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At least 775 records · Page 43Linked to original sources
PubMed1988

Prevention of uric acid stone formation by sodium bicarbonate in an ileostomy patient--a case report.

A 38 year old female underwent a proctocolectomy and ileostomy for ulcerative colitis in February, 1974. For 8 year post-operatively, she excreted innumerable renal stones, mainly composed of uric acid. Her urine was highly acidic and hyperuricosuric with a low concentration of sodium. Sodium bicarbonate 4 gm/day, t.i.d., was started in October 1985, after which her renal stone excretion completely ceased (up until March, 1987), except for one incidence of stone excretion when she discontinued therapy for a week. During the sodium bicarbonate therapy, her urinary pH and Na concentration were elevated. Furthermore, sodium bicarbonate significantly elevated the urinary pH and Na concentration of other ileostomy patients. Thus, sodium bicarbonate could be used for the possible prophylaxis of uric acid formation in selected ileostomy patients.

Adult↗
PubMed2004

Molecular mechanisms of electrogenic sodium bicarbonate cotransport: structural and equilibrium thermodynamic considerations.

The electrogenic Na(+)-HCO(3)(-) cotransporters play an essential role in regulating intracellular pH and extracellular acid-base homeostasis. Of the known members of the bicarbonate transporter superfamily (BTS), NBC1 and NBC4 proteins have been shown to be electrogenic. The electrogenic nature of these transporters results from the unequal coupling of anionic and cationic fluxes during each transport cycle. This unique property distinguishes NBC1 and NBC4 proteins from other sodium bicarbonate cotransporters and members of the bicarbonate transporter superfamily that are known to be electroneutral. Structure-function studies have played an essential role in revealing the basis for the modulation of the coupling ratio of NBC1 proteins. In addition, the recent transmembrane topographic analysis of pNBC1 has shed light on the potential structural determinants that are responsible for ion permeation through the cotransporter. The experimentally difficult problem of determining the nature of anionic species being transported by these proteins (HCO(3)(-) versus CO(3)(2-)) is analyzed using a theoretical equilibrium thermodynamics approach. Finally, our current understanding of the molecular mechanisms responsible for the regulation of ion coupling and flux through electrogenic sodium bicarbonate cotransporters is reviewed in detail.

Acid-Base Equilibrium↗
PubMed1990

Bicarbonate effects on photo-inhibition. Including an explanation for the sensitivity to photo-inhibition under anaerobic conditions.

Isolated thylakoid membranes were found to be efficiently protected against photo-inhibition by sodium bicarbonate (20 mM NaHCO3) under both anaerobic and aerobic conditions. Furthermore, data are presented which indicate that the pronounced sensitivity to photo-inhibition under anaerobic compared to aerobic conditions is due to the removal of protecting bicarbonate, rather than oxygen, from the medium. A second type of bicarbonate effect on photo-inhibition, in apparent contradiction to the protective effect of added NaHCO3, is that thylakoid membranes that were depleted in their endogenous bicarbonate by treatment with formate were found to be less susceptible to photo-inhibition than thylakoids in the normal non-depleted state.

Aerobiosis↗
PubMed1985

Bicarbonate therapy for the cardiovascular toxicity of amitriptyline in an animal model.

The beneficial hemodynamic effects of sodium bicarbonate as treatment for tricyclic antidepressant poisoning were investigated in an animal model. Seven adult dogs (17.5 to 20 kg) were poisoned by an intravenous infusion of amitriptyline. Toxicity was defined as a doubling of the initial QRS width. A continuous infusion was used to maintain toxicity for 30 minutes after which 44.5 mEq of sodium bicarbonate was administered intravenously. Five of the animals survived to completion of the experiment. Three of the surviving animals developed dysrhythmias. All dysrhythmias ceased within one minute of administration of sodium bicarbonate. An increase in mean blood pressure (P less than .05) and serum pH (P less than .05) and a decrease in mean QRS width (P less than .05) occurred following administration of sodium bicarbonate. The maintenance of toxicity for 30 minutes suggests that this model can be used for future studies of tricyclic antidepressant poisoning.

Amitriptyline↗
PubMed1993

Sodium bicarbonate alleviates penile pain induced by intracavernous injections for erectile dysfunction.

In an attempt to determine whether penile pain associated with intracorporeal injections could be due to the acidity of the medication, we performed a randomized study comparing the incidence of penile pain following intracorporeal injections with or without the addition of sodium bicarbonate to the intracorporeal medications. A total of 38 consecutive patients who presented to our clinic with impotence received 0.2 ml. of a combination of 3 drugs: 6 mg. papaverine, 100 micrograms. phentolamine and 10 micrograms. prostaglandin E1 with (pH 7.05) or without (pH 4.17) the addition of sodium bicarbonate (0.03 mEq.). Of the 19 patients without sodium bicarbonate added to the medication 11 (58%) complained of penile pain due to the medication, while only 1 of the 19 men (5%) who received sodium bicarbonate complained of penile pain. From these data we conclude that the penile pain following intracorporeal injections is most likely due to the acidity of the medication, which can be overcome by elevating the pH to a neutral level.

Adult↗
PubMed1985

Comparison of intraosseous, central, and peripheral routes of sodium bicarbonate administration during CPR in pigs.

Obtaining venous access continues to be one of the most difficult problems faced by a physician caring for the pediatric patient in cardiac arrest. Our study examined the use of the intraosseous route (through the bone) to obtain venous access for sodium bicarbonate administration in a cardiac arrest model. Ventricular fibrillation was induced in 23 domestic swine. Cardiopulmonary resuscitation was performed for five minutes and sodium bicarbonate (1 mEq/kg) was administered through a peripheral IV line (n = 6), a central IV line (n = 5), or intraosseously (n = 6). Controls (n = 6) did not receive bicarbonate. Blood pH was sampled every two minutes for 30 minutes from the right ventricle, left ventricle, and femoral artery. An analysis of variance revealed that the central and intraosseous routes were significantly different (P less than .05) from the peripheral group, and that all three groups were significantly different (P less than .05) from the control. Pathology studies revealed only minor damage to bone when sodium bicarbonate was administered intraosseously. These data demonstrate that the intraosseous route is a rapid and effective alternative for venous access in a cardiac arrest model.

Animals↗
PubMed1986

Experimental amitriptyline intoxication: treatment of cardiac toxicity with sodium bicarbonate.

Overdose with amitriptyline and other tricyclic antidepressants can result in ventricular conduction abnormalities as well as severe ventricular arrhythmias. The arrhythmogenic effects of these compounds may be attributed to their direct local anesthetic actions in blocking sodium channels in cardiac membranes. Thus tricyclic-induced ventricular arrhythmias usually do not respond well to therapy with standard Class I antiarrhythmic drugs that also have the same direct local anesthetic action and may potentiate the adverse effects of tricyclic antidepressants. Cardiac toxicity was produced in dogs by the administration of amitriptyline, both orally and IV. At serum concentrations less than 2,000 ng/mL, sinus tachycardia occurred with widened QRS complexes. At higher concentrations, QRS duration became more markedly prolonged and was followed by ventricular tachyarrhythmias. Occurrence of ventricular tachyarrhythmias was associated with QRS durations of more than 0.11 second. Sodium bicarbonate (18 to 36 mEq) administered IV over either 30 seconds or two minutes rapidly converted ventricular tachycardia to normal sinus rhythm. Conversion was associated with abbreviation of the QRS complex and was accompanied by a rise in both systolic and diastolic pressures. The duration of sodium bicarbonate effect paralleled the duration of the changes in arterial pH and plasma bicarbonate concentrations. In vitro studies in cardiac Purkinje fibers suggested that reversal of amitriptyline-induced cardiac membrane effects by sodium bicarbonate may be attributed not only to alkalinization but also to increased in extracellular sodium concentration, diminishing the local anesthetic action of amitriptyline and resulting in less sodium channel block.(ABSTRACT TRUNCATED AT 250 WORDS)

Amitriptyline↗
PubMed1981

Intracranial hemorrhage following administration of sodium bicarbonate in rabbits.

Studies on the correlation between hyperosmolality and brain damage, especially intracranial hemorrhage, were carried out on young and newborn rabbits following infusion with 7% sodium bicarbonate. 1) All the young rabbits injected with 7% sodium bicarbonate died of hyperosmolality at over 380 mOsm/L (the mean was 462 mOsm/L) after drip infusion at the rate of 20-60 ml/kg/hr. Young rabbits under a 10% hypoxic environment died even at the 350 mOsm/L level (the mean was 392 mOsm/L) during infusion of 7% sodium bicarbonate. Half of the case of newborn rabbits injected with 7% sodium bicarbonate at 10 ml/kg, intraperitoneally, had intracranial hemorrhage at 335 mOsm/L. When the hyperosmolality reached 392 mOsm/L (50 ml/kg), intracranial hemorrhage was observed in all cases. 2) The main cause of death in young and newborn rabbits was subdural hemorrhage in the subtentorial region. Intraventricular hemorrhage was observed in about 40% of the cases of young and newborn rabbits. 3) The blood pH was elevated by the drip infusion, but when the hyperosmolality reached about 400 mOsm/L, the blood pH began to fall. At the same osmolality, pCO2 showed a marked elevation. It is likely that the decrease of the blood pH was caused by the elevation of pCO2 and the outflow of H+ from intracellular compartments resulting from the hyperosmolality. These results apparently indicate that fatal intracranial hemorrhage was induced by hyperosmolality and was enhanced by the combination of hypoxia and immaturity.

Animals↗
PubMed1986

The effect of sodium bicarbonate on the flow-dependency of urinary prostaglandin excretion in man.

The influence of oral water loading on the excretion rate of prostaglandin (PG) E was investigated in healthy human subjects in a control study where the urine was acidic (pH 5.7) and after oral sodium bicarbonate, which made the urine mildly alkaline (pH 7.2). PGE was immediately extracted from urine and measured by a radioimmunoassay technique. After sodium bicarbonate (5 g) the urinary PGE excretion rate was some three-fold higher (P less than 0.01) than in the control study, in the absence of any significant difference in the urine flow (approximately 80 ml/h). In the control study (urine pH 5.7) the urinary PGE excretion rate increased significantly (P less than 0.01) as the urine flow rose in response to the oral fluid load. However, after sodium bicarbonate, PGE excretion did not alter after the fluid load despite a 10-fold increase in urine flow. Since after bicarbonate administration PGE excretion is independent of urine flow, mildly alkaline urine may represent a condition under which renal PGE synthesis can be effectively assessed from measurements of urinary PGE excretion, in the presence of changes in urine flow. In addition, the results are compatible with the hypothesis that, in man, PGE may be passively reabsorbed in the distal nephron, and a reduction in this reabsorption could contribute to or be responsible for the dependency of the excretion rate of PGE on urine flow.

Adult↗
PubMed1998

Molecular cloning, chromosomal localization, tissue distribution, and functional expression of the human pancreatic sodium bicarbonate cotransporter.

We report the cloning, sequence analysis, tissue distribution, functional expression, and chromosomal localization of the human pancreatic sodium bicarbonate cotransport protein (pancreatic NBC (pNBC)). The transporter was identified by searching the human expressed sequence tag data base. An I.M.A.G.E. clone W39298 was identified, and a polymerase chain reaction probe was generated to screen a human pancreas cDNA library. pNBC encodes a 1079-residue polypeptide that differs at the N terminus from the recently cloned human sodium bicarbonate cotransporter isolated from kidney (kNBC) (Burnham, C. E., Amlal, H., Wang, Z., Shull, G. E., and Soleimani, M. (1997) J. Biol. Chem. 272, 19111-19114). Northern blot analysis using a probe specific for the N terminus of pNBC revealed an approximately 7.7-kilobase transcript expressed predominantly in pancreas, with less expression in kidney, brain, liver, prostate, colon, stomach, thyroid, and spinal chord. In contrast, a probe to the unique 5' region of kNBC detected an approximately 7.6-kilobase transcript only in the kidney. In situ hybridization studies in pancreas revealed expression in the acini and ductal cells. The gene was mapped to chromosome 4q21 using fluorescent in situ hybridization. Expression of pNBC in Xenopus laevis oocytes induced sodium bicarbonate cotransport. These data demonstrate that pNBC encodes the sodium bicarbonate cotransporter in the mammalian pancreas. pNBC is also expressed at a lower level in several other organs, whereas kNBC is expressed uniquely in kidney.

Amino Acid Sequence↗
PubMed1986

The effect of replacement of 0.30% sodium chloride by 0.43% sodium bicarbonate in rations of fattening pigs on leg weakness, osteochondrosis and growth.

The effect of replacing dietary sodium chloride by sodium bicarbonate on leg weakness, osteochondrosis and growth in young fattening pigs was studied in two experiments using 104 and 126 animals. The experimental pigs were fed 0.43% dietary sodium bicarbonate, which replaced the sodium chloride (0.30%), was present in the diets of the control groups. It was found that the clinical symptoms of leg weakness could be improved significantly in the experimental group which received bicarbonate. No positive effects on osteochondrosis, however, could be shown. The treated animals even tended to have more severe osteochondral lesions. Reasons for the negative tendency are discussed. Daily weight gain and food conversion were not influenced by the experimental bicarbonate diet excluding a chloride deficiency. Differences in carcass grading were not significant, although barrows fed the NaHCO3-containing diet tended to score better, while the carcass quality of the experimental gilts was slightly less in comparison to the control animals.

Animal Feed↗
PubMed2000

The effect of sodium bicarbonate on propranolol-induced cardiovascular toxicity in a canine model.

STUDY OBJECTIVE: To evaluate the potential utility of sodium bicarbonate in an established model of acute propranolol toxicity. METHODS: Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of 1.5 mEq/kg of sodium bicarbonate solution (1 mEq/mL) followed by an infusion of 1.5 mEq/kg over the next 26 minutes (n = 6) or an equivalent timing and volume of 5% dextrose solution (n = 6) was administered in each dog. Targeted cardiovascular parameters included heart rate, mean arterial pressure, left ventricular dP/dtmax, and QRS interval. RESULTS: Propranolol infusion significantly depressed heart rate (p < 0.0001), mean arterial pressure (p < 0.0001), dP/dtmax (p < 0.0001) and prolonged the QRS interval (p < 0.0001). Sodium bicarbonate failed to significantly improve these targeted parameters when compared to control animals. CONCLUSION: In this canine model of propranolol toxicity, intravenous sodium bicarbonate appears to be an ineffective single therapy. Furthermore, these results may suggest a different mechanism of sodium channel blockade for propanolol than that of type IA antiarrhythmic agents.

Animals↗
PubMed2005

Bicarbonate and bovine serum albumin reversibly 'switch' capacitation-induced events in human spermatozoa.

We have investigated the reversibility of biochemical and physiological changes that occur upon suspension of ejaculated human spermatozoa during in vitro capacitation. Cells were swum up in a simple HEPES-based saline [lacking bicarbonate and bovine serum albumin (BSA)], then resuspended either in supplemented Earle's balanced salt solution (sEBSS) (25 mM bicarbonate) with 0.3% BSA (for in vitro capacitation) or in medium-lacking bicarbonate and/or BSA. Progesterone-induced acrosome reaction (AR) developed during in vitro capacitation (6 h). A progesterone-induced [Ca2+]i signal was detectable in cells maintained in the simple HEPES-based saline, but upon transfer to sEBSS, the response increased three- to four-fold, saturating within <30 min. Serine/threonine phosphorylation saturated within minutes of resuspension, but tyrosine phosphorylation developed over 3 h. Return of cells to non-capacitating conditions caused reversal of all capacitation-dependent changes. The [Ca2+]i signal reverted to its 'uncapacitated' size within <30 min. Protein phosphorylation reversed gradually and could be reinduced (kinetics resembling the first response) upon resuspension in sEBSS. The ability of cells to undergo progesterone-induced AR fell to levels similar to those in uncapacitated cells within 1 h of resuspension in medium not supporting capacitation. Loss of protein phosphorylation occurred only in the absence of both bicarbonate and BSA, but effects on [Ca2+]i signalling and AR could be seen after removal of only one of these factors. We conclude that key events in the capacitation of human spermatozoa are both reversible and repeatable.

Acrosome Reaction↗
PubMed1989

Effects of bicarbonate therapy on tissue oxygenation during resuscitation of hemorrhagic shock.

We investigated the effects of clinically appropriate doses of NaHCO3 on tissue oxygenation when hemorrhagic shock was corrected with hydroxyethyl starch (hetastarch) in 12 piglets. Six animals received colloid only while six received colloid and bicarbonate. Both groups recovered rapidly hemodynamically, but conjunctival, subcutaneous, and liver tissue PO2 values returned to baseline more slowly after bicarbonate administration. In the NaHCO3 group, pulmonary artery wedge pressure and arterial bicarbonate concentration were higher during early resuscitation, and arterial plasma lactate remained higher than in the control group at the end of the follow-up period. The delayed increase in tissue PO2 values after bicarbonate infusion may be explained, at least partly, by decreased arterial blood oxygenation and a shift of the oxyhemoglobin curve to the left. NaHCO3 adjunct has no added beneficial effect on hemodynamics and may be harmful to tissue oxygenation in hemorrhagic shock resuscitated with hetastarch.

Animals↗
PubMedDate not supplied

The sodium bicarbonate controversy.

Sodium bicarbonate has been deleted from the advanced cardiac life support protocol. Sodium bicarbonate is no longer endorsed as the method of choice for the management of metabolic acidosis in the early rounds of cardiopulmonary resuscitation. This paper discusses mechanisms of acidosis occurring during cardiopulmonary arrest, past and present protocols for sodium bicarbonate administration and rationale for the deletion of sodium bicarbonate from resuscitation protocols.

Acidosis, Lactic↗
PubMed1983

Increment in dialysate sodium with sodium chloride or bicarbonate addition.

Hemodialysis was performed in 12 patients for 2 weeks each utilizing acetate dialysate containing 134 mEq/L sodium and dialysate containing 143 mEq/L sodium, achieved by the addition of sodium chloride or sodium bicarbonate to the acetate dialysate. Intradialytic morbidity was lower, dialysis hypoxemia less marked, and predialysis blood pH higher with the bicarbonate-than with the chloride-added dialysate. The long-term use of sodium bicarbonate-added dialysate in three patients was safe. Dialysate pH adjustment was not required. These findings suggest that the addition of sodium bicarbonate (50-75 g) to acetate dialysate may be preferred to sodium chloride for increasing dialysate sodium in selected patients.

Aged↗
PubMed1987

Sodium bicarbonate reduces viability and alters aflatoxin distribution of Aspergillus parasiticus in Czapek's agar.

The potential of sodium bicarbonate to inhibit growth of and aflatoxin synthesis by Aspergillus parasiticus was examined in Czapek's agar (CA), a medium in which fluorescence under UV light indicates aflatoxin production. Incorporation of sodium bicarbonate (SB) into CA at 0.011, 0.022, and 0.033 mol% reduced cell viability 63-, 10(3)-, and greater than 10(7)-fold, respectively. Colonies resulting from surviving cells did not fluoresce under UV light, but thin-layer chromatography analysis of culture extracts detected aflatoxins. Potassium bicarbonate (KB) at 0.011 and 0.022 mol% produced inhibitory effects similar to those of SB, but NaCl and silica had no effect. After 7 days, control cultures had the normal aflatoxin distribution (B1 greater than G1 greater than B2 greater than G2), but this distribution shifted to B2 greater than B1 approximately equal to G2 greater than G1 during prolonged incubation. Cultures supplemented with SB and KB contained mostly aflatoxins B1 and G1 after 28 days. Both SB and KB raised the pH of CA to 7.5 to 8.5 at the time of growth. Culture growth on CA adjusted to pH 7.5 to 8.5 with NaOH was not inhibited but exhibited reduced fluorescence and elevated levels of aflatoxins B1 and G1. Thus, while bicarbonate inhibition of growth could not be attributed to pH elevation, the lack of culture fluorescence on CA-SB and CA-KB and the altered aflatoxin distribution were caused by the ability of SB and KB to elevate pH.

Aflatoxins↗
PubMed1964

EFFECTS OF BICARBONATE ON GROWTH OF PASTEURELLA PESTIS. I. DIFFERENTIAL RESPONSE OF VIRULENT AND AVIRULENT CELLS.

Surgalla, M. J. (Fort Detrick, Frederick, Md.), A. W. Andrews, and C. L. Baugh. Effects of bicarbonate on growth of Pasteurella pestis. I. Differential response of virulent and avirulent cells. J. Bacteriol. 88:269-272. 1964.-Virulent Pasteurella pestis and the avirulent mutants always present in a virulent inoculum have been demonstrated to give growth responses in opposite directions upon addition of bicarbonate to broth cultures under certain conditions. The effect of supplemental bicarbonate on initiation of growth from a virulent inoculum was found to be either stimulation of both virulent and avirulent cells at low levels of added bicarbonate, depression of both virulent and avirulent cells at higher initial concentrations, or depression of avirulent mutants with simultaneous stimulation of virulent cells at a narrow range of intermediate levels.

Animals↗