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At least 379 records · Page 21Linked to original sources
PubMed1989

Bicarbonate reabsorption by the kidney of the newborn rabbit.

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.

Animals↗
PubMed2005

Prediction of dilutional acidosis based on the revised classical dilution concept for bicarbonate.

Due to the controversy surrounding the term dilutional acidosis, the classical dilution concept for bicarbonate has been rigorously revised for the prediction of pH, actual bicarbonate concentration, and base excess. In the algorithms derived for buffer solutions, blood, and whole body (1-, 2-, and 3-fluid compartment), only bicarbonate is considered. On dilution at constant Pco(2), the final concentration of bicarbonate is the sum in terms of pH, due to the following processes: dilution, formation from chemical reaction with the nonbicarbonate buffers phosphate, hemoglobin, and plasma proteins, and transfer from erythrocytes and interstitial fluid to plasma. At constant Pco(2), the level of carbonic acid is held constant, whereas those of the buffer bases are reduced by dilution, resulting in acidosis. In mixed bicarbonate/phosphate buffer, the final concentration of HCO(3)(-) exceeds the diluted value due to additional buffering of H(2)CO(3) by HPO(4)(2-). For whole blood in vitro, pH, and actual bicarbonate concentration are predicted from dilution with 0.9% saline from initial Hb (100%) to infinite dilution (pure saline). The acidosis from dilution of plasma bicarbonate is mitigated by contributions from plasma proteins (<1 mmol/l) and from the erythrocytes ( approximately 5 mmol/l). Similarly, for whole body, the main contributions to combat primary dilutional acidosis in the range of hemodilution (relative Hb: 100-50%) are from the erythrocytes (1.2-2.2 mmol/l) and from the interstitial fluid (3.3-7.2 mmol/l). Perioperatively measured nonrespiratory acidosis is predictable if caused by hemodilution with fluids containing neither bicarbonate nor its precursors, irrespective of other electrolytes.

Acidosis↗
PubMed1990

Chronic haemodialysis with bicarbonate dialysate. Technical and clinical aspects.

Bicarbonate as a physiological buffer should be preferred in haemodialysis treatments. The use of bicarbonate dialysis, however, varies from 30 to 100% in the different industrialised countries. Except for the many advantages using bicarbonate dialysate, there are also clinical pitfalls in the use of the bicarbonate buffer substrate. Furthermore, technical problems can be expected in the use of varying dialysate bicarbonate concentrations, as in the concomitant use of acetate and bicarbonate dialysate in the same dialysis unit. This paper deals with the clinical and technical aspects of bicarbonate dialysis.

Acetates↗
PubMed1990

Duodenal disappearance rate of acid during inhibition of mucosal bicarbonate secretion.

In order to investigate the relation between duodenal mucosal and pancreaticobiliary bicarbonate secretion, we have studied the effect of inhibition of mucosal bicarbonate secretion by indomethacin on the disappearance rate of acid and the concomitant plasma secretin concentrations. 10 healthy subjects were studied twice, with and without indomethacin pretreatment. By means of a double-lumen tube the duodenum was perfused with increasing amounts of acid (0, 3.0, 6.0 and 9.5 mmol/h) and the disappearance rate of acid, pH of duodenal aspirate and plasma secretin were measured. In both experiments nearly all acid, even at the highest acid load, disappeared (pH greater than 6). Inhibition of the duodenal mucosal bicarbonate secretion did not decrease the acid-neutralizing capacity of the human duodenum. In fact, the disappearance rate of acid at the highest acid load was a little greater when mucosal bicarbonate secretion had been inhibited than when not (10.3 +/- 0.5 vs. 9.2 +/- 0.2 mmol/h). The pancreaticobiliary secretion of bicarbonate, as judged by plasma secretin concentrations, increased, however, earlier when mucosal bicarbonate secretion had been inhibited than when not (3.7 vs. 3.0 pmol/l at an acid load of 6.0 mmol/h). This indicates that bicarbonate from the duodenal mucosa normally plays a role in the in lumen neutralization of acid in the human duodenum.

Adult↗
PubMed1997

Tris-hydroxymethyl aminomethane and sodium bicarbonate to buffer metabolic acidosis in an isolated heart model.

Metabolic acidosis induces a decrease in the developed force of cardiac muscle by affecting every step of the excitation--contraction coupling pathway. Due to transient worsening in intracellular acidosis, the value of administering sodium bicarbonate therapeutically during acute acidosis has been questioned. An alternative therapeutic drug, Tris-hydroxymethyl aminomethane (THAM) has the advantage of diffusing into the intracellular space. This study was designed to evaluate the effects of metabolic acidosis on myocardial performance and to determine the effects of alkalinization with sodium bicarbonate, THAM, and their combination. Using a blood-perfused isolated heart preparation, left ventricular contractility and relaxation were measured at normal pH and during metabolic acidosis (pH = 7.0). Acidosis dramatically impaired myocardial contractility and relaxation. After buffering with sodium bicarbonate, although plasma bicarbonate concentration was normalized, pH remained below normal owing to an increased PaCO2. Contractility and relation were initially worsened, then slightly improved to return to control values. THAM uncompletely buffered acidosis but significantly improved contractility and relaxation. The combination of THAM with sodium bicarbonate perfectly buffered acidosis without modifying PaCO2 and significantly improved contractility. The combination of THAM with sodium bicarbonate is based on the ability of THAM to capture the CO2 produced by the sodium bicarbonate buffer. This combination achieves a perfect correction of metabolic acidosis and improves myocardial performance.

Acidosis↗
PubMed1974

Effects of glucose on bicarbonate reabsorption in the dog kidney.

The effects of glucose on renal bicarbonate reabsorption were investigated in the dog. The infusion of small amounts of glucose calculated to slightly exceed the renal threshold for glucose absorption increased bicarbonate reabsorption in bicarbonate loaded dogs. Galactose in similar doses also increased the reabsorption of filtered bicarbonate. This effect is not due to insulin secretion since insulin alone did not alter bicarbonate reabsorption and the infusion of glucose into alloxan-diabetic dogs given a steady infusion of insulin also enhanced bicarbonate reabsorption. It is more likely that the increased tubular reabsorption of glucose, secondary to an increased filtered load, resulted in the increase in bicarbonate reabsorption since phlorizin reversibly inhibits the effect of glucose.

Analysis of Variance↗
PubMed1986

Renal bicarbonate reabsorption in the rat. I. Effects of hypokalemia and carbonic anhydrase.

Free-flow micropuncture studies were carried out on superficial rat proximal and distal tubules to assess the participation of different nephron segments in bicarbonate transport. Particular emphasis was placed on the role of the distal tubule, and micro-calorimetric methods used to quantitate bicarbonate reabsorption. Experiments were carried out in control conditions, during dietary potassium withdrawal, and after acute intravenous infusions of carbonic anhydrase. We observed highly significant net bicarbonate reabsorption in normal acid-base conditions as evidenced by the maintenance of significant bicarbonate concentration gradients in the presence of vigorous fluid absorption. Distal bicarbonate reabsorption persisted in hypokalemic alkalosis and even steeper transepithelial concentration gradients of bicarbonate were maintained. Enhancement of net bicarbonate reabsorption followed the acute intravenous administration of carbonic anhydrase but was limited to the nephron segments between the late proximal and early distal tubule. The latter observation is consistent with a disequilibrium pH along the proximal straight tubule (S3 segment), the thick ascending limb of Henle, and/or the early distal tubule.

Absorption↗
PubMed1989

Lack of effect of carbonic anhydrase inhibition on direct measurements of endolymph bicarbonate.

In the past, sodium, potassium, and chloride have been measured in endolymph directly, but bicarbonate has been measured only indirectly. We sampled endolymph directly while monitoring endocochlear potentials in normal and methazolamide-treated guinea pigs. Bicarbonate was determined in samples by use of a method that depends on reduction of NADH to NAD linked to malate formation from oxaloacetate. In 11 normal animals, the bicarbonate in endolymph was 20.2 mM +/- 4,4 mM (mean +/- standard deviation); in six of these, plasma bicarbonate was 23.1 mM +/- 3.5 mM. Nine animals treated with methazolamide (carbonic anhydrase inhibitor) had an endolymph bicarbonate of 19.5 mM +/- 3.9 mM; plasma bicarbonate in five of these was 25 mM +/- 3.2 mM. Carbonic anhydrase inhibition did not significantly affect endolymphatic bicarbonate levels.

Animals↗
PubMed2001

Bicarbonate stimulated phospholipid scrambling induces cholesterol redistribution and enables cholesterol depletion in the sperm plasma membrane.

Mammalian sperm cells are activated prior to fertilization by high bicarbonate levels, which facilitate lipoprotein-mediated cholesterol efflux. The role of bicarbonate and cholesterol acceptors on the cholesterol organization in the sperm plasma membrane was tested. Bicarbonate induced an albumin-independent change in lipid architecture that was detectable by an increase in merocyanine staining (due to protein kinase A-mediated phospholipid scrambling). The response was limited to a subpopulation of viable sperm cells that were sorted from the non-responding subpopulation by flow cytometry. The responding cells had reduced cholesterol levels (30% reduction) compared with non-responding cells. The subpopulation differences were caused by variable efficiencies in epididymal maturation as judged by cell morphology. Membrane cholesterol organization was observed with filipin, which labeled the entire sperm surface of non-stimulated and non-responding cells, but labeled only the apical surface area of bicarbonate-responding cells. Addition of albumin caused cholesterol efflux, but only in bicarbonate-responding cells that exhibited virtually no filipin labeling in the sperm head area. Albumin had no effect on other lipid components, and no affinity for cholesterol in the absence of bicarbonate. Therefore, bicarbonate induces first a lateral redistribution in the low cholesterol containing spermatozoa, which in turn facilitates cholesterol extraction by albumin. A model is proposed in which phospholipid scrambling induces the formation of an apical membrane raft in the sperm head surface that enables albumin mediated efflux of cholesterol.

Acrosome Reaction↗
PubMed1990

Bicarbonate-dependent action of Bay K 8644 in the smooth muscle of the rat vas deferens.

Effects of Bay K 8644, partial depolarization with high potassium, and nifedipine on the dose-response curves of the rat vas deferens to norepinephrine, methacholine and KCI were investigated in HEPES-buffered physiological salt solution (PSS) with or without 20 mM sodium bicarbonate. In the bicarbonate-containing PSS, Bay K 8644 at 10(-6) M enhanced the maximal contractions in response to norepinephrine, methacholine and KCI by 31.4, 103.3 and 40.1%, respectively. In the bicarbonate-free PSS, where the maximal contractions induced by norepinephrine, methacholine and KCI were 77.5, 75.0 and 68.2% of those in the bicarbonate-containing PSS, respectively. Bay K 8644 did not enhance the maximal contractile response to any of the agonists, although the contractions induced by low concentrations of KCI were increased by Bay K 8644. Increasing the potassium concentration in the PSS from 6 to 20 mM enhanced the maximal contractions in response to norepinephrine and methacholine in the bicarbonate-containing PSS, whereas in the bicarbonate-free PSS, the treatment decreased the contractions. In the two PSSs, nifedipine similarly inhibited the contraction in response to either 10(-5) M norepinephrine or 68 mM KCI. These results suggest that bicarbonate ion modulates the function of the voltage-dependent calcium channel in the smooth muscle of the rat vas deferens.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Angiotensin stimulates bicarbonate transport and Na+/K+ ATPase in rat proximal straight tubules.

The effect of angiotensin on HCO3- absorption, fluid absorption, and Na+/K+ ATPase activity in isolated rat proximal straight tubules was investigated. During the control period, tubules absorbed fluid at 0.66 +/- 0.12 nL/mm.min and bicarbonate at 60.2 +/- 10.7 pmol/mm.min. After 10(-10) M angiotensin was added to the bath, tubules absorbed fluid at 0.93 +/- 0.19 nL/mm.min and bicarbonate at 77.4 +/- 15.2 pmol/mm.min, indicating stimulation of both parameters. Time controls showed no significant change in the rate of bicarbonate or fluid absorption. To determine whether this stimulation was due to an increase in the maximum rate of transport, tubules were perfused at greater than or equal to 20 nL/mm.min. During the control period, tubules absorbed bicarbonate at 82.5 +/- 13.0 pmol/mm.min. After 10(-10) M angiotensin was added to the bath, these same tubules absorbed bicarbonate at 75.9 +/- 11.9 pmol/mm.min. Thus, angiotensin did not alter the maximum rate of transport. Angiotensin also had no effect on bicarbonate permeability, which was 1.1 +/- 0.2 x 10(-4) cm/s before treatment and 1.3 +/- 0.3 x 10(-4) cm/s afterward. Finally, the effect of angiotensin on Na+/K+ ATPase activity was measured in paired experiments. Na+/K+ ATPase activity of control tubules was 36 +/- 6 pmol of ADP/mm.min; after angiotensin treatment, it was 47 +/- 6 pmol ADP/mm.min. From these data it was concluded that: (1) angiotensin stimulates bicarbonate absorption in the rat proximal straight tubule; (2) this stimulation is the result of a change in Km rather than of an increase in the maximum rate of transport or permeability; and (3) angiotensin directly stimulates Na+/K+ ATPase activity in the proximal nephron.

Absorption↗
PubMed1985

Continuous computerized determination of gastric bicarbonate secretion in man.

A method for continuous determination of gastric bicarbonate secretion in man has been developed. A computer-based system calculated the total bicarbonate secretion every 30 sec throughout the experiment on the basis of the continuously recorded pH and Pco2 measurements. A high gastric perfusion rate facilitated the identification of duodenogastric reflux, which was observed as rather short-lived spikes on the curves. The contribution of alkaline saliva to the measured gastric bicarbonate secretion was minimized by continuous salivary suction and was corrected for after determining amylase in the gastric aspirate. Validation of the measuring system, by introducing bicarbonate in the range of 50-400 mumol into the stomach, demonstrated a correlation value of 0.91 (p less than 0.001) between added and recovered bicarbonate. Basal gastric bicarbonate output in seven healthy subjects was 379 +/- 105 mumol/h (mean +/- SEM). Intragastric instillation of 16,16-dimethyl prostaglandin E2 in five subjects resulted in a fourfold increase in gastric bicarbonate output.

Bicarbonates↗
PubMed1987

Effect of fundic distension on gastric bicarbonate secretion in man.

Human gastric mucosa secretes small amounts of bicarbonate into the mucus layer to maintain the pH at the cell surface as close to neutrality as possible. We have measured gastric bicarbonate secretion continuously with a computer-based system, using recordings of pH and PCO2. The formula of Henderson and Hasselbalch was used in the calculations. Graded fundic distension of the stomach with a balloon in six healthy subjects increased the gastric bicarbonate output by 46% (p less than 0.05), 28% (NS), and 84% (p less than 0.05) during 1 h of distension to 150 ml, 300 ml, and 600 ml, respectively. Continuous fundic distension during 2 1/2 h with a volume of 300 ml elicited a response that peaked after 45 min and vanished after 90 min. The rather short duration of gastric bicarbonate secretion response to fundic distension may be due to a fading caused by a volume adaptation or, alternatively, to an activation of inhibitory mechanisms. Seven duodenal ulcer patients who had undergone proximal gastric vagotomy showed virtually the same gastric bicarbonate secretion response to graded fundic distension. The anticholinergic drug benzilonium bromide totally inhibited the gastric bicarbonate response to 30 min of fundic distension to 150 ml, whereas indomethacin did not significantly affect the response to distension. These studies indicate that the gastric bicarbonate response to fundic distension is mainly mediated by short intramural neural cholinergic pathways and is independent of mucosal production of prostaglandins.

Adult↗
PubMed1993

Motility-related cyclic fluctuations of interdigestive gastric acid and bicarbonate secretion in man. A source of substantial variability in gastric secretion studies.

The relationship between interdigestive gastric motility and secretion was studied in eight healthy volunteers. Acid and bicarbonate output rates were measured with a high time resolution, using a perfusion system based on continuous registration of pH and PCO2 of gastric effluent. Antral pressure was measured by manometry. The total duration of the interdigestive motility cycle (time between two phase-III complexes) was 96 +/- 12 min (mean +/- SE). In late migrating motor complex phase II, acid output, bicarbonate output, and bile reflux increased significantly. Acid secretion reached a peak in association with motor phase III. The gastric lumen was then rapidly alkalinized; this phenomenon was due to a simultaneous decrease in acid secretion and a short-lasting (15 +/- 2 min, mean +/- SE) phasic increase in bicarbonate output, which was not associated with bile reflux (bilirubin). After these phase-III-related events both acid and bicarbonate output rates reached a relatively stable level during phase I and early phase II. This period of stability constituted 47 +/- 3% (acid) and 41 +/- 6% (bicarbonate, means +/- SE), respectively, of the cycle. The peak to base line output ratio was 6.6 +/- 1.2 (p < 0.001) for acid and 2.8 +/- 0.3 (p < 0.001) for bicarbonate (means +/- SE). The results show a marked variability in acid and bicarbonate output rates during the interdigestive motility cycle. The magnitude of this variability has previously been underestimated owing to poor time resolution of the secretion measurements. If not taken into account, these 'spontaneous' secretory variations may constitute a considerable source of error in gastric secretion studies.

Adult↗
PubMed1995

The presence of bicarbonate in oral rehydration solution does not influence fluid absorption in cholera.

BACKGROUND: On the basis of human perfusion studies it has been speculated that bicarbonate ions in oral rehydration salt solutions (ORS) to treat diarrhoea are more efficiently absorbed from the small bowel. We evaluated the role of bicarbonate in ORS by using a reduced purging rate in cholera as a proxy indicator for absorption efficiency in cholera-like severe diarrhoea. METHODS: In a double-blind randomized trial 60 patients received standard ORS containing bicarbonate or an identical solution except that sodium bicarbonate was replaced by an equimolar amount of sodium chloride (sodium, 90 mmol/l; potassium, 20 mmol/l; chloride, 80 mmol/l; bicarbonate, 30 mmol/l; glucose, 111 mmol/l; and osmolality, 331 mmol/l) after initial intravenous rehydration to correct initial dehydration and shock and until diarrhoea ceased. RESULTS: Five patients receiving standard ORS and eight receiving bicarbonate-free ORS required unscheduled intravenous therapy for recurrence of severe dehydration in spite of receiving ORS solution. ORS intake and purging rate, in ml/kg body weight/day, both including and excluding stool output during unscheduled intravenous therapy are closely similar in the two treatment groups. CONCLUSION: The results indicate that bicarbonate-containing ORS solution does not have any clinically significant effect on the absorption efficiency of ORS, either beneficial or adverse, and its use is relevant only for correction of metabolic acidosis of diarrhoeal dehydration.

Administration, Oral↗
PubMed1995

Indomethacin decreases gastroduodenal mucosal bicarbonate secretion in humans.

BACKGROUND: Cyclooxygenase inhibitors reduce mucosal bicarbonate secretion in the duodenum, but the evidence for their effect on bicarbonate secretion in the stomach remains controversial. We have, therefore, studied how indomethacin influences gastroduodenal bicarbonate secretion and luminal release of prostaglandin (PG) E2 by means of a method that enables simultaneous measurements in the stomach and the duodenum. METHODS: Gastric and duodenal perfusions were performed twice in random order during control conditions or after pretreatment with indomethacin (100 mg intravenously) in eight healthy volunteers. Bicarbonate and PGE2 were measured in the gastroduodenal effluents by back-titration and radioimmunoassay, respectively. RESULTS: Vagal stimulation and duodenal luminal acidification (0.1 M HCl; 20 ml; 5 min) increased gastroduodenal bicarbonate secretion (p < 0.05). Indomethacin markedly inhibited both basal and stimulated gastric and duodenal mucosal bicarbonate secretion, and this reduction was similar to the degree of cyclooxygenase inhibition estimated by the luminal release of PGE2 (p < 0.05). CONCLUSION: These results unequivocally demonstrate that endogenous PG modulates basal and stimulated bicarbonate secretion, both in the stomach and in the duodenum.

Adult↗
PubMed1996

Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects.

BACKGROUND: Duodenal ulcer (DU) patients have impaired proximal duodenal mucosal bicarbonate secretion at rest and in response to luminal acid with higher acid-stimulated mucosal release of prostaglandin (PG) E2 than healthy subjects. Our purpose was to determine whether this abnormality was present also in the stomach of DU patients. METHODS: Simultaneous determinations of gastric and duodenal bicarbonate secretion and luminal release of PGE2 were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positive). RESULTS: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE2 were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mumol/h; mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mumol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mumol/h and 543 +/- 99 versus 778 +/- 69 mumol/h) in duodenal bicarbonate secretion were lower (p < 0.05). In addition, inactive DU patients had higher basal (148 +/- 32 versus 53 +/- 5 ng/h) and stimulated (291 +/- 84 versus 131 +/- 25 ng/h) gastric release of PGE2, but only the basal release of PGE2 into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). CONCLUSION: Increased mucosal production of PGE2 may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. The defective duodenal secretion of bicarbonate observed in these patients may be a consequence of previous ulceration rather than the mere presence of H. pylori infection.

Adult↗
PubMed1980

Effect of dietary sodium bicarbonate and magnesium oxide on production and physiology in early lactation.

Twenty cows were in an experiment to measure effects of dietary buffers, sodium bicarbonate and magnesium oxide, on ration adjustment and incidence of metabolic problems in the first 8 wk postpartum. Cows were fed 2.7 kg grain per day and alfalfa ad libitum prepartum and switched immediately to a complete ration of 40% corn silage and 60% concentrate (dry matter) postpartum. Treatments included 1.5% sodium bicarbonate and .8% magnesium oxide (total ration dry matter) fed in a 2 x 2 factorial arrangement. Cows receiving bicarbonate peaked 2 to 3 wk earlier in intake and averaged 2.1 kg per day greater intake than those fed the control diet. Actual milk production was increased by sodium bicarbonate with greatest differences for cows receiving both buffers averaging 3.8 kg per day more milk than control cows. Increases over co ntrols were 2.6 and 5.6 kg fat-corrected milk per day for cows receiving sodium bicarbonate alone or in combination with magnesium oxide, respectively. Sodium bicarbonate increased acetate to propionate molar ratios in rumen samples taken at 1 and 2 wk postpartum whereas neither buffer had any effect on rumen pH. Blood hematocrit and urine pH were not affected by treament. Magnesium oxide increased fecal pH .8 units and slightly decreased fecal starch, but sodium bicarbonate had no effect.

Animals↗