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PubMedDate not supplied

Bicarbonate versus lactate buffer in peritoneal dialysis solutions: the beneficial effect on RBC metabolism.

OBJECTIVE: Using the erythrocyte as a model for other kinds of cells not directly exposed to peritoneal dialysis (PD) solutions, we investigated the tolerance of the cell metabolism to lactate and bicarbonate buffers. DESIGN: We studied, in vivo (in two groups of 5 PD patients each) and in vitro, the Embden-Meyerhof pathway (EMP) because it represents a potential target for the unphysiological effects of lactate or bicarbonate buffers. The EMP is the main glucose-utilizing route in the red blood cell (RBC), producing energy and reducing power. METHODS: The enzymatic activities of the key steps in the glycolytic pathway and the energy charge (EC), determined by the levels of phosphorylated adenine nucleotides, were investigated spectrophotometrically and by high performance liquid chromatography (HPLC) in two groups of patients undergoing lactate (L-group) and bicarbonate (B-group) PD, respectively. The in vitro effects of both bicarbonate and lactate buffers on some EMP enzyme activities and energy production were determined. Cellular pH (pHi) was also investigated. RESULTS: The B-group showed an EC value near the control levels, while in the L-group a significantly lower EC value was observed (t-test: p < 0.05 vs both B-group and controls). The key enzymes in the EMP, and in particular hexokinase, were higher in the L-versus B-group (p < 0.03 for the comparison of the Hk mean values). As demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, the bound form of glyceraldehyde-3-phosphate dehydrogenase (G-3-PD), an inactive form of this EMP enzyme, was significantly higher in the L-group with respect to the B-group (p < 0.004). In the in vitro experiments, high lactate concentrations acutely inhibited the key enzymatic steps of glycolysis, producing a significant decrease in glucose consumption and adenosine triphosphate production. These effects were not observed when bicarbonate was used in the incubations. Both in vivo and in vitro lactate, but not bicarbonate, induce a significant drop in pHi (p < 0.05). Decreased levels of pHi like those observed in the lactate-incubated RBC were demonstrated to be able to inhibit G-3-PD activity (25 +/- 2%) here used as an indicator of the actual decrease in pH. CONCLUSION: This study provides evidence for a damaging action of lactate with respect to bicarbonate buffer on the RBC metabolism. This condition was demonstrated observing a cell energy depletion, which coincides in vitro with an acute EMP impairment; the lactate accumulation together with the consequent lowering of pHi seem to be responsible for this effect, which was not observed when bicarbonate was used instead of lactate.

Adenine Nucleotides↗
PubMed1980

A proposed mechanism for the stimulatory effect of bicarbonate ions on ATP synthesis in isolated chloroplasts.

The effect of bicarbonate ions on induction of Mg(2+)-ATPase activity, on the N-ethylmaleimide inhibition of phosphorylation and on energy-dependent adenine nucleotide exchange has been examined with pea seedling chloroplasts. Incubation of chloroplasts with N-ethylmaleimide in the presence of 15 millimolar bicarbonate in the light results in enhanced inhibition of ATP synthesis when the preillumination pH is maintained between 7.0 and 7.5. Bicarbonate also enhances Mg(2+)-ATPase activity when it is included in the light-triggering stage at pH 7.0. The conditions (medium pH, bicarbonate concentration, etc.) for demonstrating the bicarbonate-induced enhancement of the N-ethylmaleimide inhibition and ATPase activity are similar to those required for the direct effect of bicarbonate on phosphorylation. Bicarbonate, under the same conditions, does not affect adenine nucleotide exchange (binding or release). It is concluded that the stimulatory effect of bicarbonate on ATP synthesis may be related to its ability to alter directly the conformation of the chloroplast coupling factor under conditions (suboptimal pH) where the enzyme shows minimal activity.

Journal Article↗
PubMed1989

A comparison of sodium bicarbonate and sodium lactate infusion in the induction of panic attacks.

Infusion of sodium lactate has been shown by a number of investigators to induce panic in patients with panic disorder, but the pathophysiology underlying this phenomenon is unknown. One theory to explain lactate's anxiety-producing effects involves its ability to induce alkalosis because of metabolic conversion to bicarbonate. To test this hypothesis, we administered both sodium lactate and sodium bicarbonate infusions in counterbalanced order to patients with panic disorder. Thirteen of 22 subjects panicked in response to lactate and nine of 20 subjects panicked in response to bicarbonate. Although the rate of panic between the two infusion responses was not significantly different, several aspects of response to the two infusions indicated that lactate may be a more potent producer of anxiety than bicarbonate. An unexpected finding was that bicarbonate panickers had a reduction in arterial carbon dioxide pressure during the infusion, while bicarbonate nonpanickers had an increase in arterial carbon dioxide pressure during the infusion. Induction of hyperventilation and subsequent hypocapnia appears to be a common denominator between lactate- and bicarbonate-induced panic.

Adult↗
PubMed1990

Bicarbonate dependence of cAMP accumulation induced by phorbol esters in hamster spermatozoa.

Phorbol esters stimulate cyclic adenosine 3',5'-monophosphate (cAMP) accumulation in hamster spermatozoa under conditions for in vitro capacitation. The 20-50-fold elevation of cAMP levels induced by 1 microM phorbol 12-myristate 13-acetate (PMA) in spermatozoa depends on the presence of sodium bicarbonate in the medium (ED50: 15 mM) and it is independent of extracellular pH. Sodium bicarbonate stimulates adenylate cyclase activity in membrane preparations by 4-fold (ED50: 40 mM). After solubilization, the bicarbonate-sensitive moiety elutes as a single peak of 55 kDa in a gel filtration column. Blockers of bicarbonate chloride antiporters diisothiocyanate stilbene 2,2'-disulfonic acid (DIDS) or acetamido 4'-isothiocyanate stilbene 2,2'-disulfonic acid (SITS) inhibit the bicarbonate dependent PMA effect on cAMP in living spermatozoa (ED50: 100 microM). Maximal (85%) inhibition in cAMP accumulation is observed at 1 mM. Motility is inhibited only at high concentrations of the blockers. Pretreatment of living cells with 1 mM DIDS does not affect membrane adenylate cyclase activity which remains responsive to bicarbonate. These results suggest that controlled transport of bicarbonate through the sperm plasma membrane could be associated to the regulation of cAMP synthesis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Are inter-center differences in EMS-management and sodium-bicarbonate administration important for the outcome of CPR? The Cerebral Resuscitation Study Group.

The hospital of Brugge relies on selection of the emergency calls and sends a Mobile Intensive Care Unit (MICU) whenever cardiac arrest (CA) is suspected. The University Hospital of Leuven does no selection of calls and responds to every emergency call by sending an ambulance with an advanced life support (ALS) trained nurse. The MICU is called when the ambulance crew recognizes the emergency to be a CA. The Leuven system is a so-called tiered system. Although MICU-response times are significantly longer in Leuven than in Brugge, no difference is found as to the success of CPCR. The immediate response to all emergency calls by specialized E.D. nurses (paramedic) capable of ALS, seems to make up for the difference in MICU-response times. The University Hospital of Jette has a higher success-rate for CPCR for in-hospital CA, than the University Hospitals of Leuven. Due to size and lay-out differences, the MICU-response times are shorter in Jette than in Leuven. Basic life support (BLS) provided by doctors and nurses present at the scene, does not seem to be able to compensate for longer MICU-arrival times. The introduction of semi-automatic or automatic defibrillators, to be used by the BLS trained medical and nursing personnel, might be able to make up for the longer MICU-intervention times. Inter-center differences were witnessed as far as the amount of sodium-bicarbonate infused during CPR. Within each group of total duration of CPR an inverse correlation exists between the amount of bicarbonate infused and the success rate of CPCR. Partial correlation between the bicarbonate infused and the survival with regaining of consciousness at 14 days post-CPR, with constant CPR-time, is statistically significant. This indicates that long-term CPCR success is inversely correlated with increasing amounts of sodium-bicarbonate infused. Short duration of CPR and low adrenaline dosage correlate with immediate and long-term success of CPR. On the contrary, low versus high bicarbonate dosage has hardly any influence on immediate success (restoration of spontaneous circulatory activity) but low bicarbonate dosage favours long-term success (survival accompanied by recuperation of brain function). Our data support a negative effect on long-term survival with recuperation of consciousness from infusion of more than 1 mEq/kg body weight of sodium-bicarbonate during CPR. No final conclusions can be drawn so far as to the mechanisms of this negative effect at the level of the brain.

Ambulances↗
PubMed1993

The effect of sodium bicarbonate administration on the vasopressor effect of high-dose epinephrine during cardiopulmonary resuscitation in swine.

Sodium bicarbonate is administered during cardiopulmonary resuscitation (CPR) for the treatment of systemic acidemia. However, the effect of administering standard-dose sodium bicarbonate on the vasopressor effect of epinephrine is unknown. This study compared the effects of sodium bicarbonate or normal saline on the vasopressor effect of epinephrine in 18 pigs. After 10 minutes of unassisted ventricular fibrillation, CPR was started using a pneumatic chest compression device. Two minutes after the start of CPR, sodium bicarbonate (1 mEq/kg) or normal saline (1 mL/kg) was administered into the right ventricule followed 1 minute later by epinephrine (0.2 mg/kg). Defibrillation was attempted at 8 minutes of CPR (18 minutes of ventricular fibrillation). Results demonstrated no significant differences in aortic systolic, aortic diastolic, or coronary perfusion pressure (CPP) between the two groups (1 minute after epinephrine, CPP was 22.6 +/- 13.3 mm Hg versus 21.1 +/- 20.7 mm Hg for the sodium bicarbonate and normal saline groups, respectively). However, when the data were stratified according to pH < 7.4 and pH > 7.4, the peak change in CPP was 12.7 +/- 21 mm Hg when pH < 7.4 and was 5.2 +/- 7.4 when pH > 7.4 (P = .33). Resuscitation was also similar between the two groups (two of nine for sodium bicarbonate and one of nine for normal saline). In conclusion, the standard recommended dose of sodium bicarbonate did not alter the vasopressor effect of epinephrine or resuscitation compared with normal saline in this closed chest model of ventricular fibrillation and CPR.

Acidosis↗
PubMed1965

REVERSIBLE EFFECT OF BICARBONATE ON THE INHIBITION OF MYCOBACTERIAL AND YEAST TRANSGLUCOSYLASES BY MYCORIBNIN.

Lornitzo, Frank A. (Veterans Administration Hospital, Madison, Wis.), and Dexter S. Goldman. Reversible effect of bicarbonate on the inhibition of mycobacterial and yeast transglucosylases by mycoribnin. J. Bacteriol. 89:1086-1091. 1965.-The transglucosylase which catalyzes the formation of trehalose-6-phosphate from uridine diphosphate (UDP)-glucose and glucose-6-phosphate was purified from cell-free extracts of Mycobacterium tuberculosis H37Ra. During the purification procedure, the transglucosylase loses its sensitivity to mycoribnin, an inhibitor also found in these extracts. Sensitivity of the transglucosylase to mycoribnin is regained when the bicarbonate concentration of either enzyme or mycoribnin preparations is reduced to about 0.01 mm; sensitivity to mycoribnin is lost when low concentrations (< 1 mm) of bicarbonate are present in the reaction mixture. Transglucosylase preparations retain their bicarbonate-induced insensitivity to mycoribnin after dilution to a bicarbonate concentration which is ineffective for the initial conversion to insensitivity. The transglucosylases of brewer's yeast and of physiologically young (9-day) H37Ra cells, previously reported as insensitive to mycoribnin, have been partially purified. If bicarbonate is excluded from these preparations, the transglucosylases become sensitive to mycoribnin; bicarbonate abolishes this sensitivity. The H37Ra transglucosylase is specific for UDP-glucose and glucose-6-phosphate as substrates. UDP-galactose does not serve as a glycosyl donor; galactose-6-phosphate, ribose-5-phosphate, and glucose-1-phosphate do not act as glucosyl acceptors. Oligoribonucleotide analogues of mycoribnin do not inhibit substantially the H37Ra transglucosylase.

Bicarbonates↗
PubMed1984

Grocery store baking soda. A source of sodium bicarbonate in the management of chronic metabolic acidosis.

Oral sodium bicarbonate is used to treat metabolic acidosis in patients with renal tubular acidosis. Since infants and young children are unable to swallow tablets, those affected must ingest sodium bicarbonate in a powder or liquid form. Pharmacy-weighed sodium bicarbonate is expensive and inconvenient to obtain; some pharmacists are reluctant to provide it. We determined that the sodium bicarbonate contained in 8-oz boxes of Arm and Hammer Baking Soda was sufficiently constant in weight that, dissolved in water to a given volume, it yielded a quantitatively acceptable therapeutic solution of sodium bicarbonate at a cost of approximately 3 percent of that of pharmacy-weighed sodium bicarbonate. Grocery store baking soda can be a safe, economical, and convenient source of sodium bicarbonate for the treatment of chronic metabolic acidosis in infants and young children.

Acidosis, Renal Tubular↗
PubMed1982

Dietary sodium bicarbonate and magnesium oxide for early postpartum lactating dairy cows: effects on production, acid-base metabolism, and digestion.

In two experiments with cows in early lactation fed 40% corn silage and 60% concentrate diets (dry basis), we examined effects of 1.0% dietary sodium bicarbonate and .8% magnesium oxide in a 2 x 2 factorial arrangement on performance, acid-base metabolism, and digestion. In Experiment 1 with 20 Holstein and 4 Jersey cows, intake and milk production were not affected by treatment through 12 wk postpartum. In digestion trials at 3, 6, 9, and 12 wk postpartum, addition of magnesium oxide increased digestibility of dry matter 1.8% units by sodium bicarbonate whereas acid detergent fiber digestion increased 9 to 12% units with addition of either buffer. In Experiment 2, with four fistulated Holstein cows in a Latin square design, intake per unit body weight was increased .18% units by dietary sodium bicarbonate while milk production was unaffected. Dry matter and acid detergent fiber digestion were increased slightly by sodium bicarbonate plus magnesium oxide addition whereas nitrogen balance increased 23 g/day in cows fed magnesium oxide alone. Because of the low fiber content of the ration, milk fat percent increased .5 to .9% by addition of either buffer in both experiments and resulted in corresponding increased in fat-corrected milk. Sodium bicarbonate and magnesium oxide prevented rapid declines in rumen pH associated with feeding in Experiment 2, which related to changes in acid detergent fiber digestion. Blood acid-base metabolites were relatively unchanged by treatment in either experiment. Urinary bicarbonate and net acid excretion rates were changed on the average by +41 and +43 meq/h by sodium bicarbonate or magnesium oxide but could not be related to changes in intake and production.

Acid-Base Equilibrium↗
PubMed1984

Effect of sodium bicarbonate addition to alfalfa hay-based diets on digestibility of dietary fractions and rumen characteristics.

Three trials were to evaluate effects of sodium bicarbonate in alfalfa hay-based diets. In Experiment 1, four Jersey cows were fed diets of 40:60 chopped alfalfa hay:grain with either 0, .25, .5, and .75% sodium bicarbonate in a 4 X 4 Latin square digestion trial. Dry matter and fiber digestion were unaffected. Volatile fatty acids of ruminal fluid and milk fatty acids were not different. In Experiment 2, two rumen fistulated cattle were fed diets of Experiment 1 for changes of ruminal fluid characteristics at -1, 2, 4, and 8 h postfeeding. Volatile fatty acids of ruminal fluid and hydrogen ion concentration were not different across time with sodium bicarbonate. In Experiment 3, four Holstein cows with rumen cannulae were fed diets of 30:70 chopped alfalfa hay:grain with 0, .4, .8, and 1.2% sodium bicarbonate in a 4 X 4 Latin square. Dry matter and fiber digestion were unaffected. Ruminal fluid samples were collected at -1, 3, 6, and 9 h postfeeding. Volatile fatty acids were different only at 6 h with 0 and 1.2% sodium bicarbonate diets displaying lower concentrations. Rate of increase of hydrogen ion concentration was greater for diets containing 0 and .4% compared with .8 and 1.2% sodium bicarbonate between -1 and 6 h. Milk fatty acid composition, ruminal liquid dilution rate, and dry matter disappearance from nylon bags suspended in the rumen were not affected by sodium bicarbonate.

Ammonia↗
PubMedDate not supplied

Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial.

Intravenous sodium bicarbonate has been used for a long time in the treatment of diabetic ketoacidosis. However, there are no clinical studies showing its effectiveness in improving arterial pH in this condition. We therefore designed this study to investigate if bicarbonate therapy improves the rate of increase of arterial pH and to find out its effects on the recovery rate of the other metabolic abnormalities. Twenty patients with severe diabetic ketoacidosis (pH less than 7.15) entered a double-blind, randomized, placebo controlled trial: nine were included in the bicarbonate group and eleven in the placebo group. All patients were studied during the first 24 hours of treatment. Their management was similar, except for the use of sodium bicarbonate in one group and 0.9% saline solution in the placebo group. Heart rate, respiratory rate, arterial pressure, mental status, blood gases, blood glucose, sodium, potassium, and urea were assessed at the beginning of treatment, and then at 2, 6, 12 and 24 hours. No clinical or metabolic differences were found between groups. Two hours after therapy was begun, the arterial pH rose in the bicarbonate group from 7.05 +/- 0.08 to 7.24 +/- 0.04, while it only rose from 7.04 +/- 0.08 to 7.11 +/- 0.09 in the placebo group (p less than 0.02). Simultaneously, arterial bicarbonate increased from 2.87 +/- 1.2 to 6.1 +/- 1.5 mEq/L in the bicarbonate group and from 2.55 +/- 0.81 to 3.6 +/- 2 mEq/L in the placebo group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effect of interval between doses on response of the pony to sodium bicarbonate.

Three pony geldings were given sodium bicarbonate orally in order to study the effect on blood pH and bicarbonate and to determine if frequency of dosing influences the response. In a preliminary study, it appeared that a carry-over effect might occur if the interval between dosing was only 2 days. The ponies received 2 doses of sodium bicarbonate (400 mg/kg) 7 days apart in trial one and then in trial two they received 2 doses of sodium bicarbonate 4 days apart. The sodium bicarbonate was mixed with 2 liters of warm water and given through a nasogastric tube on each trial day. Blood samples were taken before dosing, and every half hour after for five and a half hours. The blood was analyzed for pH and bicarbonate. There did not seem to be a carry-over effect due to sodium bicarbonate administration since there was little difference in the responses between the first and second doses of each trial.

Animals↗
PubMed1986

Dietary sodium bicarbonate as a treatment for exertional rhabdomyolysis in a horse.

A 3-year-old mare repeatedly had clinical signs of rhabdomyolysis on mild exertion. Serum creatine kinase and aspartate transaminase activities were high at rest. Responses to dietary sodium bicarbonate were tested through 7 alternating periods of supplementation of a basal ration of timothy hay and oats. Physical signs; venous blood pH and gases; blood glucose and lactate; serum electrolytes, enzymes, and creatinine; and urine pH were monitored before and after exercise. Dietary sodium bicarbonate raised resting venous blood pH and bicarbonate slightly and significantly increased urine pH from pH 7.46 to 8.2 (P less than 0.001). An exercise test included 5 minutes at the walk followed by 20 minutes at the trot. The exercise induced gait stiffness, muscle fasciculations, and muscle induration when the diet was not supplemented, but not when it was supplemented with sodium bicarbonate. Myoglobin was present in 16 of 21 urine samples after exercise during nonsupplemented periods, but only in 3 of 28 urine samples during supplemented periods (P less than 0.0001). Bicarbonate supplementation significantly decreased the responses of blood lactic acid, serum creatine kinase, and aspartate transaminase to exercise. Supplementation of the diet was associated with higher venous blood pH and bicarbonate ion concentrations throughout exercise. Dietary sodium bicarbonate apparently mitigated or prevented physical, chemical, and enzymatic characteristics of exertional rhabdomyolysis in this mare, possibly through its enhancement of buffering capacity in muscle tissue fluids.

Animals↗
PubMed1984

Effects of peroperative myocardial ischemia on early and late hemodynamic response to hypertonic sodium bicarbonate in dogs.

Because hypotension induced by the administration of hypertonic sodium bicarbonate is more severe when cardiac performance is impaired, the authors evaluated the hemodynamic consequences of peroperative myocardial ischemia upon the response of conscious dogs to an intravenous bolus of sodium bicarbonate. Twenty-two control dogs (group 1) were equipped with an electromagnetic flow probe positioned around the ascending aorta. Seventeen dogs (group 2), equipped in the same manner, were subjected to 1 hour of myocardial ischemia combined with topical cardiac hypothermia. Hemodynamic studies were performed daily for 1 month before and during the administration of sodium bicarbonate. Baseline hemodynamic values in group 1 were always within normal limits. In group 2, cardiac failure was evident in the immediate postoperative period but hemodynamic values reached normal limits 24 hours postoperatively. For both groups, the peak hypotensive response to sodium bicarbonate was combined with a substantial reduction in all hemodynamic values reflecting the left ventricular performance. However, this response is significantly (p less than 0.01) more pronounced in group 2 during the first 4 postoperative days, being maximal 3 and 24 hours after operation. Afterwards, the hemodynamic response to sodium bicarbonate was similar in both groups. These results indicated that an intravenous bolus of sodium bicarbonate decreases left ventricular performance and that this decrement is greater when cardiac performance is impaired following peroperative myocardial ischemia. Long-term hemodynamic studies show that this temporary myocardial ischemia is not deleterious to cardiovascular adaptability to hypertonic sodium bicarbonate administration.

Animals↗
PubMedDate not supplied

Effect of high-dose sodium bicarbonate on the vasopressor effects of epinephrine during cardiopulmonary resuscitation.

We attempted to determine the effect of extreme alkalemia induced by highdose sodium bicarbonate on the vasopressor effects of epinephrine during cardiopulmonary resuscitation (CPR). Subjects in this randomized, blinded study performed in a controlled laboratory environment were 12 mongrel dogs that had had a previous episode of CPR. Each dog underwent 3 minutes of ventricular fibrillation (VF) followed by 7 minutes of closed-chest CPR. Animals were assigned to receive either sodium bicarbonate 3 mEq/kg and epinephrine 0.1 mg/kg, or normal saline 3 ml/kg and epinephrine 0.1 mg/kg. The sodium bicarbonate or normal saline was infused over 2 minutes beginning at 4 minutes of VF (1 min of CPR) followed by bolus epinephrine. Arterial pH in the sodium bicarbonate group was significantly higher at each sampling point (7.7 +/- 0.1 vs 7.29 +/- 0.06 at 1 min after drug, p < 0.001). However, there were no statistically or clinically significant differences in coronary perfusion pressure between the groups at any time: 29 +/- 13 versus 32 +/- 21 mm Hg 1 minute, and 22 +/- 12 versus 26 +/- 19 mm Hg 4 minutes after epinephrine for sodium bicarbonate and normal saline, respectively (p > 0.7). Increased arterial pH (alkalemia) induced by high-dose sodium bicarbonate administration did not improve the vasopressor effects of epinephrine during CPR in this canine model. These results suggest the limited value of administering sodium bicarbonate during CPR to improve the responsiveness to epinephrine.

Animals↗
PubMed2004

Rapid PKA-catalysed phosphorylation of boar sperm proteins induced by the capacitating agent bicarbonate.

In boar spermatozoa, the capacitating agent bicarbonate has been shown to induce rapid changes both in plasma membrane lipid architecture and in motility; in each case, a PKA-dependent pathway is involved. Early bicarbonate-induced changes in protein phosphorylation were probed using a commercial antibody against the phosphorylated form of the consensus substrate site for cyclic AMP-dependent protein kinase. The antibody detected relatively few bands in sperm extracts, of which only a small number showed incubation-dependent changes. While the quantitative response varied between boar ejaculates, in general terms bicarbonate induced phosphorylation increases in bands of 96, 64, and 59 kDa within 80 sec. The changes reached a maximum after about 160 sec, declined somewhat thereafter, and then increased again slowly as incubation progressed further (up to 21 min). The bicarbonate-induced increases were strongly dependent on the presence of BSA in the incubation medium. They were inhibited by H89 (PKA inhibitor) but not by GF (PKC inhibitor), and were enhanced by papaverine (phosphodiesterase inhibitor) and by calyculin (protein phosphatase inhibitor). The cyclic AMP analogue cBIMPS was able to mimic bicarbonate action though its effect was less dramatic. Stearated Ht31, a permeable inhibitor of PKA's binding to A-kinase anchoring protein, did not affect either the intensity or the specificity of the bicarbonate-induced phosphorylation changes, though it blocked motility entirely. Immunocytochemical studies revealed marked bicarbonate-dependent phosphorylation changes in the post-acrosomal region of the head and in the neck, midpiece, and anterior regions of the tail. Fractionation of stimulated spermatozoa showed that all bands detectable with the antibody were bound to heads and to midpieces and associated large tail fragments; no bands were detected in either small tail or membrane fragments or in the cytoplasmic fraction. Differential extraction of the midpiece/large tail fraction revealed two protein bands with closely similar electrophoretic mobilities to the 96- and 59-kDa phosphorylated bands; MALDI-TOF analyses of these bands revealed both to be members of the Odf2 family.

Animals↗
PubMed1982

Fast bicarbonate-chloride exchange between plasma and brain extracellular fluid at maintained PCO2.

The aim of this paper was to investigate the kinetics and mechanism of bicarbonate exchange at the blood-brain ECF barrier. The experiments were performed on anaesthetized and artificially ventilated cats in such a way that acid-base parameters of the brain extracellular fluid were continuously measured while an approximately rectangular increase in the arterial plasma bicarbonate concentration was produced at maintained PCO2. The results from such a preparation were: 1. A rapid increase in the brain extracellular bicarbonate concentration was observed in response to an i.v. bolus injection of 3 ml molar NaHCO3. The bolus was followed by a slow infusion of bicarbonate solution. The brain extracellular bicarbonate reached a new steady state within a minute. 2. This increase was almost simultaneously accompanied by a decrease in the extracellular chloride concentration. The HCO-3-Cl- exchange ratio very closely approached one. 3. The extracellular bicarbonate concentration in the brain, after an initial increase, returned towards control in spite of elevated arterial bicarbonate at maintained PCO2. 4. The results are discussed in terms of a 5-compartment model, where the extracellular fluid is interposed between the glial cells and the interstitial side of the endothelial cells, similar to the blood plasma being interposed between the red cells and the luminal side of the endothelial cells. 5. A non-electrogenic carrier-mediated HCO-3-Cl- exchange at the interphase of the blood brain barrier is postulated.

Animals↗
PubMed1981

Bicarbonate reabsorption in the papillary collecting duct of rats.

Using the technique of capillary perfusion and simultaneous luminal stop flow microperfusion the reabsorption of bicarbonate and glycodiazine from the papillary collecting duct was evaluated. Starting with equal H14CO3- and 3H-glycodiazine concentrations in the luminal and peritubular perfusates, the decrease in the luminal concentration at 10 and 45 s contact time was measured. In control rats with 25 mmol/l HCO3- in the perfusates the rate of HCO3- reabsorption calculated from the 10 s values was 0.34 nmol cm-2 s-1. In acute metabolic acidosis, the rate of bicarbonate reabsorption was 2,3 times higher. In metabolic alkalosis, the rate of bicarbonate absorption dropped to 13% of the control values. Also the 45 s values of acidotic and alkalotic animals differed significantly from each other. With 25 mmol/l glycodiazine in both perfusates the rate of buffer reabsorption as calculated from the 10 s values was 0.76 nmol cm-2 s-1 in control rats and did not deviate significantly from this value in acidotic and alkalotic animals. In control rats the bicarbonate reabsorption in % was the same, no matter whether both luminal and capillary perfusate contained 25 mmol/l bicarbonate or 10 mmol/l. In acidotic rats the rate of HCO3- reabsorption did not change significantly if all Na+ in the perfusates was replaced by choline (0.88 versus 0.79 nmol cm-2 s-1 at 25 mmol/l HCO3-). When in acidotic rats. 0.1 mmol/l acetazolamide or 1 mmol/l SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid) was added to both perfusates the rate of HCO3- reabsorption dropped by 75 and 58%, respectively. A potassium deficient diet for one week and DOCa administration had no influence on the bicarbonate reabsorption of rats which were on standard diet. The data indicate that (1) the buffer reabsorption from the papillary collecting duct is rather due to H+ ion secretion than to buffer anion reabsorption. (2) The adaptation to metabolic acidosis and alkalosis is specific for bicarbonate and not seen with glycodiazine. (3) Within the concentration range tested the HCO3- reabsorption rises linearly with the HCO3- concentration. (4) The HCO3- reabsorption in the papillary collecting duct is Na+-independent, it can be inhibited by acetazolamide and SITS, but is not influenced by K+-deficient diet plus DOCA.

Absorption↗