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 1,045 records · Page 58Linked to original sources

Whole animal and rumen digestive parameters of sheep given a concentrate diet supplemented with sodium bicarbonate.

Mature wether sheep were continuously given a concentrate-type diet and intraruminally infused with treatments of sodium bicarbonate (NaHCO3) at 0, 20 or 40 g/l per day according to a 3 x 3 Latin-square design. No effects of NaHCO3 on digestive parameters were statistically significant (P greater than 0.1). However, NaHCO3 additions decreased dietary intake and at 20 g/day supplementation, apparent digestibilities of dry matter, organic matter and nitrogen were increased, but 40 g/day bicarbonate reduced these values. Additions of NaHCO3 tended to increase rumen pH values, buffering capacities, concentrations of ammonia and acetate: propionate ratios. Water intakes, rumen volumes and population densities of rumen bacteria and protozoa were also higher with NaHCO3 supplementation, but these were not reflected by consistent changes in either rumen dilution rates or rumen microbial nitrogen concentrations. Interrelationships of digestive parameters that might be produced by the neutralising, buffering and osmotic pressure effects of sodium bicarbonate are discussed.

Animal Feed↗

Calculation of sodium bicarbonate requirement in metabolic acidosis.

Despite the host of complications which may be associated with intravenous sodium bicarbonate infusion, the use of this agent is a frequent necessity in patients with metabolic acidosis. No satisfactory formula for calculating bicarbonate dose had previously been described, although such an approach might be expected to reduce the incidence of these complications. The authors have devised a simple formula for bedside calculation of bicarbonate requirement in metabolic acidosis, designed to elevate th pH to the region about 7.30, and report their experience with the use of this formula in 13 instances. In all but one, the post-infusion pH was between 7.25 and 7.37, with a mean of 7.30 +/- 0.04 and no instances of serious overtitration. It is concluded that the formula is useful as a pragmatic aid in the management of patients with metabolic acidosis.

Acid-Base Imbalance↗

Comparison of external jugular and peripheral venous administration of sodium bicarbonate in puppies.

We compared the administration of sodium bicarbonate via a catheter inserted in the external jugular and extending to the junction with the subclavian vein (group 1) and a peripheral hindpaw vein (group 2) in puppies. During spontaneous cardiac activity, the increases in pH (0.12 +/- 0.04 in group 1 vs. 0.08 +/- 0.04 in group 2) and PCO2 (11 +/- 2.8 torr in group 1 vs. 6 +/- 3.2 torr in group 2) in blood from the right atrium 10 sec after the injection of bicarbonate differed significantly. However, the increases in pH (0.31 +/- 0.07 in group 1 vs. 0.30 +/- 0.15 in group 2) and PCO2 (86 +/- 33 torr in group 1 vs. 72 +/- 35 torr in group 2) in blood from the right atrium during closed chest CPR were similar in the two groups. We found that the sodium bicarbonate reached the central circulation more rapidly when administered in the external jugular vein as compared to a peripheral site, but this difference was small and did not reach the level of significance during CPR. Our findings do not provide evidence of any advantage to obtaining central venous access (a potentially complicated procedure) in children with cardiac arrest in regard to the delivery of medications to the heart.

Animals↗

Mechanism of hepatic bicarbonate secretion and bile acid independent bile secretion.

To examine hepatic bicarbonate transport and bile acid independent bile secretion, bile was sampled via a T-tube inserted into the common bile duct of anaesthetized pigs. Secretin was infused intravenously at a rate of 2.7 C.U./kg body weight h-1 (large dose) or 0.45 C.U./kg body weight h-1 (small dose). Hepatic water and electrolyte secretion were studied during systemic acid-base disturbances while secretin was continuously administered. Systemic acidosis reduced the rate of NaHCO3 secretion which fell in proportion to changes in plasma pH, by 9% and 2% per 0.1 pH unit for the large and small dose of secretin, respectively. Plasma pCO2 and bicarbonate concentration had little influence on NaHCO3 secretion. Consequently, plasma pH appeared to be the main determinant of hepatic NaHCO3 secretion during acid-base changes. Secretion of 1 mol NaHCO3 was accompanied by an isotonic solution containing water and 0.25 mol NaCl. After secretin infusion, 14C-erythritol clearance increased in proportion to bile flow. Bicarbonate secretion is determined by a gradient limited H+-pump at the contraluminal cell. During secretin stimulation bile acid independent bile secretion is osmotically driven by bile NaHCO3 flux.

Acid-Base Equilibrium↗

Evaluation of the 13CO2 kinetics in humans after oral application of sodium bicarbonate as a model for breath testing.

The kinetics of 13CO2 have been investigated following oral administration at five doses between 12.5 and 100 mg of 13C labelled sodium bicarbonate to 10 healthy subjects in a randomized study. Sodium bicarbonate in this study served as a model compound for carbon dioxide/bicarbonate generated in breath tests. Exhalation of 13CO2 into breath was monitored by stable isotope ratio mass spectrometry. The kinetics of 13CO2 were characterized by an apparent terminal elimination half-life of 1 h and a mean recovery of 0.630 of the dose administered. The kinetics were not dose-dependent. These results were in agreement with the findings reported previously after i.v. application of sodium bicarbonate.

Administration, Oral↗

Comparison of intra-and extracellular buffering of clinically used buffer substances: tris and bicarbonate.

A large and important group of acid-base disturbances are the metabolic acidoses. In general, every type of metabolic acidosis can be treated with infusion of base when the underlying cause of the disturbances is removed. In our medical centers, the use of tris and bicarbonate is common. For a long time they were competitive agents and until now it was not possible to decide by available clinical methods which of these substances was more suitable for correction of metabolic acidosis. The intracellular pH of the whole rat (mean lcf-pH) was determined from the distribution of 14C labelled DMO (5,5-dimethyl-2,4-oxazolidinedione) and monitored for 6 h following intravenous application of tris or sodiumbiarbonate in a dose of 10 mmol per kg body mass. Arterial plasma pH and PCO2 were also measured. To determine and compare the effectiveness of the two buffer substances, intra- and extracellular bicarbonate were calculated from the Henderson-Hasselbalch equation. It was found that the buffering following bicarbonate infusion is more effective in both body compartments. Sodiumbicarbonate should be preferred in daily practice.

Acidosis↗

Slc26a6: a cardiac chloride-hydroxyl exchanger and predominant chloride-bicarbonate exchanger of the mouse heart.

Bicarbonate facilitate more than 50% of pH recovery in the acidotic myocardium, and have roles in cardiac hypertrophy and steady-state pH regulation. To determine which bicarbonate transporters are responsible for this activity, we measured the expression levels of all known HCO3(-)-anion exchange proteins in mouse heart, by quantitative real time RT-PCR. Bicarbonate-anion exchangers are members of either the SLC4A or the SLC26A gene families. In neonatal and adult myocardium, AE1 (Slc4a1), AE2 (Slc4a2), AE3 (Slc4a3) (AE3fl and AE3c variants), Slc26a3 and Slc26a6 were expressed. Adult hearts expressed Slc26a3 and Slc4a1-3 mRNAs at similar levels, while Slc26a6 mRNA was about seven-fold higher than AE3, which was more abundant than any other. Immunohistochemistry revealed that Slc26a6 and AE3 are present in the plasma membrane of ventricular myocytes. Slc26a6 expression levels were higher in ventricle than atrium, whereas AE3 was detected only in ventricle. Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchange activity of SLC26A6 and AE3 were investigated in transfected HEK293 cells, using intracellular fluorescence measurements of 2',7'-bis (2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF), to monitor intracellular pH (pH(i)). Rates of pH(i) change were measured under HCO3(-)-containing (Cl(-)-HCO(3)(-)) or nominally HCO3(-)-free (Cl(-)-OH(-)) conditions. HCO3(-) fluxes were similar for cells expressing AE3fl, SLC26A6 or Slc26a3, suggesting that they have similar transport activity. However, only SLC26A6 and Slc26a3 functioned as Cl(-)-OH(-) exchangers. Activation of alpha-adrenergic receptors, which stimulates protein kinase C, inhibited SLC26A6 Cl(-)-HCO(3)(-) exchange activity. We conclude that Slc26a6 is the predominant Cl(-)-HCO(3)(-) and Cl(-)-OH(-) exchanger of the myocardium and that Slc26a6 is negatively regulated upon alpha-adrenergic stimulation.

Animals↗

Can potassium citrate replace sodium bicarbonate and potassium chloride of oral rehydration solution?

Ninety four children aged less than 5 years with diarrhoeal dehydration and acidosis were treated randomly with either World Health Organisation (WHO) oral rehydration solution containing sodium chloride, potassium chloride, sodium bicarbonate and glucose or an oral solution with tripotassium citrate monohydrate replacing the sodium bicarbonate and potassium chloride in the WHO solution. Fifty five children (58%) were hypokalaemic (potassium less than 3.5 mmol/l) on admission. All but two in the citrate group were successfully treated. There were no significant differences in rehydration solution intake, stool output, gain in body weight, and fall in plasma specific gravity and haematocrit between the two treatment groups after 48 hours' treatment. Significant improvement in the serum potassium concentration was observed in the hypokalaemic children receiving potassium citrate solution compared with children receiving WHO solution after 24 and 48 hours' treatment. None developed hyperkalaemia. Although children receiving potassium citrate solution corrected their acidosis at a slower rate than the WHO solution group during the first 24 hours, by 48 hours satisfactory correction was observed in all. Tripotassium citrate can safely replace sodium bicarbonate and potassium chloride and may be the most useful and beneficial treatment for diarrhoea and associated hypokalaemia.

Acidosis↗

Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis.

The effect of intravenous bicarbonate on the changes in intermediary metabolites during the initial treatment of diabetic ketoacidosis was examined in 16 patients. The results were compared with the changes seen in 16 patients receiving intravenous saline. Infusion of 150 mmol (mEq) bicarbonate significantly delayed the fall in blood lactate, lactate:pyruvate ratio, and total ketone bodies observed in the saline treated group. No difference in the rate of fall of blood glucose concentration was found. There is no metabolic indication for the use of intravenous bicarbonate in the treatment of diabetic ketoacidosis.

Adolescent↗

Oral rehydration therapy: efficacy of sodium citrate equals to sodium bicarbonate for correction of acidosis in diarrhoea.

Forty patients with moderate degrees of dehydration and acidosis because of acute watery diarrhoea were successfully treated randomly with either WHO recommended oral rehydration solution containing 2.5 g sodium bicarbonate or an oral solution containing 2.94 g sodium citrate in place of sodium bicarbonate per litre of oral rehydration rehydration solution. Efficacies were compared by measuring oral fluid intake, stool and vomitus output, change in body weight, hydration status, and rate of correction of acidosis during a period of 48 hours. Seventy five per cent (21 cases) in the citrate group and 83% (19 cases) in the bicarbonate group were successfully rehydrated (p greater than 0.05). There were no significant differences in intake, output, gain in body weight, fall in haematocrit and plasma specific gravity, and correction of acidosis between the two groups of patients within 48 hours after initiation of therapy. The solution with sodium citrate base was as effective as WHO-oral rehydration solution for management of diarrhoea. This study shows the efficacy, safety, and acceptability of citrate containing oral rehydration solution for rehydration and correction of acidosis in diarrhoea.

Acidosis↗

Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis.

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

Acidosis↗

Exercise in the heat: effects of saline or bicarbonate infusion.

Adult male rats (n = 17/group, 300-320 g, physically untrained) were exercised (9.14 m/min) in the heat (35 degrees C) to hyperthermic exhaustion (rectal temperature 43 degrees C) after infusion of 2 ml of 7.5% sodium bicarbonate (BIC) or 2 ml of 0.9% sodium chloride (SAL). Rats receiving BIC or SAL had no effects on endurance when compared with rats receiving no exogenous fluid [control (CON]), whereas the rate of heat gain, was significantly increased in the BIC-treated group. After exercise, the BIC group manifested significantly decreased hematocrit and plasma protein levels but exaggerated increments in plasma osmolality. Lactate levels were significantly increased in all three groups with no notable intergroup differences. Although venous blood pH and bicarbonate levels were decreased after exercise in the SAL and CON groups, they were unchanged in the BIC group. Although venous PCO2 was unaffected by fluid administration in all three groups, venous PO2 was significantly increased after exercise in the heat in all groups. We concluded from these experiments that even though BIC infusion prevented the acidosis and hypobicarbonatemia induced by exercise in the heat to hyperthermic exhaustion, the hypertonicity and Na+ content of the bicarbonate solution may have increased the rate of heat gain and precluded beneficial effects on physical performance.

Acidosis↗

Effect of sodium bicarbonate preloading on ischemic renal failure.

Rats pretreated with sodium bicarbonate were functionally protected from the damage of bilateral renal artery occlusion. The rise in serum creatinine (day 1 minus day 0) during the first 24 h after ischemia was 2.88 +/- 0.28 mg% in the bicarbonate-loaded animals versus 3.90 +/- 0.26 mg% in their matched controls (p less than or equal to 0.01). Pretreatment with acetazolamide produced a similar alkaline urine as the bicarbonate loading (pH 8.3 vs. 7.0 in controls) and a similar degree of protection (delta creatinine 2.85 +/- 0.41 vs. 4.23 +/- 0.26 mg%; p less than or equal to 0.01). A direct effect of sodium loading was excluded by comparing NH4HCO3 with NaHCO3 loading and observing no difference in delta creatinine levels after ischemia (3.39 +/- 0.69 vs. 3.20 +/- 0.61 mg%). These data indicate that NaHCO3 protects in this model of acute renal failure and further suggest that the mechanism of protection is not related to either systemic alkalosis or sodium loading.

Acetazolamide↗

[Differential effect of sodium bicarbonate on disposition of sulfadimethoxine and sulfisoxazole in rabbits].

The orally co-administered sodium bicarbonate significantly enhanced the blood concentration of sulfadimethoxine at the early stage after oral administration to rabbits, by increasing its intestinal absorption. On the other hand, the sodium bicarbonate significantly reduced the blood concentration of sulfisoxazole at the elimination phase after oral administration to rabbits, by increasing its urinary excretion. The fact that sodium bicarbonate exhibits different effects in the disposition of these two sulfonamides is an interesting example to gain a better understanding for the complexity of drug interaction.

Animals↗

The effect of sodium bicarbonate and hydrogen peroxide on the microbial flora of periodontal pockets. A preliminary report.

This study investigated the effects of sodium bicarbonate and hydrogen peroxide on the microbial flora of 4 to 7 mm periodontal pockets. Four selected patients were instructed to brush assigned quadrants daily with a sodium bicarbonate-3% hydrogen peroxide paste utilizing a split-mouth design. The paste was pumped between the teeth and gingiva via sulcular brushing and a Perio Aid. The control sides were treated in the identical manner with fluoridated paste. Probing depths on each patient were taken on Days 1 and 21 and examined under dark-field microscopy. For each sample, morphology and motility of all cells were recorded. The data were analyzed by three factor repeated measures analysis of variance. No statistically significant differences were found between the control and medicament sites at the 0.005 level regarding changes in the microbial flora. Probing depths were reduced during the study. However, similar results were found on both medicament and control sites. It appeared that sodium bicarbonate and hydrogen peroxide have no unusual benefits in reducing the microbial flora of periodontal pockets.

Adult↗

Addition of sodium bicarbonate to rations of pre- and postpartum dairy cows.

Sodium bicarbonate was added to complete mixed rations to evaluate the effect of buffer addition on adaptation to high-energy rations by dairy cows in elderly lactation. Forty-five Holstein cows were assigned to one of three treatment groups: control pre- and postpartum; control prepartum, buffer postpartum; and buffer pre- and postpartum. Rations consisted of 85% chopped grass hay: 15% concentrate prepartum and 60% corn silage:40% concentrate postpartum. On day 4 postpartum, cows were switched abruptly to the postpartum ration for 9 wk. Buffered rations contained .6% sodium bicarbonate prepartum and .7% postpartum. Daily dry matter intake as a percent of body weight for cows fed buffer postpartum (3.51%) was greater than for cows fed no buffer (3.04%) of buffer pre- and postpartum (3.14%). Average production of 4% fat-corrected milk was greater for cows fed buffer postpartum and buffer pre- and postpartum (31.9 kg/day and 31.7 kg/day) than for cows fed no buffer (28.9 kg/day). Milk fat tests were not different. Cows fed the buffered rations lost body weight between wk 1 and 9 as compared to a net gain for cows fed no buffer. Cows fed buffers consumed more dry matter during wk 1 than did cows fed no buffer. Samples of rumen fluid, feces, and serum showed few differences that could be attributed to treatments. Compared to controls, cows fed sodium bicarbonate adapted to rations more rapidly postpartum as indicated by increased feed intake during the first 2 wk and by increased milk production during the first 4 wk of the trial.

Animal Feed↗

Addition of sodium bicarbonate to rations of postpartum dairy cows: physiological and metabolic effects.

Sodium bicarbonate was added to complete mixed rations to characterize physiological, metabolic, and ruminal changes immediately postpartum when dairy cows are switched abruptly from a low energy ration prepartum to a high energy ration postpartum. Twelve Holstein cows were paired and assigned randomly to either a control or buffered ration containing .8% sodium bicarbonate. Rations consisted of 50% corn silage:50% concentrate. All All cows were fed a similar dry cow ration for a minimum of 7 days prepartum and experimental rations for 2 wk beginning at parturition. Blood, feces, and urine were sampled on days 1, 2, 4, 7, 10, and 14 postpartum. Rumen fluid was sampled on days 7 and 14. Dry matter intake and milk production were 2.75% of body weight and 30.3 kg/day for cows fed buffer and 2.49% and 27.6 kg/day for cows fed control. Higher partial pressure of carbon dioxide and base excess in blood in cows fed buffer existed on days 2 and 4 postpartum than for cows fed the control ration. Cows fed buffer had higher concentrations of ruminal ammonia than cows fed control. This difference was less pronounced in blood urea nitrogen and urinary ammonia. Urine pH was higher for cows fed buffer than for control. Addition of sodium bicarbonate improved the acid-base status after abrupt change of ration and may be associated with increased dry matter intake and improved ration adaptation. Concentrations of most minerals and metabolites in blood serum did not differ between rations.

Animal Feed↗

Rumen volatile fatty acid production and nutrient utilization in steers fed a diet supplemented with sodium bicarbonate and monensin.

Effects of feeding dietary supplements of monensin and sodium bicarbonate singly or in combination on production of rumen volatile fatty acids, nitrogen balance, and rumen water kinetics were studied. Four rumen fistulated steers were fed a diet (50% concentrate mix and 50% corn silage) ad libitum in a 4 X 4 Latin square design (21-day periods) with a 2 X 2 factorial arrangement of treatments. Sodium bicarbonate increased feed intake, water intake, rumen pH, fluid dilution rate, and decreased both molar proportion and production rate of propionate in the rumen. Alteration of the ratio of acetate to propionate reflects the large decrease in propionate production relative to the small increase in acetate production. In contrast, monensin did not alter significantly rumen fluid dilution rate or ruminal pH but did decrease the molar proportion of acetate and increase that of propionate. Monensin increased production of both acetate and propionate in the rumen; however, the large increase in propionate production appears to account for more of the increase in molar proportion of propionate in the rumen. Increases in total volatile fatty acid production per kilogram of dry matter consumed with monensin supplementation appears to result from decrease in feed intake, thereby increasing ruminal retention time of dry matter and potentially the extent of digestion. Efficiency of nitrogen utilization was not altered by either sodium bicarbonate or monensin.

Animals↗