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PubMed1987

The renin-angiotensin-aldosterone system during haemodialysis with acetate or bicarbonate at different dialysate sodium concentrations.

The hormones of the renin angiotensin aldosterone system were measured during regular haemodialysis with acetate or bicarbonate at dialysate sodium concentrations of 135, 140, 145, and 150 mmol/l. Plasma renin activity and aldosterone concentration were higher during acetate haemodialysis than during bicarbonate haemodialysis. At lower dialysate sodium concentrations, plasma renin activity (acetate dialysis and bicarbonate dialysis) and aldosterone concentration (only acetate dialysis) were higher than they were at higher dialysate sodium concentrations. Plasma renin activity increased during acetate dialysis, but did not change during bicarbonate dialysis. Aldosterone and potassium concentrations were positively correlated. Aldosterone decreased during haemodialysis (increase to predialysis values at the end of haemodialysis (4 h) at lower dialysate sodium concentrations). It is concluded that the renin angiotensin aldosterone system is activated more during acetate dialysis than during bicarbonate dialysis. Aldosterone concentrations seem to be related more closely to serum potassium than to renin-angiotensin-aldosterone system and to serum sodium intradialytically.

Acetates↗
PubMed1988

[Bicarbonate hemodialysis in the therapy of chronic kidney failure].

A method of random sampling was applied to 10 CRI patients to analyze the results of 24 hemodialyses with acetate solution for dialysis (35 mmol/l) and 34 hemodialyses with bicarbonate solution for dialysis (35 mmol/l). Significant reduction of complications like headache, nausea, vomiting, tachycardia, dyspnea, extrasystole was observed in bicarbonate dialysis. The concentration of mean molecular uremic toxins was decreased from 5.75 +/- 0.84 mmol/l in acetate dialysis up to 2.63 +/- 0.21 mmol/l in bicarbonate dialysis. The content of intracellular potassium returned to normal. The concentration of serum cholesterol was decreased from 5.6 +/- 0.4 up to 4.8 +/- 0.2 mmol/l. These data indicated a favorable effect of bicarbonate dialysis on intracellular metabolism. Preliminary data did not confirm the normalizing effect of bicarbonate dialysis on the development of uremic osteopathy.

Acetates↗
PubMed1977

Effect of graded amounts of acid instilled into the duodenum on pancreatic bicarbonate secretion and plasma secretin in duodenal ulcer patients and normal subjects.

Pancreatic bicarbonate secretion and plasma secretin were measured in response to graded amounts of hydrochloric acid (0.94, 1.88, 3.75, and 7.5 mEq per 5 min) instilled directly into the duodenum in duodenal ulcer patients and in normal subjects. These graded amounts of acid produced graded increases in pancreatic bicarbonate in both groups. Mean bicarbonate secretion was significantly greater in the duodenal ulcer patients than in the normal subjects basally and after the lowest dose of hydrochloric acid. Mean (+/- SE) peak 30-min bicarbonate output (in milliequivalents) after duodenal acidification was 3.0 +/- 1.0 in the duodenal ulcer patients and 2.1 +/- 0.6 in the normal subjects (P less than 0.5). A significant (P less than 0.05) increase in plasma secretin occurred after duodenal acidification, but the increase in the duodenal ulcer and normal subjects was not significantly different (P less than 0.2). These results indicate that pancreatic bicarbonate secretion and increase in plasma secretin in response to graded amounts of duodenal acid are at least as great in patients with duodenal ulcer as in normal subjects.

Adult↗
PubMed1988

[Personal preparation of bicarbonate solutions--cost comparison and quality control].

Haemodialysis with bicarbonate dialysate is well established in the treatment of chronic renal failure. The costs of bicarbonate haemodialysis are higher than acetate haemodialysis. Commercially available bicarbonate solutions are sold from AS 129.- to AS 189.- per 8 litre canister (December 1987). The self-prepared solution contains 650 g bicarbonate (for AS 8.-) in 8 litres of deionized water. In 10 patients on regular dialysis treatment haemodialysis were performed with both commercially available and self-prepared solutions for a 3 week period. Blood and dialysate samples were obtained before and 10 minutes, 1 h, 2 h, 3 h and 4 h after starting haemodialysis. Osmolality, Na+, K+, Cl-, pO2, pCO2 and pH were measured in the dialysate and in the serum, as well as serum lactate levels. There were no significant differences and the biochemical changes were similar with both preparations. In our centre with about 4000 bicarbonate dialyses yearly, AS 500,000.- to AS 700,000.- could be saved by self preparation of the dialysate.

Bicarbonates↗
PubMed1987

Increase in P50 with the use of bicarbonate hemodialysis.

We studied the effect of bicarbonate and acetate on oxygenation during dialysis in ten male chronic dialysis patients. The dialysis delivery system and dialysate constituents were identical except for the use of either bicarbonate or acetate. We found no hemodynamic differences between the two kinds of dialysis. Blood PO2 fell by a similar amount, but blood PCO2 was higher during bicarbonate dialysis. The blood pH became alkalotic by the second hour of bicarbonate dialysis and remained so throughout the dialysis, whereas blood pH became alkalotic only at the end of acetate dialysis. The P50 increased significantly only during bicarbonate dialysis, but 2.3 DPG concentration did not change. Red cell volume, assessed by the mean corpuscular hemoglobin concentration, was unchanged. Without changes in the red cell volume we cannot explain the observed changes in P50 in the absence of concomitant changes in 2.3 DPG concentration.

2,3-Diphosphoglycerate↗
PubMed1986

Correction of uremic acid-base imbalance in biofiltration: standardization of the amount of bicarbonate infused.

Beneficial effects of biofiltration on acid-base balance have been described, especially in patients showing poor tolerance to standard hemodialysis. This study was designed to standardize the amounts of bicarbonate to be infused for optimal control of the acid-base balance, without the adverse reactions of symptomatic metabolic alkalosis. In three adult patients (body weight greater than 55 kg) a 300 mEq. bicarbonate infusion achieved normal pre- and post-dialysis plasma levels of bicarbonate and normal pre- dialysis pH. Conversely, in three adolescent patients (body weight less than 40 kg) pre- dialysis plasma bicarbonate levels and pre- dialysis pH could not be adequately corrected in spite of increasingly high doses of bicarbonate infused up to a maximum of 240 mEq per treatment. Larger amounts brought on symptoms of metabolic alkalosis.

Acid-Base Imbalance↗
PubMed1979

Bicarbonate hemodialysis using a sorbent regenerative system.

In light of the concern about the use of acetate in dialyzate a simplified means of performing acetate-free hemodialysis has been developed using the sorbent regenerative system (RED). Fifteen sorbent bicarbonate hemodialyses free of acetate were performed on two patients for 4 or 6 hours. The initial dialyzate mixture contained 135 mEq/l NaHCO3 only. The infusate cations of K, Ca and Mg were in the form of chloride salts. A 30-minute titration of the sorbent cartridge with the bicarbonate dialyzate was necessary to release the excessive hydrogen ion from the cartridge which allowed the dialyzate bicarbonate to stabilize. The dialyzate Na fell during titration but rose during dialysis. The dialyzate Cl rose throughout titration and dialyses. The plasma bicarbonate rose significantly by the end of 4 and 6 hour dialyses. The blood pO2 and pCO2 did not change during dialysis and a significant rise in blood pH resulted. We conclude that bicarbonate dialysis is feasible and relatively easily accomplished in the sorbent system.

Bicarbonates↗
PubMed1983

[Long-term effects of acid-base equilibrium of bicarbonate dialysis].

The acid-base effects of long-term bicarbonate hemodialysis (BDH) were evaluated in five patients previously stabilized on acetate hemodialysis (AHD). Following 12 weeks on BHD, the patients were studied an additional 6 weeks on return to AHD. Hydrogen ion generation rate (calculated from urea generation rate), and pre- and post-dialysis pH, and blood gases were measured every 2 weeks. The results of the study show that, while pre-dialysis blood bicarbonate and pH did not change significantly during the stabilization period, during BHD, and following return to AHD, hydrogen ion generation rate increased substantially on the average during BHD (+6 mmol/24 h) and fell precipitously on return to AHD (-9 mmol/24 h). Pre- to post-dialysis changes in blood bicarbonate, and pH were significantly greater during BDH than during AHD. We conclude that the increase in hydrogen ion generation rate during BDH indicates that the patients increased their intake of fixed acid. Because of extreme increases observed intra-dialytically in blood bicarbonate and pH during BHD, the ability to vary bicarbonate delivery to the patient may have to be an integral part of equipment used in BDH.

Acid-Base Equilibrium↗
PubMed1984

Carbonic anhydrase independent bicarbonate reabsorption in rats with chronic papillary necrosis.

The present study was designed to indirectly localize the tubular sites of carbonic anhydrase independent bicarbonate reabsorption in the rat. Papillary necrosis was induced in rats by intravenous administration of bromoethyleneamine hydrobromide (BEA) 6 weeks prior to the study, in order to assess the role of deep nephrons in this process. Acetazolamide alone, acetazolamide plus amiloride, and acetazolamide, amiloride plus furosemide were infused into rats with intact papillae (groups I, III, V) and rats with BEA-induced papillary necrosis (groups II, IV, VI). Our results show that chronic papillary necrosis does not alter carbonic anhydrase independent bicarbonate reabsorption, since the fractional excretion of bicarbonate (FEHCO3) was not significantly higher when acetazolamide was infused into animals with BEA-induced papillary necrosis as compared to those rats with intact papillae (FEHCO3 group I vs. group II: NS). The addition of amiloride hydrochloride, a blocker of distal acidification at the administered doses, increased FEHCO3 significantly in both, animals with intact papillae and those with papillary necrosis, to a similar degree. The addition of furosemide to acetazolamide and amiloride further induced a significant increase in FEHCO3 only in the group of animals with papillary necrosis (FEHCO3 group V 43.0 +/- 2.9% vs. group VI 52.1 +/- 0.9%; p less than 0.05). It appears from our study that deeper nephrons and papillary structures are not indispensable for carbonic anhydrase independent bicarbonate reabsorption in the rat on a chronic basis. The cortical collecting duct appears to have a significant capacity to reabsorb bicarbonate independent of carbonic anhydrase which can be blocked by amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1981

Effects of [Na+], [Cl-], carbonic anhydrase, and intracellular pH on corneal endothelial bicarbonate transport.

Sodium removal from the solution bathing the isolated rabbit corneal endothelium caused a reduction in both unidirectional and net flux of bicarbonate, whereas chloride withdrawal from the solution had no effect on the net bicarbonate flux but increased the unidirectional fluxes. These data correlate with previously published data on the effects of similar solution manipulations on both fluid movement and potential difference across the endothelium and strongly implicate bicarbonate as the primary ion involved in the maintenance of corneal hydration. Carbonic anhydrase (1 mg/ml) added to the solution bathing both sides of the endothelium markedly increased unidirectional and net bicarbonate fluxes, possibly by maintaining a high bicarbonate/CO2 concentration close to the membrane and thereby eliminating chemical gradients in the unstirred layer adjacent to the membrane. Determinations of intracellular pH with the 5,5-dimethyl-2,4-oxazolidine-dione method indicate that at more acid ambient conditions there is a lesser gradient between cell and bathing medium for H+; similar ambient conditions in other experiments resulted in larger unidirectional bicarbonate fluxes than at neutral pH. The data are suggestive of a nonvectorial H+-HCO3- exchange occurring across the endothelial cellular membranes.

Animals↗
PubMed1981

Ethacrynic acid inhibits transcellular NaCl reabsorption in dog kidneys in doses of 1 to 10 mg.kg-1 and proximal bicarbonate-dependent reabsorption at higher doses.

In anesthetized dogs, sodium reabsorption in the kidney tubule was continuously reduced with increasing dosage of ethacrynic acid until 59% of the filtered load was excreted with 25 mg.kg-1 at constant glomerular filtration rate. With 50 mg.kg-1, glomerular filtration rate fell, but fractional sodium reabsorption was further reduced by 7%. In the dosage range of 1 to 10 mg.kg-1, ethacrynic acid inhibited chloride but not bicarbonate reabsorption, and the ratio between reductions in sodium reabsorption and oxygen consumption (delta Na/delta O2) averaged 25.5 +/- 5.2. With doses of 25 and 50 mg.kg-1, ethacrynic acid further reduced chloride reabsorption, reduced fractional bicarbonate reabsorption by 17% and almost halved phosphate reabsorption, whereas delta Na/delta O2 rose significantly to 65.3 +/- 12.2. Renal cortical carbonic anhydrase activity was normal and the inhibitory effect of acetazolamide, a carbonic anhydrase inhibitor, on bicarbonate reabsorption was unimpaired. We conclude that ethacrynic acid in doses up to 10 mg.kg-1 exclusively inhibits transcellular NaCl reabsorption, but in higher doses interferes with bicarbonate reabsorption and bicarbonate-dependent passive reabsorption of NaCl in the proximal tubules without inhibiting carbonic anhydrase activity.

Absorption↗
PubMed1981

[Exchange of chloride and bicarbonate at terminal ileum in rabbit: the process active character and physiological sense (author's transl)].

The process of chloride and bicarbonate exchange at the terminal ileum in rabbit and the way it is affected by the alkalinization or acidification of the caecum have been studied. Chloride absorption and bicarbonate secretion takes place at the terminal ileum in rabbit. Administration of DNP (5 X 10(-4) M) in the solution together with an i.v. injection of the same substance (0.11 mg/100 g weight) decreased chloride absorption and, quite markedly, bicarbonate secretion in the ileum. Introduction of an alkaline solution into the caecum reduces bicarbonate secretion in the ileum and simultaneously decreases chloride absorption. Introduction of an acid solution into the caecum produces an increase in ileal bicarbonate secretion, while it reduces chloride absorption.

2,4-Dinitrophenol↗
PubMed1981

Gastric mucus and bicarbonate secretion in relation to mucosal protection.

Gastric mucus, a viscous gel that coats the entire gastric mucosa, is produced by and secreted from the surface epithelial cells. Although 95% water by weight, gel mucus is a polymer of four equal-sized subunits joined by disulfide bridges. Carbohydrate side chains include N-acetylglucosamine, N-acetylgalactosamine, galactose, fucose, neuraminic acid, and sialic acid. At a concentration of about 20 mg/ml, the viscosity begins to rise, and a gel is formed. The thickness of the gel mucus layer is dynamic, and a function of release from surface epithelial cells and mechanical and proteolytic degradation within the lumen. An increase in luminal fluid glycoprotein output has been observed in response to splanchnic and vagal nerve stimulation, topical acetylcholine, prostaglandins, carbenoxolone, and parenteral secretin. Topical prostaglandins and carbenoxolone have been observed to increase mucus gel thickness. Gastric bicarbonate secretion is also thought to be a function of the surface epithelial cell. The magnitude of stimulated gastric bicarbonate secretion is 5 to 10% of maximal acid secretion for a given surface area of mucosa. Stimulants of gastric bicarbonate secretion are carbachol, Ca++, c-GMP, 16-16 dimethyl PGE2, and PGF2 alpha. Inhibitors of gastric bicarbonate secretion include atropine, metabolic inhibitors, acetazolamide, alpha-adrenergic agents, and inhibitors of prostaglandin synthesis. Taken together, these observations lend credence to the hypothesis that an unstirred layer of mucus, rich in bicarbonate, may offer significant protection against acid-peptic mucosal injury by neutralizing luminal acid and thereby providing the apical membrane of the surface epithelial cell with a near neutral pH milieu.

Animals↗
PubMed1980

Light-evoked disc shedding by rod photoreceptors in vitro: relationship to medium bicarbonate concentration.

Although studies on the control of photoperiod-related shedding by rod photoreceptors in frogs suggested that the mechanisms which initiate shedding are intrinsic features of the eye, attempts to observe light-evoked shedding in opened eye cups in balanced salt solutions have been unsuccessful. We have examined disc shedding in eye cups kept in a complex tissue culture medium. Eye cups were prepared in red light from dark-adapted animals or in white light from constant light-treated animals. Light-evoked shedding did not occur in the standard medium with -20 mM sodium bicarbonate, but a large light-evoked response was consistently seen when medium bicarbonate was raised to 030 mM. In high-bicarbonate medium, light-evoked shedding was comparable in magnitude, size distribution of phagosomes, and time course to similar responses observed in intact animals. Preliminary analysis of culture conditions which support shedding suggests that bicarbonate ion concentration is of critical importance. However, lack of light-evoked shedding in a high-bicarbonate Ringer solution suggests that some additional unidentified factor(s) in the complex medium is also necessary. The data indicate that both light- and dark-dependent processes involved in the control of photoperiod-related shedding are sustained in appropriate culture medium.

Animals↗
PubMed1995

Induced acute ruminal acidosis in goats treated with yeast (Saccharomyces cerevisiae) and bicarbonate.

Ruminal acidosis was induced in twenty-one 10-month-old West African Dwarf Goats by feeding a suspension of 80 g wheat flour per kg bodyweight (day 0) through a stomach tube. Ruminal and systemic acidosis was diagnosed on day 1 in all goats. Clinical signs included loss of rumination and appetite, trembling, and watery diarrhoea. The detection of acidic faeces during the first 24h was considered of diagnostic importance. Subgroups were treated orally on days 1, 2, and 3 either with 1 g of sodium bicarbonate per kg bodyweight, with 1 g of baking yeast per kg, or with a combination of these treatments at 0.5 g of each per kg. A fourth group served as untreated controls. Peroral bicarbonate neutralization was highly effective in the treatment of rumen acidosis, whereas the use of yeast was found ineffective. The combined treatment had a moderate effect probably due to the bicarbonate. Three fatal cases (60%) occurred in the untreated group compared with none in the bicarbonate group, and 2 in each of the remaining groups. This corresponded to 33% of the yeast treated group and 40% of the combined treated group. Details were given on post mortem examinations performed on all survivors on day 11. Lesions included subacute rumenitis and abomasal ulcers. No lesions were found in 3 of the bicarbonate treated goats and in 2 of the animals receiving combined treatment.

Acidosis↗
PubMed1994

[Some indices of peripheral blood oxidative metabolism during acetate and bicarbonate hemodialysis in patients with chronic uremia].

Whole blood superoxide anion generation, erythrocyte superoxide dismutase (SOD-1) and catalase activities and erythrocyte and plasma malonyldialdehyde concentrations were evaluated during cuprophane hemodialysis using bicarbonate and acetate dialysate. Superoxide anion generation by resting phagocytes was found to be significantly higher during bicarbonate hemodialysis, while its generation by opsonized zymosan--stimulated phagocytes did not differ between hemodialyses with both kinds of dialysates. Changes in the erythrocytes SOD-1 activities, found in the initial period of hemodialysis, were independent of the kind of dialysate, while erythrocyte catalase activity was higher during acetate hemodialysis in comparison with bicarbonate one. The kind of dialysate did not affect extent of erythrocyte membrane lipid peroxidation, while plasma lipid peroxidation was lower during acetate hemodialysis in comparison with bicarbonate one. In vitro studies with blood cells incubated with acetate or bicarbonate ions in concentrations, which are observed in vivo during hemodialysis, suggest that probably these ions do not directly affect superoxide anions generation, erythrocyte SOD-1 and catalase activities and erythrocyte membrane lipid peroxidation.

Acetates↗
PubMed1994

Mechanisms of acid-base homeostasis in acetate and bicarbonate dialysis, lactate hemofiltration and hemodiafiltration.

The different mechanisms of acidosis buffering were investigated in 15 RDT patients dialyzed in cross-over with four depurative techniques: acetate dialysis (AD), bicarbonate dialysis (BD), lactate hemofiltration (LHF) and hemodiafiltration (HDF) with acetate bath and lactate reinfusion fluid. Blood pH, bicarbonate, blood gases, intraerythrocytic pH - on red cell hemolisates - anion gap, L-lactate, pyruvate, adenosinmonophosphate (ADP) and 2-3 Diphosphoglycerate (2-3 DPG) levels were evaluated. During AD the intradialytic buffering is initially achieved by the CO2 fall and later by the acetate metabolism and an important bicarbonate shift from the intra to the extracellular space. A physiological compensation is obtained during BD with bicarbonate administration and a mild ventilatory response to the pCO2 increase. In LHF the massive lactate administration, with plasma levels of 7 mmol/l, strongly alters the Central Nervous System elettroneutrality inducing a hyperventilatory response with a purely pulmonary acidosis buffering. Furthermore the lactate/pyruvate ratio rose as high as 40:1 with ADP increase and cellular energy depletion. In HDF several different mechanisms are associated: the CO2 fixation, the acetate muscular metabolism, the intra-extracellular bicarbonate shift with the pulmonary response driven by lactate Central Nervous System penetration.

2,3-Diphosphoglycerate↗
PubMed1995

Bicarbonate therapy in the treatment of lactic acidosis: medicine or toxin?

The metabolic acidosis resulting from poor tissue perfusion is considered to have several significant hemodynamic effects. Correction of the acidosis with sodium bicarbonate seems to be a rational approach to this problem. However, the current medical literature shows little clinical benefit to this tactic. In fact, indiscriminate bicarbonate administration may, itself, have deleterious effects. Concurring with the absence of a consistent therapeutic advantage to the use of sodium bicarbonate in the treatment of lactic acidosis due to inadequate tissue perfusion, the American Heart Association removed the routine use of sodium bicarbonate from the treatment of cardiac arrest in the algorithms of the Advanced Cardiac Life Support course. Although the debate continues, a detailed review of the medical literature does not support the use of sodium bicarbonate in this setting.

Acidosis, Lactic↗