Controlled Sodium Bicarbonate Infusion and Maternal Acid-Base Balance During Labor

1980 ◽  
Vol 59 (3) ◽  
pp. 225-230
Author(s):  
Raphael Ron-El ◽  
Eliahu Caspi ◽  
David Modai
Keyword(s):  
Sodium Bicarbonate ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Bicarbonate Infusion ◽  
Sodium Bicarbonate Infusion

Decrease in ureagenesis by partial hepatectomy does not influence acid-base balance

1989 ◽  
Vol 257 (4) ◽  
pp. F696-F699
Author(s):  
T. Almdal ◽  
H. Vilstrup ◽  
K. Bjerrum ◽  
L. O. Kristensen
Keyword(s):  
Sodium Chloride ◽  
Sodium Bicarbonate ◽  
Synthesis Rate ◽  
Urea Synthesis ◽  
Ph Homeostasis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Bicarbonate Infusion

It has been suggested that urea synthesis participates directly in body pH homeostasis by removal of bicarbonate. To elucidate this hypothesis sodium bicarbonate or sodium chloride was infused (11.5 mumol/min) for 90 min into control rats and into rats that had undergone an 85% hepatectomy immediately before starting the infusion. Urea synthesis rate was 2.6 +/- 0.3 mumol/min (mean +/- SE) in controls, and was significantly (P less than 0.01) reduced to 1.0 +/- 0.2 mumol/min in partially hepatectomized rats. At the start of bicarbonate infusion, pH was 7.38 and 7.34 in control and partially hepatectomized rats, respectively, and at the end of infusion, pH was 7.56 and 7.51. Standard bicarbonate at start of bicarbonate infusion was 21.9 and 21.3 mM in controls and partially hepatectomized, respectively, and it increased to 32.7 and 29.9 mM at end of infusion. In saline-infused rats a slight decrease of approximately 0.05 pH units was observed during the experiment, but again no difference emerged between control and partially hepatectomized rats. It is concluded that a major role of the liver in the regulation of acid-base balance is unlikely.

Branchial mechanisms of ion and acid–base regulation in the freshwater rainbow trout, Salmo gairdneri

1988 ◽  
Vol 66 (12) ◽  
pp. 2699-2708 ◽  
Author(s):  
D. G. McDonald ◽  
E. T. Prior
Keyword(s):  
Lactic Acid ◽  
Rainbow Trout ◽  
Sodium Bicarbonate ◽  
Ammonium Sulphate ◽  
Ammonia Excretion ◽  
Salmo Gairdneri ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Blood acid–base balance and branchial fluxes of Na+, Cl−, and acidic equivalents were examined in rainbow trout (Salmo gairdneri) in response to variations in external [NaCl] and following experimental acid or base loads (intravascular infusion of ammonium sulphate, lactic acid, or sodium bicarbonate). NaCl influx, NaCl efflux, and ammonia excretion covaried with external [NaCl]. Large fluxes of acidic equivalents across the gills were produced by infusion of both ammonium sulphate and sodium bicarbonate, but both treatments had little effect upon Na+ and Cl− uptake. We interpret this result as indicating that apical [Formula: see text] and [Formula: see text] exchange played little role in the branchial clearance of acidic equivalents. Instead, the results are consistent with the notion that acidic equivalents were excreted via diffusion through paracellular channels. A model is presented which suggests that the paracellular channels are the normal route for ionic efflux across the gills and that excretion of acidic equivalents results from modulation of the permselectivity of this pathway.

Mechanisms of antinatriuresis during low-frequency renal nerve stimulation in anesthetized dogs

1985 ◽  
Vol 249 (3) ◽  
pp. R360-R367
Author(s):  
J. L. Osborn ◽  
R. J. Roman ◽  
R. W. Harland
Keyword(s):  
Sodium Bicarbonate ◽  
Nerve Stimulation ◽  
Low Frequency ◽  
Acid Base Balance ◽  
Renal Nerve ◽  
Bicarbonate Reabsorption ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation ◽  
Bicarbonate Infusion ◽  
Sodium Bicarbonate Infusion

The influence of 1.0 Hz renal nerve stimulation (RNS) on the renal excretion of sodium and bicarbonate was determined in anesthetized dogs before and during inhibition of renal bicarbonate reabsorption. RNS decreased both urinary sodium and bicarbonate excretion without changing arterial pressure, renal blood flow, or glomerular filtration rate. Pharmacological blockade of bicarbonate reabsorption with acetazolamide prevented RNS-induced decreases in bicarbonate excretion and reduced the antinatriuretic response. Physiological blockade of tubular bicarbonate reabsorption with intrarenal sodium bicarbonate infusion (1 M) abolished both the antinatriuretic response to RNS and the decrease in bicarbonate excretion. This physiological blockade of neurogenic antinatriuresis resulted from alkalinization of the urine and/or peritubular blood rather than an increase in filtered sodium load, because during intrarenal infusion of 1 M sodium chloride RNS concomitantly decreased sodium and urinary bicarbonate excretion. Since antinatriuretic responses and the decrease in bicarbonate excretion response to RNS were significantly decreased by blockade of bicarbonate reabsorption (with acetazolamide and intrarenal sodium bicarbonate infusion), antinatriuresis during RNS is partly mediated by a mechanism dependent on intact bicarbonate reabsorption. The data suggest that renal nerve activity may participate in the normal regulation of acid-base balance via changes in bicarbonate excretion.

scholarly journals Ingestion of Sodium Bicarbonate (NaHCO3) Following a Fatiguing Bout of Exercise Accelerates Postexercise Acid-Base Balance Recovery and Improves Subsequent High-Intensity Cycling Time to Exhaustion

2017 ◽  
Vol 27 (5) ◽  
pp. 429-438 ◽  
Author(s):  
Lewis A. Gough ◽  
Steven Rimmer ◽  
Callum J. Osler ◽  
Matthew F. Higgins
Keyword(s):  
Sodium Bicarbonate ◽  
Body Mass ◽  
High Intensity ◽  
Recovery Period ◽  
Time To Exhaustion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Experimental Trials ◽  
Cycling Time

This study evaluated the ingestion of sodium bicarbonate (NaHCO3) on postexercise acid-base balance recovery kinetics and subsequent high-intensity cycling time to exhaustion. In a counterbalanced, crossover design, nine healthy and active males (age: 23 ± 2 years, height: 179 ± 5 cm, body mass: 74 ± 9 kg, peak mean minute power (Wpeak) 256 ± 45 W, peak oxygen uptake (V̇O2peak) 46 ± 8 ml.kg-1.min-1) performed a graded incremental exercise test, two familiarization and two experimental trials. Experimental trials consisted of cycling to volitional exhaustion (TLIM1) at 100% WPEAK on two occasions (TLIM1 and TLIM2) interspersed by a 90 min passive recovery period. Using a double-blind approach, 30 min into a 90 min recovery period participants ingested either 0.3 g.kg-1 body mass sodium bicarbonate (NaHCO3) or a placebo (PLA) containing 0.1 g.kg-1 body mass sodium chloride (NaCl) mixed with 4 ml.kg-1 tap water and 1 ml.kg-1 orange squash. The mean differences between TLIM2 and TLIM1 was larger for PLA compared with NaHCO3 (-53 ± 53 vs. -20 ± 48 s; p = .008, d = 0.7, CI =-0.3, 1.6), indicating superior subsequent exercise time to exhaustion following NaHCO3. Blood lactate [Bla-] was similar between treatments post TLIM1, but greater for NaHCO3 post TLIM2 and 5 min post TLIM2. Ingestion of NaHCO3 induced marked increases (p < .01) in both blood pH (+0.07 ± 0.02, d = 2.6, CI = 1.2, 3.7) and bicarbonate ion concentration [HCO3-] (+6.8 ± 1.6 mmo.l-1, d = 3.4, CI = 1.8, 4.7) compared with the PLA treatment, before TLIM2. It is likely both the acceleration of recovery, and the marked increases of acid-base after TLIM1 contributed to greater TLIM2 performance compared with the PLA condition.

An Approach to the Problems of Acid-Base Balance

1970 ◽  
Vol 39 (2) ◽  
pp. 169-182 ◽  
Author(s):  
C. T. Kappagoda ◽  
R. J. Linden ◽  
H. M. Snow
Keyword(s):  
Sodium Bicarbonate ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Titration Curves ◽  
Base Parameters ◽  
Base Balance ◽  
Acid Base Disturbance ◽  
Direct Extrapolation

1. The existing methods for assessing states of acidosis are discussed with particular reference to non-respiratory acidosis. Most of these methods are based either on the Henderson—Hasselbalch equation or on the direct extrapolation of in vitro studies on blood to the whole animal. The evidence available shows that these methods cannot be used to obtain an accurate assessment of disturbances of acid-base balance in the whole animal. 2. The experiments were designed to investigate the acid-base parameters of an animal when a respiratory acidosis was superimposed on a non-respiratory acidosis caused by the infusion of n HCl; from these experiments it was possible to construct CO2 titration curves at various levels of non-respiratory acidosis. 3. A scheme which is based upon the CO2 titration curves, has been proposed for assessing an acute acid-base disturbance in terms of its respiratory and non-respiratory components. 4. The use of sodium bicarbonate to correct a non-respiratory acidosis was investigated, and it was shown that the amount of sodium bicarbonate required varied with the rate of infusion. No firm predictions could be made regarding the dose of bicarbonate required, but from the results of the present experiments an infusion rate of 0·1 mEq kg−1 min−1 is recommended in dogs.

Differentiation of the effects of protein status and acid-base balance on the appetite of sheep for lucerne silage

1992 ◽  
Vol 118 (2) ◽  
pp. 249-257 ◽  
Author(s):  
L. E. Phillip ◽  
M. V. Simpson
Keyword(s):  
Organic Matter ◽  
Food Intake ◽  
Sodium Bicarbonate ◽  
Ammonium Chloride ◽  
Ammonium Bicarbonate ◽  
Acid Base Balance ◽  
Acid Base ◽  
Protein Status ◽  
Base Balance ◽  
Voluntary Intake

SUMMARYFive cross-bred Suffolk lambs (liveweight 24–29 kg) were fed lucerne silage and made acidotic or offered supplemental protein with the objective of determining the effects of acidosis and amino acid undersupply on food intake from silage. In this study, at McGill University, Quebec, Canada in January 1989, lucerne silage (25% DM) was supplemented with equimolar amounts (450 mmol/kg DM) of ammonium chloride, ammonium bicarbonate and sodium bicarbonate; fishmeal was added at 100 g/kg silage DM. The lambs were fedad libitumaccording to a 5 × 5 Latin square with 21-day periods.Digestibility of organic matter (OM) from silage ranged from 78 to 82% and was not significantly affected by diet (P> 0·05). Voluntary intake of digestible organic matter (DOM) from silage was. Fishmeal supplementation of lucerne silage improved nitrogen retention (P> 0·05) but not intake of DOM. The addition of ammonium chloride to silage reduced blood concentration (p< 0·05) and urinary output of HCO3, increased ammonia excretion in urine (P< 0·05), and depressed intake of DOM (P< 0·05). Ammonium bicarbonate also reduced voluntary intake of DOM (P< 0·05) but had no significant effect (P> 0·05) on the acid-base status of the lambs. Sodium bicarbonate depressed food intake but had no significant effect on measures of acid-base balance.The results suggest that metabolic acidosis is not an underlying mechanism restricting food intake by sheep and that neither acid-base imbalance nor inadequate protein status is likely to explain the limitation in food intake from ensiled lucerne.

Complementary role of citrate and bicarbonate excretion in acid-base balance in the rat

1988 ◽  
Vol 255 (1) ◽  
pp. F182-F187 ◽  
Author(s):  
A. M. Kaufman ◽  
T. Kahn
Keyword(s):  
Sodium Bicarbonate ◽  
Potassium Chloride ◽  
Metabolic Alkalosis ◽  
Reciprocal Relationship ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Chloride Depletion ◽  
Base Balance

Studies were performed to evaluate whether alterations in the excretion of citrate, a metabolic precursor of bicarbonate, play a quantitatively important role in acid-base balance during bicarbonate feeding in the rat. Potassium depletion (K-DEPL), chloride depletion (Cl-DEPL), or potassium plus chloride depletion (KCl-DEPL) was produced by eliminating potassium, chloride, or potassium chloride from the diet. After 3 days of depletion, sodium bicarbonate (4,000 mueq/24 h) was added to the diet for 7 days. In all groups plasma bicarbonate concentration increased minimally during bicarbonate administration and was similar to normal controls receiving bicarbonate. In K-DEPL, citrate excretion was less than normal but bicarbonate excretion was greater than normal. In Cl-DEPL, bicarbonate excretion was less than normal but citrate excretion was greater than normal. In KCl-DEPL, bicarbonate and citrate excretion were similar to normal. Sodium bicarbonate was also administered to K-DEPL and KCl-DEPL rats in which plasma bicarbonate concentration averaged 32.9 meq/1. The reciprocal relationship between citrate and bicarbonate excretion was not altered by the profound metabolic alkalosis. Again, plasma bicarbonate concentration changed little with sodium bicarbonate administration. These studies suggest that the ability to excrete a base load remains intact despite potassium or chloride depletion or metabolic alkalosis. Complementary alterations of citrate and bicarbonate excretion play an important role in acid-base balance under these conditions.

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