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PubMed1984

Calcium balance and acid-base status of women as affected by increased protein intake and by sodium bicarbonate ingestion.

Six women, aged 38 to 62 yr, participated in a 40-day metabolic study to investigate the effect of level of protein intake and of sodium bicarbonate ingestion on urinary calcium, net calcium balance, net renal acid excretion, and arterialized venous blood pH and bicarbonate ion concentration. The diet contained 44 g protein during the first 16 days and 102 g during the remaining 24 days. During the last 10 days of the study, 5.85 g of sodium bicarbonate was ingested concomitantly with the higher protein intake. Calcium, phosphorus, and magnesium intakes were held constant at 500, 900, and 300 mg, respectively. The increase in protein intake significantly increased urinary calcium and net renal acid excretion and the mean net calcium balance became negative. The ingestion of sodium bicarbonate alkalinized the urine and reversed the increase in urinary calcium associated with the higher protein intake; the mean net calcium balance became positive. The arterialized venous blood pH and bicarbonate ion concentrations were not significantly affected by dietary treatments. The results suggest that the ingestion of a small amount of sodium bicarbonate may be an effective way to increase calcium retention in women with protein-induced hypercalciuria.

Acid-Base Equilibrium↗
PubMed1993

Acute haemodynamic effect of sodium bicarbonate in canine respiratory or metabolic acidosis.

This study has examined the acute haemodynamic effects of 7% sodium bicarbonate solution 1 mmol kg-1 (1.2 ml kg-1) administered into the right atrium over 5 s in 25 anaesthetized dogs allocated randomly to respiratory (arterial pH (pHa) 7.18, PaCO2 10.1 kPa (n = 8)) or metabolic acidosis (pHa 7.27, base deficit -9.0 mmol litre-1 (n = 7)) or metabolic neutrality (pHa 7.39 (n = 10)). The pHa and PaCO2 in the respiratory acidosis group differed from those in the two other groups (P < 0.01). One dog with respiratory acidosis developed progressive circulatory depression and cardiac arrest 6 min after injection of sodium bicarbonate. In the remaining seven dogs with respiratory acidosis, administration of sodium bicarbonate 1 mmol kg-1 produced transient decreases in mean arterial pressure, right ventricular dP/dt, and pulmonary blood flow, with increased right atrial pressure, followed by a gradual return of these variables to the baseline. The magnitude of reduction in pulmonary blood flow after sodium bicarbonate was greater in dogs with respiratory acidosis (P < 0.05) compared with the changes in the two other groups. The haemodynamic depression after bicarbonate was pronounced during respiratory acidosis and this may be attributed to a smaller pHa in the respiratory acidosis group, further reduction of intracellular pH, or both. It is suggested that when metabolic acidosis is corrected, bicarbonate should be administered with caution in the presence of respiratory acidosis.

Acid-Base Equilibrium↗
PubMed1988

Effects of sodium bicarbonate in canine hemorrhagic shock.

We studied the use of sodium bicarbonate administration in a canine model of hemorrhagic shock to determine its effect on hemodynamics, arterial and venous blood gases, respiratory gases, and blood lactate levels. Thirteen dogs were anesthetized, paralyzed, mechanically ventilated, and hemodynamically monitored. Hypotension was induced and maintained at a mean arterial pressure of 40 to 45 mm Hg using controlled hemorrhage and reinfusion. After 2.5 h of shock, the dogs were randomized into two groups: one group (n = 6) received NaCl infusion; the other (n = 7) received sodium bicarbonate (1 mEq/kg followed by a continuous infusion of 2.5 mEq/kg.h for 2.5 h). CO2 production was increased in the alkali group, but there was no statistically significant difference between groups in any measured hemodynamic, blood gas, or respiratory gas variable. These included heart rate, BP, cardiac output, arterial and venous pH, CO2 production, and bicarbonate levels. Blood lactate levels, however, in the bicarbonate treated animals were significantly (p less than .01) higher than in the group treated with NaCl alone (10.1 +/- 3.2 vs. 5.1 +/- 1.2 mEq/L). These results are similar to the effects of bicarbonate found in other models of lactic acidosis, and suggest that bicarbonate therapy may have limited usefulness in the treatment of lactic acidosis.

Acidosis, Lactic↗
PubMed2003

Oral sodium bicarbonate for the treatment of metabolic acidosis in peritoneal dialysis patients: a randomized placebo-control trial.

Acidosis causes malnutrition in peritoneal dialysis (PD) patients. The effect of oral bicarbonate in PD patients with Kt/V <2.1 has not been studied. We randomly assigned 60 PD patients with acidosis and Kt/V <2.1 to oral sodium bicarbonate (0.9 g thrice daily) or placebo. Patients were followed for 12 mo. We compared their nutritional status, including subjective global assessment (SGA) score and normalized protein nitrogen appearance (NPNA), hospitalization and all-cause mortality. Treatment with oral bicarbonate resulted in a higher plasma bicarbonate level at 4 wk (27.8 +/- 2.6 versus 24.7 +/- 3.9 mmol/L, P = 0.002), and the difference persisted until 52 wk. Bicarbonate treatment had a significant effect on the change in overall SGA score (repeated measures ANOVA, P = 0.0003). The overall SGA score of the treatment group was higher than the placebo group at 24 wk (5.07 +/- 0.94 versus 4.40 +/- 1.00, P = 0.015), and the difference persisted thereafter. NPNA rose in the treatment group (1.17 +/- 0.32 to 1.28 +/- 0.26 g/kg per d, P = 0.034), but declined in placebo group (1.13 +/- 0.25 to 1.03 +/- 0.28 g/kg per d, P = 0.054). The treatment group had a shorter hospitalization than the placebo group (8.4 +/- 17.7 versus 16.8 +/- 21.7 d/yr; P = 0.02). Mortality was not significantly different. Although our trial has limited statistical power, we find that in PD patients with mild acidosis and Kt/V <2.1, oral sodium bicarbonate probably improve nutritional status and reduce the duration of hospitalization.

Acidosis↗
PubMed1989

Sodium bicarbonate as a single dose antacid in obstetric anaesthesia.

Gastric pH and volumes were measured in 84 women who had general anaesthesia for emergency Caesarean section. Forty-eight received only 20 ml 8.4% sodium bicarbonate immediately before induction of anaesthesia and 36 ranitidine 150 mg 6-hourly during labour in combination with NaHCO3. Gastric pH was less than 2.5 in four women who received only bicarbonate. All aspirates from the ranitidine plus bicarbonate group had a pH greater than 2.5. Mean volumes of gastric content aspirated were 87 (SD 87.4) and 60 (SD 46.3) ml for the bicarbonate alone and bicarbonate plus ranitidine series respectively. These differences were not significant. Twenty millilitres of 8.4% NaHCO3 cannot be recommended as a single dose antacid for emergency Caesarean section. Ranitidine plus bicarbonate is considered a reliable antacid regimen to ensure elevation of gastric pH to safe levels.

Anesthesia, General↗
PubMed1981

Effects of sodium acetate, bicarbonate and lactate on acid-base status in anaesthetized dogs.

Equal doses of sodium acetate, bicarbonate and lactate (6.6 mEq/L) infused intravenously over 30 min into three groups of halothane-anaesthetized dogs caused changes in acid-base status. Arterial carbon dioxide tension (PaCO2), pHa, base excess (BE) and standard bicarbonate (SB) increased. Sodium bicarbonate caused the most rapid and greatest changes. The bicarbonate group was significantly different (P less than 0.05) from the other groups at 15 and 30 min after the start of infusion for pHa, BE and SB. The greater effects of bicarbonate are due to its production of alkalinization without a requirement for metabolism; acetate and lactate require oxidation to be effective. The acetate and bicarbonate groups were not statistically different at 45 min after the onset of drug infusion, but both had significantly higher SB and BE mean values than the lactate group. All measurements made after 45 min revealed no significant differences among groups. Thus, after the earlier differences noted above, the three alkalinizers caused similar effects on acid-base status. PaCO2 was elevated in all groups, but there were no differences among groups. Cardiovascular effects caused by infusion of the three drugs were minimal.

Acetates↗
PubMed2001

Phosphorylation of Ser(982) in the sodium bicarbonate cotransporter kNBC1 shifts the HCO(3)(-) : Na(+) stoichiometry from 3 : 1 to 2 : 1 in murine proximal tubule cells.

1. Adenosine 3',5'-cyclic monophosphate (cAMP) modulates proximal tubule sodium and bicarbonate absorption by decreasing the rate of apical Na(+)-H(+) exchange and basolateral sodium bicarbonate efflux, through activation of protein kinase A (PKA). The electrogenic sodium bicarbonate cotransporter kNBC1 mediates basolateral sodium and bicarbonate efflux in the proximal tubule by coupling the transport of 1 Na(+) cation to that of 3 HCO(3)(-) anions. In this work we studied the effects of cAMP on the function of kNBC1 expressed heterologously in a proximal tubule cell line. 2. A mouse renal proximal tubule cell line, deficient in electrogenic sodium bicarbonate cotransport function, was transfected with kNBC1. Cells were grown on a permeable support to confluence, mounted in an Ussing chamber and permeabilized apically with amphotericin B. Current through the cotransporter was isolated as the difference current due to the reversible inhibitor dinitrostilbene disulfonate. The HCO(3)(-) : Na(+) stoichiometry of kNBC1 was calculated from its reversal potential by measuring the current-voltage relationships of the cotransporter at different Na(+) concentration gradients. 3. Addition of the potent cAMP agonist 8-Br-cAMP caused the stoichiometry of kNBC1 to shift from 3 HCO(3)(-) : 1 Na(+) to 2 HCO(3)(-) : 1 Na(+). Pretreatment of the cells with the PKA inhibitor H-89 abolished the effect of the agonist on the stoichiometry change. Replacing Ser(982) at the C-terminus consensus PKA phosphorylation site with alanine resulted in a failure of PKA to phosphorylate the transporter and induce a stoichiometry shift. 4. Our data indicate that cAMP modulates the stoichiometry of kNBC1 through activation of PKA. The change in stoichiometry from 3 : 1 to 2 : 1 is predicted to cause a shift in the direction of basolateral membrane sodium bicarbonate transport from efflux to influx. Ser(982) in the C-terminus of kNBC1 is a target for PKA phosphorylation. This is the first example of modulation of the stoichiometry of a membrane transporter by phosphorylation.

Amino Acid Sequence↗
PubMed2002

The functional and physical relationship between the DRA bicarbonate transporter and carbonic anhydrase II.

COOH-terminal cytoplasmic tails of chloride/bicarbonate anion exchangers (AE) bind cytosolic carbonic anhydrase II (CAII) to form a bicarbonate transport metabolon, a membrane protein complex that accelerates transmembrane bicarbonate flux. To determine whether interaction with CAII affects the downregulated in adenoma (DRA) chloride/bicarbonate exchanger, anion exchange activity of DRA-transfected HEK-293 cells was monitored by following changes in intracellular pH associated with bicarbonate transport. DRA-mediated bicarbonate transport activity of 18 +/- 1 mM H+ equivalents/min was inhibited 53 +/- 2% by 100 mM of the CAII inhibitor, acetazolamide, but was unaffected by the membrane-impermeant carbonic anhydrase inhibitor, 1-[5-sulfamoyl-1,3,4-thiadiazol-2-yl-(aminosulfonyl-4-phenyl)]-2,6-dimethyl-4-phenyl-pyridinium perchlorate. Compared with AE1, the COOH-terminal tail of DRA interacted weakly with CAII. Overexpression of a functionally inactive CAII mutant, V143Y, reduced AE1 transport activity by 61 +/- 4% without effect on DRA transport activity (105 +/- 7% transport activity relative to DRA alone). We conclude that cytosolic CAII is required for full DRA-mediated bicarbonate transport. However, DRA differs from other bicarbonate transport proteins because its transport activity is not stimulated by direct interaction with CAII.

Acetazolamide↗
PubMed2000

Bicarbonate exacerbates oxidative injury induced by antitumor antibiotic doxorubicin in cardiomyocytes.

Doxorubicin, a broad-spectrum antitumor antibiotic, causes dose-dependent cardiomyopathy and heart failure. Although the exact molecular mechanisms of cardiotoxicity are not well established, oxidative mechanisms involving doxorubicin-induced superoxide anion production have been proposed. In this study, we show that bicarbonate, a physiologically relevant tissue component, greatly amplified doxorubicin-induced cardiomyocyte injury. Bicarbonate also enhanced inactivation of aconitase, a crucial tricarboxylic acid cycle enzyme, in cardiomyocytes exposed to doxorubicin. The cell-permeable superoxide dismutase mimetic, Mn(III)tetrakis (4-benzoic acid) porphyrin, reversed doxorubicin-induced cardiomyocyte injury. Bicarbonate enhanced the inactivation of purified mitochondrial aconitase in the xanthine/xanthine oxidase system, generating superoxide. The results suggest that bicarbonate amplifies the prooxidant effect of superoxide. Bicarbonate also caused an increased loading of cardiomyocytes with doxorubicin. We conclude that the bicarbonate-mediated increase in doxorubicin toxicity is due to increased intracellular loading of doxorubicin in cardiomyocytes and subsequent exacerbation of superoxide-mediated cardiomyocyte injury.

Aconitate Hydratase↗
PubMed1984

Rapid determination of whole-body bicarbonate kinetics by use of a digital infusion.

Accurate determination of substrate oxidation rates from breath 13CO2 levels often requires information on the bicarbonate status of the subject. We have developed a rapid method to obtain a complete set of bicarbonate kinetic parameters, prime bicarbonate pools with 13C, clamp breath 13CO2 levels rapidly and accurately with predetermined ranges, and provide a steady base-line enrichment of 13C for a subsequent substrate oxidation measurement. The method consists of administering NaH13CO3 intravenously as a combination of a bolus dose, an exponentially decreasing infusion, and a constant infusion. A Harvard model 2729 microprocessor-controlled syringe pump was modified for external control and coupled to a Hewlett-Packard HP-85 desk-top computer to deliver the complex infusion. An infusion algorithm that would rapidly attain and maintain an increase of 50% 13C enrichment of breath CO2 was derived by using the SAAM-27 program to interrogate a three-compartmental model of bicarbonate kinetics in normal, fasted, resting adult subjects. When the method was tested on five adult fasted subjects who had rested for 1.5 h, plateau enrichments were achieved within 10-20 min. The bicarbonate pool sizes and kinetic parameters obtained by compartmental analysis of their 13CO2 data were used to obtain a refined infusion protocol, which resulted in more rapid attainment of plateau enrichments. If carried out immediately before a substrate oxidation test, the method can provide a complete description of bicarbonate kinetics for use in the compartmental and noncompartmental analysis of substrate catabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effect of sodium bicarbonate and Tris (THAM) infusion on intra- and extracellular acid-base status during experimental uremia in the rat.

The intra- and extracellular acid-base status of nephrectomized rats was determined following infusion of 10 mmol/kg body mass Tris (THAM) or sodium bicarbonate. The 'mean whole body pHi', an overall estimate of the intracellular pH (complementary to the in vivo determined arterial plasma pH) was calculated from the distribution of 14C-labelled 5,5-dimethyl-2,4-oxazolidinedione. For evaluation of buffer effect of Tris or sodium bicarbonate, extra- and intracellular bicarbonate concentration was calculated from the Henderson-Hasselbalch equation. Intracellular and extracellular pH and bicarbonate concentration were significantly more increased when sodium bicarbonate was infused, while PCO2 increased significantly more when Tris was administered. On the basis of these results it is concluded that treatment of both in intracellular and extracellular uremic acidosis can be performed more efficiently with bicarbonate than with Tris buffer.

Acid-Base Equilibrium↗
PubMed2001

Cellular bicarbonate protects rat duodenal mucosa from acid-induced injury.

Secretion of bicarbonate from epithelial cells is considered to be the primary mechanism by which the duodenal mucosa is protected from acid-related injury. Against this view is the finding that patients with cystic fibrosis, who have impaired duodenal bicarbonate secretion, are paradoxically protected from developing duodenal ulcers. Therefore, we hypothesized that epithelial cell intracellular pH regulation, rather than secreted extracellular bicarbonate, was the principal means by which duodenal epithelial cells are protected from acidification and injury. Using a novel in vivo microscopic method, we have measured bicarbonate secretion and epithelial cell intracellular pH (pH(i)), and we have followed cell injury in the presence of the anion transport inhibitor DIDS and the Cl(-) channel inhibitor, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB). DIDS and NPPB abolished the increase of duodenal bicarbonate secretion following luminal acid perfusion. DIDS decreased basal pH(i), whereas NPPB increased pH(i); DIDS further decreased pH(i) during acid challenge and abolished the pH(i) overshoot over baseline observed after acid challenge, whereas NPPB attenuated the fall of pH(i) and exaggerated the overshoot. Finally, acid-induced epithelial injury was enhanced by DIDS and decreased by NPPB. The results support the role of intracellular bicarbonate in the protection of duodenal epithelial cells from luminal gastric acid.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Effect of chewing gum containing sodium bicarbonate on human interproximal plaque pH.

The effect of chewing sorbitol gum containing sodium bicarbonate on interproximal plaque pH was determined by use of an ion-sensitive field-effect transistor (ISFET) electrode system with four human volunteers. Plaque pH was lowered by 2 min of chewing of a sucrose-containing toffee. After 20 min, either sodium bicarbonate or control gum was chewed for 10 min, and the pH was followed for an additional 20 min. The minimum pH after toffee chewing was elevated by both the control gum (4.5 +/- 0.3 to 5.2 +/- 0.5) and the sodium-bicarbonate-containing product (4.3 +/- 0.3 to 6.1 +/- 0.6) to levels which were significantly different (p less than 0.01). The rate of rise in pH was 2.6 times faster with the gum containing buffer compared with the control gum. In comparison with the control gum, the sodium bicarbonate gum caused the pH to remain at a higher level, approximately 0.5 pH units, for 20 min after gum chewing. The addition of sodium bicarbonate to gum containing sorbitol markedly enhanced its capacity to cause and maintain an elevation of interproximal plaque pH previously lowered by exposure to fermentable carbohydrate. Sodium bicarbonate may be useful in products designed to reduce the acidogenic challenge to the teeth following food ingestion.

Adult↗
PubMed1989

Exacerbation of hypercapnia and acidosis of central venous blood and tissue following administration of sodium bicarbonate during cardiopulmonary resuscitation.

Administration of sodium bicarbonate during cardiopulmonary resuscitation (CPR) is controversial, and our aim was to elucidate whether or not its administration is beneficial by analyzing the acid-base status and the level of carbon dioxide in central venous blood during CPR, and their changes following administration of sodium bicarbonate. Six patients were studied. They had all been admitted to the intensive care unit (ICU), had already had pulmonary arterial or central venous catheters inserted, and had acute episodes of circulatory collapse during their stay in the ICU. The following phenomena were observed: 1) hypercapnia and acidosis of central venous blood were prominent during both cardiogenic shock and CPR, although arterial hypocapnia was maintained by hyperventilation; 2) administration of sodium bicarbonate during cardiogenic shock and CPR induced exacerbation of hypercapnia and acidosis of central venous blood; 3) when arterial hypercapnia was present due to disturbed ventilation, administration of sodium bicarbonate exacerbated hypercapnia and acidosis of both arterial and central venous blood; 4) administration of sodium bicarbonate did not induce hypercapnia of central venous blood in a septic shock patient in whom the septic hyperdynamic state was prevalent in spite of low systemic perfusion pressure. It was concluded that hypercapnia and acidosis of the central venous blood and tissues were exacerbated by administration of sodium bicarbonate during CPR, and that such an effect might be dependent on the severity of the decrease in tissue perfusion.

Acid-Base Equilibrium↗
PubMed1984

Response of milking cows fed a high concentrate, low roughage diet plus sodium bicarbonate, magnesium oxide, or magnesium hydroxide.

To determine the ability of mineral supplements to elevate depressed milk fat percent, we placed 42 Holstein cows in early to midlactation in seven blocks and assigned each to one of six treatments: control (25% corn silage and alfalfa haylage, 75% concentrate, mostly corn, dry matter); control plus magnesium oxide ground to pass a .425-mm sieve; control plus prilled magnesium oxide sieved to between 1.70 and .425 mm; control plus sodium bicarbonate; control plus reactive powdered magnesium oxide to pass a 45 microns sieve; and control plus powdered magnesium hydroxide. Sodium bicarbonate was 1% of diet as fed, magnesium oxide .5%, magnesium hydroxide .7% later reduced to .5%. Cows were fed control ration for 3 wk to induce milk fat depression, then were changed to treatment rations for 5 wk. Five cows (unblocked) were continued on each dietary treatment for a digestibility study after the feeding trial. All mineral supplements produced greater milk fat percent and yield of milk fat per day than control and all magnesium treatments produced greater milk fat percent than sodium bicarbonate. Magnesium oxide passing a .425-mm sieve produced the greatest increase of milk fat percent. Milk production was most for sodium bicarbonate treatment. Supplementation with magnesium increased ruminal magnesium concentration by factors of 1.26 to 3.75. Blood serum, urine, and fecal magnesium concentrations and fecal pH were more for cows fed magnesium than those fed sodium bicarbonate treatments. Kidney filtration ratios of element to creatinine increased for magnesium when diets were supplemented with magnesium and increased for phosphorus and sodium when diets were supplemented with sodium bicarbonate.

Animal Feed↗
PubMed1984

Influence of dietary sodium and potassium bicarbonate and total potassium on heat-stressed lactating dairy cows.

Objectives were to study effects of heat stress, 0 or .85% sodium bicarbonate, 0 or 1.0% potassium bicarbonate, and 1.0 or 1.5% total dietary potassium on production and physiological responses of dairy cows. Eighteen lactating Holsteins were assigned to shade (control) or no shade (heat stress) lots continuously for three consecutive 35-day periods and to different dietary treatments each period. Basal diet was 25% cottonseed hulls and 75% concentrate. Daytime and nighttime feed intake and production were measured the last 2 wk of each period, and milk and blood were sampled the final day of each period. Black globe temperature, rectal temperature, respiration rate, and blood pH were higher in no shade. Daytime intake was 132% greater in shade, nighttime intake was not different between environments. Milk production was about 19% greater for evening and morning milkings in shade. Daytime intake, daytime and nighttime milk production were higher with sodium bicarbonate. Potassium bicarbonate reduced intake and production. Higher total dietary potassium increased total daily milk production. Lactating cows appear adept at withstanding environmental and dietary challenges to acid-base homeostasis. Supplementation of sodium bicarbonate and 1.5% dietary potassium, but not potassium bicarbonate, were beneficial to lactating dairy cows.

Animals↗
PubMed1985

Dietary sodium bicarbonate for high-producing Holstein cows over complete lactations.

Several concentrates with sodium bicarbonate (experimental) were compared with the same concentrates without sodium bicarbonate (control) throughout two lactations. During first lactation, two control concentrates were used in sequence in one comparison and three in another. Toward the end of first lactation, sodium bicarbonate was increased from 1.5 to 2.5% in concentrates, and that concentration was continued throughout the second lactation. During second lactation high-moisture corn with soybean meal was one concentrate; the other included half high-moisture barley and half dry corn and soybean meal. Fifty-two and 60 lactations of cows fed control and experimental rations contributed feed intake and production data. Ninety-four and 95 lactations of cows fed control or experimental rations contributed 305-day, mature-equivalent production data over three lactations. Inclusion of sodium bicarbonate in these rations had little effect on feed consumption, milk production, fat content of milk, efficiency of milk production, or change of body weight. The kind of concentrate did not alter the effect of sodium bicarbonate. Cows consuming control rations produced 8898 kg milk with 312 kg fat (305-day mature equivalent). Cows using bicarbonate produced 8972 kg milk with 312 kg fat.

Animals↗
PubMed1988

Effects of feed intake and sodium bicarbonate on milk production and concentrations of hormones and metabolites in plasma of cows.

Eight Holstein cows were used to investigate the effects of DM intake and sodium bicarbonate on lactational performance and concentrations of hormones and metabolites in plasma. Cows were fed a diet with or without 1.0% sodium bicarbonate (dry matter basis) in a switchback design. Four cows were fed ad libitum and four cows were fed approximately 80% of their recommended nutrient requirements by restriction of DM intake throughout the three 21-d periods. Supplementing the diet with sodium bicarbonate increased DM intake of cows fed ad libitum. There was a feed intake by sodium bicarbonate interaction for production of 4% FCM. This interaction may be explained by the difference in DM intake of cows fed ad libitum or restricted amounts of feed and supplemented with sodium bicarbonate. Cows fed restricted amounts of feed had lower milk, milk fat, milk protein, milk SNF, and milk energy yields. Restriction of feed intake increased plasma concentrations of somatotropin and nonesterified fatty acids but decreased concentrations of insulin, triidothyronine, thyroxine, glucagon, and prolactin. In contrast, feeding supplemental sodium bicarbonate did not affect concentrations of hormones or metabolites in plasma at either feed intake.

Animals↗