarbonate may provide additional protection against the loss of tooth enamel. Such effects may be significant for the design of new high-bicarbonate products.

Animals↗
PubMed2002

Physostigmine, sodium bicarbonate, or hypertonic saline to treat diphenhydramine toxicity.

Diphenhydramine (DPH) is a commonly reported overdose that shares similar toxicities with other agents. such as tricyclic antidepressants, that interact with the fast sodium channels. Although physostigmine is considered an acceptable antidote for severe DPH toxicity, adverse effects such as seizures and cholinergic crisis may occur. We hypothesized that hypertonic saline or bicarbonate is equivalent or are better antidotes in an animal model of DPH toxicity. In a preliminary study. Sprague-Dawley rats were given toxic doses of DPH while continuous ECG, EEG, and blood pressure monitoring was performed. Seizures were the common toxic effect observed and was chosen. Four groups of 10 rats each were established as control physostigmine, hypertonic sodium bicarbonate, and hypertonic saline(3%) treatment. Control had initial "drop-off" seizure burst rates over time; seizure bursts in the treatment groups were compared to these rates. Hypertonic sodium bicarbonate was the most effective treatment, followed closely by hypertonic saline. Hypertonic sodium bicarbonate may interact with DPH neuronal sodium channels and may be considered adjuvant therapy in humans with DPH-induced seizures.

Animals↗
PubMed2001

Bicarbonate-regulated soluble adenylyl cyclase.

Soluble adenylyl cyclase (sAC) represents a novel form of mammalian adenylyl cyclase structurally, molecularly, and biochemically distinct from the G protein-regulated, transmembrane adenylyl cyclases (tmACs). sAC possesses no transmembrane domains and is insensitive to classic modulators of tmACs, such as heterotrimeric G proteins and P site ligands. Thus, sAC defines an independently regulated cAMP signaling system within mammalian cells. sAC is directly stimulated by bicarbonate ion both in vivo in heterologously expressing cells and in vitro using purified protein. sAC appears to be the predominant form of adenylyl cyclase (AC) in mammalian sperm, and its direct activation by bicarbonate provides a mechanism for generating the cAMP required to complete the bicarbonate-induced processes necessary for fertilization, including hyperactivated motility, capacitation, and the acrosome reaction. Immunolocalization studies reveal sAC is also abundantly expressed in other tissues which respond to bicarbonate or carbon dioxide levels suggesting it may function as a general bicarbonate/CO(2) sensor throughout the body.

Adenylyl Cyclases↗
PubMed1997

Effects of a high-bicarbonate dentifrice on intraoral demineralization.

Dentifrices available on the market today contain sodium bicarbonate in a wide range of concentrations. Anticaries efficacy has been demonstrated for these dentifrices in a variety of tests. New insights were gained in the present study in which the effect of a high-bicarbonate dentifrice on the sucrose-induced demineralization of tooth enamel in situ was examined. With the intraoral Delta Ip system it is possible to follow the minute changes in tooth enamel that essentially model the daily episodes of demineralization accompanying the ingestion of various foods. The results revealed a pronounced effect on the pH of the test plaque and a considerable reduction in mineral loss from the enamel. The effect persisted for more than 1 hour and, during that time, appeared to predominate over the effect of fluoride. These findings suggest that bicarbonate may provide additional protection against the loss of tooth enamel. Such effects may be significant for the design of new high-bicarbonate products.

Animals↗
PubMed1999

[Perhydrit and sodium bicarbonate improve maternal gases and acid-base status during the second stage of labor].

Perhydrit and sodium bicarbonate were administered to 99 women during the second stage of labor. Gas analysis was done twice at the beginning and the end of the second stage. The results showed that 33 women received both perhydrit and sodium bicarbonate(Group I) had significantly higher pH, BE, pO2, and O2sat at the end of the second stage than those of 30 controls (Group III) (P < 0.05 and < 0.01). And 33 women received only sodium bicarbonate(Group II) showed merely higher pH and BE than those of Group III. The difference was significant(P < 0.05 and < 0.01), while PO2 and O2sat had no statistical difference between Group II and Group III. By comparing the values, we found that pH, PO2 and O2sat were much higher at the end of the second stage in Group I and Group II than those at the beginning of the second stage(P < 0.05 and < 0.01). No statistical difference of BE had been found between both groups. In contrary, BE, pH, PO2 and O2sat declined at the end of the second stage in Group III (P < 0.02 and < 0.01). There were no significant differences of PCO2 among the three groups. It is suggested that the administration of perhydrit and sodium bicarbonate may effectively improve the tendency of maternal metabolic acidosis and tissue oxygen debt caused by consumption and uterine contractions during the second stage, subsequently improve maternal gases and acid-base status.

Acid-Base Imbalance↗
PubMed1975

[Differences in the responses of taste receptors to organic and inorganic acids with changes in the concentration of bicarbonate in the solution].

The thresholds of the pH for citric acid (pH=4.9) were found to exceed by 1.4 pH the thresholds for HC1 (3.5) at 1.2 mmol/1 bicarbonate in the solution. The reaction to citric acid was higher than to HC1 at equal pH. Decreasing of bicarbonate from 1.2 mmol/1 to 0 reduced pH threshold only for sitric acid from 4.90 to 3.15. pH threshold for HC1 remained 3.5 The chorda tympani response to stimulation with solutions containing bicarbonate (1.2 mmol/1) was higher than in absence of bicarbonate. The data obtained suggest two ranges of the acids in action.

Animals↗
PubMed1976

Sodium bicarbonate administration during cardiac arrest. Effect on arterial pH PCO2, and osmolality.

Arterial pH, Pco2, and osmolality were determined serially during cardiac resuscitation in patients and in dogs, with and without administration of sodium bicarbonate. These studies demonstrate that (1) in the absence of preexisting acidosis, severe acidosis can be prevented by adequate ventilation alone; (2) sodium bicarbonate administration results in a significant rise in arterial Pco2, which parallels the rise in pH despite adequate ventilation; (3) during prolonged cardiac and resuscitation, there is a rise in arterial osmolality that is accentuated by sodium bicarbonate. These studies suggest that sodium bicarbonate should not be used during resuscitation (1) in the absence of effective hyperventilation or where carbon dioxide removal is inadequate despite adequate ventilation, (2) in repeated doses, without confirmation of substantial acidosis, or (3) when cardiac arrest has been of brief duration and preexisting acidosis is unlikely. These studies also point to the need for a reappraisal of other buffers that do not elevate the arterial Pco2.

Acidosis↗
PubMedDate not supplied

[Misinterpretation of measured bicarbonates during the administration of high doses of propofol].

A patient, admitted to intensive care unit and sedated with propofol (Diprivan), had repeatedly presented severe decreased of measured bicarbonates without metabolic acidosis and with physiologic values of calculated bicarbonates. Consecutively to the administration of high doses of propofol, an important lactescence of samples had been observed and the tests realised showed that lactescence play a key role in the interference with the measurement of bicarbonates (as described in the literature). So, in the course of propofol administration, it would be advised to interpret with caution the results of measured bicarbonates to not conclude too quickly on a case of "propofol syndrome".

Aged↗
PubMed1990

Gabexate and camostat, synthetic proteinase inhibitors, as direct inducing factors of water and bicarbonate secretion in the isolated and blood-perfused dog pancreas.

The effects of proteinase inhibitors on the secretion of pancreatic juice were investigated in preparations of the isolated and blood-perfused dog pancreas as compared with those of secretin. Each drug tested was administered i.a. Graded doses of gabexate (1-10 mg) elicited dose-dependent biphasic responses for the secretory rates, bicarbonate concentrations and outputs of pancreatic juice, with maximum effects at approximately 5 mg, but had little effect on the protein concentrations. Camostat, at a high dose of 10 mg, caused significant increases in the secretory rate, bicarbonate concentration and output of pancreatic juice over their basal levels, but had little influence on the protein concentration. Secretin (0.03-0.3 U) usually produced similar to gabexate-induced results (1-5 mg). Both bicarbonate and protein concentrations of the juice obtained with gabexate or camostat were almost the same as those obtained with secretin at a similar secretory rate of pancreatic juice, suggesting the secretory action of gabexate or camostat might be similar to that of secretin. In addition, gabexate (3 mg) and camostat (10 mg) elicited more than the respective additive secretory responses in the presence of i.a. infusion of a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (12 micrograms/min) as well as secretin (0.1 U). These results indicate that gabexate and camostat induce water and bicarbonate secretion by acting directly on ductular cells of the dog pancreas, which might be mediated at least partially through cyclic AMP.

1-Methyl-3-isobutylxanthine↗
PubMed1976

ATP-dependent reactions catalyzed by inner membrane vesicles of rat liver mitochondria. Kinetics, substrate specificity, and bicarbonate sensitivity.

Three ATP-dependent reactions catalyzed by the inner membrane of rat liver mitochondria and the ATPase reaction catalyzed by purified mitochondrial ATPase (F1), were studied with respect to kinetic properties, substrates specificity, and sensitivity to bicarbonate. The ATP-dependent transhydrogenase reaction (reduction of NADP+ by NADH) catalyzed by inner membrane vesicles displays typical Michaelis-Menten kinetics in both Tris-Cl and Tris-bicarbonate buffers, with Km (ATP) values of 0.035 mM and 0.054 mM respectively. The Vmax of transhydrogenase activity (25 nmol min-1 mg-1) is the same in Tris-bicarbonate or Tris-Cl buffer. ITP and GTP readily substitute for ATP in the transhydrogenase reaction. The ATP-P1 exchange reaction catalyzed by inner membrane vesicles displays typical Michaelis-Menten kinetics in both Tris-Cl and Tris-bicarbonate buffers with Km (ATP) values of 1.0 mM and 1.4 mM respectively. The Vmax of exchange (200 nmol min-1 mg-1) is the same in either buffer. ITP and GTP do not effectively replace ATP in the exchange reaction.

4-Nitrophenylphosphatase↗
PubMedDate not supplied

Optimal dialysate bicarbonate during hemodialysis.

Eleven stable hemodialysis patients were treated with acetate dialysate, then changed to bicarbonate dialysate at three different concentrations. Blood was drawn from the arterial limb of the arteriovenous fistula before and after dialysis for pH, partial pressure of carbon dioxide, bicarbonate radical, and partial pressure of oxygen. Both acetate (35 mEq/L) and the lowest bicarbonate concentration (25 mEq/L) resulted in inadequate control of acid-base balance. Using a bicarbonate concentration of 30 mEq/L, mild predialysis acidosis was still present; this could be abolished using 35 mEq/L, but only at the cost of postdialysis alkalosis and mild hypoxemia.

Acetates↗
PubMedDate not supplied

[The effect of acetate and bicarbonate on the tolerance for hemodialysis therapy in chronic kidney failure].

Effects of acetate and bicarbonate dialysates on tolerance to dialysis have been examined in 30 patients with chronic renal failure (CRF). Symptomatic homeostatic impairment (nausea, vomiting, headache) and cardiovascular instability (tachycardia, arrhythmia, dyspnea) were less common (p less than 0.05) in bicarbonate dialysis. The cardiovascular symptoms correlated with antihypertensive effects of acetate (p = +0.48). Tolerance to ultrafiltration was better with bicarbonate dialysis. Gas chromatographic measurement of blood acetate concentrations in 7 patients on bicarbonate dialysis showed them to be 1.4 +/- 0.31 mmol/l at the beginning of dialysis treatment and 1.7 +/- 0.24 mmol/l at its end (normal, 1.7 +/- 0.14 mmol/l). Of 26 patients on acetate dialysis, 9 patients showed initial and late acetate concentrations of 1.7 +/- 0.26 and 2.5 +/- 0.23 mmol/l, respectively, while in 17 patients an initial concentration of 4.8 +/- 0.32 mmol/l rose to 9.0 +/- 1.1 mmol/l at the end of the treatment (p less than less than 0.01). Dialysis-induced complications had a higher incidence in the latter group (p less than 0.02). Acetate dialysis was poorly tolerated by 65% of the patients. The intolerance was aggravated by myocardial lesions and slow acetate turnover indicated by blood acetate concentrations above 7-8 mmol/l.

Acetates↗
PubMed1990

Sodium and bicarbonate reabsorption in microperfused proximal tubules from the denervated rat kidney: relationship to cortical Na-K-ATPase activity.

Although numerous studies have documented the effects of the renal nerves on kidney function, the mechanisms involved in the diuresis have yet to be elucidated. The present study was undertaken to examine the effect of acute unilateral renal denervation (DNX) on proximal tubular absorption of fluid and bicarbonate and to determine if acute DNX was associated with changes in Na-K-ATPase activity. Acute DNX caused significant increases in urine flow and absolute and fractional excretions of Na, HCO3 and K compared to the contralateral control kidney (INN) or sham denervated kidneys in normal rats as well as in rats made alkalotic by the I.V. infusion of 150 mM NaHCO3. These effects were seen without significant changes in GFR. When proximal convoluted tubules (PCT) were perfused with bicarbonate-Ringer's solution DNX resulted in a 67% decrease in fluid reabsorption (INN: 3.0 +/- 0.2 vs DNX: 1.0 +/- 0.1 nl/min/mm; p less than 0.001) and a 40% decline in bicarbonate (total CO2) reabsorption (INN: 151.3 +/- 8.8 vs DNX: 94.5 +/- 10.1 pmol/min/mm; p less than 0.01). Acute DNX caused a significant reduction in Na-K-ATPase activity measured in microsomes derived from the outer cortex of the kidney (INN: 13.2 +/- 1.3 vs DNX: 10.9 +/- 0.7 mumol PO4/mg prot/hr; p less than 0.01) while Mg-ATPase was unaffected. Sham denervation had no effect on any of the above parameters. These results indicate that the renal nerves play an important role in the regulation of bicarbonate and fluid reabsorption in the PCT. The diuresis, natriuresis, and bicarbonaturia associated with acute unilateral renal denervation may be the direct result of inhibition of Na-K-ATPase activity.

Acid-Base Equilibrium↗
PubMedDate not supplied

Benefit of bicarbonate dialysis during CAVHD.

The effect of bicarbonate dialysate (BD) on acid-base status in six pediatric CAVHD patients was examined during seven episodes of metabolic acidosis. When metabolic acidosis was not corrected with CAVHD, a sterile BD was substituted for either acetate- or lactate-based dialysate. Pre- and post-BD substitution levels of lactate, HCO3, PCO2, anion gap, and pH were recorded, as well as dose of intravenous (i.v.) bicarbonate. Improvements in pH and serum HCO3 were seen in all seven cases. Anion gap decreased in all but one of the patients who were switched from lactate to bicarbonate dialysate, with improvement most marked in those patients with marked elevation of the anion gap. No adverse effect on PCO2 was noted. Lactate dialysate may be less effective when serum lactate levels are high, and may contribute to further elevation of lactate levels and anion gap. These data suggest that bicarbonate dialysate may be preferable to lactate or acetate dialysate in CAVHD patients with persistent metabolic acidosis.

Acid-Base Equilibrium↗